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Papilledema describes optic disc swelling (usually bilateral) arising from raised intracranial pressure. Due to its serious nature, there is a fear of underdiagnosis; hence, one major stumbling points is correct identification, which typically requires a thorough ocular examination including visual field testing. In this episode, Kait Nevel, MD speaks with Susan P. Mollan, MBChB, PhD, FRCOphth, author of the article “Papilledema” in the Continuum® April 2025 Neuro-ophthalmology issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Mollan is a professor and neuro-ophthalmology consultant at University Hospitals Birmingham in Birmingham, United Kingdom. Additional Resources Read the article: Papilledema Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @IUneurodocmom Guest: @DrMollan 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 Nevel: Hello, this is Dr Kait Nevel. Today I'm interviewing Dr Susan Mollan about her article Papilledema Diagnosis and Management, which appears in the April 2025 Continuum issue on neuro-ophthalmology. Susie, welcome to the podcast, and please introduce yourself to our audience. Dr Mollan: Thank you so much, Kait. It's a pleasure to be here today. I'm Susie Mollan, I'm a consultant neuro-ophthalmologist, and I work at University Hospitals Birmingham- and that's in England. Dr Nevel: Wonderful. So glad to be talking to you today about your article. To start us off, can you please share with us what you think is the most important takeaway from your article for the practicing neurologist? Dr Mollan: I think really the most important thing is about examining the fundus and actually trying to visualize the optic nerves. Because as neurologists, you're really acutely trained in examining the cranial nerves, and often people shy away from looking at the eyes. And it can give people such confidence when they're able to really work out straightaway whether there's going to be a problem or there's not going to be a problem with papilledema. And I guess maybe a little bit later on we can talk about the article and tips and tricks for looking at the fundus. But I think that would be my most important thing to take away. Dr Nevel: I'm so glad that you started with that because, you know, that's something that I find with trainees in general, that they often find one of the more daunting or challenging aspects of learning, really, how to do an excellent neurological exam is examining the fundus and feeling confident in diagnosing papilledema. What kind of advice do you give to trainees learning this skill? Dr Mollan: So, it really is practice and always carrying your ophthalmoscope with you. There's lots of different devices that people can choose to buy. But really, if you have a direct ophthalmoscope, get it out in the ward, get it out in clinic. Look at those patients that you'd know have alternative diagnosis, but it gives you that practice. I also invite everybody to come to the eye clinic because we have dilated patients there all the time. We have diabetic retinopathy clinics, and it makes it really easy to start to acquire those skills because I think it's very tricky, because you're getting a highly magnified view of the optic nerve and you've got to sort out in your head what you're actually looking at. I think it's practice. and then use every opportunity to really look at the fundus, and then ask your ophthalmology colleagues whether you can go to clinic. Dr Nevel: Wonderful advice. What do you think is most challenging about the evaluation of papilledema and why? Dr Mollan: I think there are many different aspects that are challenging, and these patients come from lots of different areas. They can come from the family doctor, they can come from an optician or another specialist. A lot of them can have headache. And, as you know, headache is almost ubiquitous in the population. So, trying to pull out the sort of salient symptoms that can go across so many different conditions. There's nothing that's pathognomonic for papilledema other than looking at the optic nerves. So, I think it's difficult because the presentation can be difficult. The actual history can be challenging. There are those rare patients that don't have headache, don't have pulsatile tinnitus, but can still have papilledema. So, I think it- the most challenging thing is actually confirming papilledema. And if you're not able to confirm it, getting that person to somebody who's able to help and confirm or refute papilledema is the most important thing. Dr Nevel: Yeah, right. Because you talk in your article the importance of distinguishing between papilledema and some other diagnoses that can look like papilledema but aren't papilledema. Can you talk about that a little bit? Dr Mollan: Absolutely. I think in the article it's quite nice because we were able to spend a bit of time on a big table going through all the pseudopapilledema diagnoses. So that includes people with shortsightedness, longsightedness, people with optic nerve head drusen. And we've been very fortunate in ophthalmology that we now have 3D imaging of the optic nerve. So, it makes it quite clear to us, when it's pseudopapilledema, it's almost unfair when you're using the direct ophthalmoscope that you don't get a cross sectional image through that optic nerve. So, I'd really sort of recommend people to delve into the article and look at that table because it nicely picks out how you could pick up pseudopapilledema versus papilledema. Dr Nevel: Perfect. In your article, you also talk about what's important to think about in terms of causes of papilledema and what to evaluate for. Can you tell us, you know, when you see someone who you diagnose with papilledema, what do you kind of run through in terms of diagnostic tests and things that you want to make sure you're evaluating for or not missing? Dr Mollan: Yeah. So, I think the first thing is, is once it's confirmed, is making sure it's isolated or whether there's any additional cranial nerve palsies. So that might be particularly important in terms of double vision and a sixth nerve palsy, but also not forgetting things like corneal sensation in the rest of the cranial nerves. I then make sure that we have a blood pressure. And that sounds a bit ridiculous in this day and age because everybody should have a blood pressure coming to clinic or into the emergency room. But sometimes it's overlooked in the panic of thinking, gosh, I need to investigate this person. And if you find that somebody does have malignant hypertension, often what we do is we kind of stop the investigational pathway and go down the route of getting the medics involved to help with lowering the blood pressure to a safe level. I would then always think about my next thing in terms of taking some bloods. I like to rule out anemia because anemia can coexist in a lot of different conditions of raised endocranial pressure. And so, taking some simple blood such as a complete blood count, checking the kidney function, I think is important in that investigational pathway. But you're not really going to stop there. You're going to move on to neuroimaging. It doesn't really matter what you do, whether you do a CT or an MRI, it's just getting that imaging pretty much on the same day as you see the patient. And the key point to that imaging is to do venography. And you want to rule out a venous sinus thrombosis cause that's the one thing that is really going to cause the patient a lot of morbidity. Once your neuroimaging is secure and you're happy, there's no structural lesion or a thrombosis, it's then reviewing that imaging to make sure it's safe to proceed with lumbar puncture. And so, we would recommend the lumbar puncture in the left lateral decubitus position and allowing the patient to be as calm and relaxed as possible to be able to get that accurate opening pressure. Once we get that, we can send the CSF for contents, looking for- making sure they don't have any signs of meningitis or raised protein. And then, really, we're at that point of saying, you know, we should have a secure diagnosis, whether it would be a structural lesion, venous sinus thrombosis, or idiopathic intracranial hypertension. Dr Nevel: Wonderful. Thank you for that really nice overview and, kind of, diagnostic pathway and stepwise thought process in the evaluations that we do. There are several different treatments for papilledema that you go through in your article, ranging from surgical to medication options. When we're taking care of an individual patient, what factors do you use to help guide you in this decision-making process of what treatment is best for the patient and how urgent treatment is? Dr Mollan: I think that's a really important question because there's two things to consider here. One is, what is the underlying diagnosis? Which, hopefully, through the investigational save, you'll have been able to achieve a secure diagnosis. But going along that investigational pathway, which determines the urgency of treatment, is, what's happening with the vision? If we have somebody where we're noting that the vision is affected- and normally it's actually through a formal visual field. And that's really challenging for lots of people to get in the emergency situation because syndromes of raised endocranial pressure often don't cause problems with the visual acuity or the color vision until it's very late. And also, you won't necessarily get a relative afferent papillary defect because often it's bilateral. So I really worry if any of those signs are there in somebody that may have papilledema. And so, a lot rests on that visual field. Now, we're quite good at doing confrontational visual fields, but I would say that most neurologists should be carrying pins to be able to look at the visual fields rather than just pointing fingers and quadrants if you're not able to get a formal visual field early. It's from that I would then determine if the vision is affected, I need to step up what I'm going to do. So, I think the sort of next thing to think about is that sort of vision. So, if we have somebody who, you know, you define as have severe sight loss at the point that you're going through this investigational pathway, you need to get an ophthalmologist or a neuro-ophthalmologist on board to help discuss either the surgery teams as to whether you need to be heading towards an intervention. And there are a number of different types of intervention. And the reason why we discuss it in the article---and we'll also be discussing it in a future issue of Continuum---is there's not high-class evidence to suggest one surgery over another surgery. We may touch on this later. So, we've got our patients with severe visual loss who we need to do something immediately. We may have people where the papilledema is moderate, but the vision isn't particularly affected. They may just have an enlarged blind spot. For those patients, I think we definitely need to be thinking about medical therapy and talking to them about what the underlying cause is. And the commonest medicine to use for raised endocranial pressure in this setting is acetazolamide, a carbonic anhydrous inhibitor. And I think that should be started at the point that you believe somebody has moderate papilledema, with a lot of discussion around the side effects of the medicine that we go into the article and also the fact that a lot of our patients find acetazolamide in an escalating dose challenging. There are some patients with very mild papilledema and no visual change where I might say, hey, I don't think we need to start treatment immediately, but you need to see somebody who understands your disease to talk to you about what's going on. And generally, I would try and get somebody out of the emergency investigational pathway and into a formal clinic as soon as possible. Dr Nevel: Thank you so much for that. One thing that I was wondering that we see clinically is you get a consult for a patient, maybe, who had an isolated episode of vertigo, back to their normal self, completely resolved… but incidentally, somebody ordered an MRI. And that MRI, in the report, it says partially empty sella, slight flattening of the posterior globe, concerns for increased intracranial pressure. What should we be doing with these patients who, you know, normal neurological exam, maybe we can't detect any definite papilledema on our endoscopic exam. What do you think the appropriate pathway is for those patients? Dr Mollan: I think it's really important. The more neuroimaging that we're doing, we're sort of seeing more people with signs that are we don't believe are normal. So, you've mentioned a few, the sort of partially empty sella, empty sella, tortuosity of the optic nerves, flattening of the globes, changes in transverse sinus. And we have quite a nice, again, table in the article that talks about these signs. But they have really low sensitivity for a diagnosis of raised endocranial pressure and isolation. And so, I think it's about understanding the context of which the neuroimaging has been taken, taking a history and going back and visiting that to make sure that they don't have escalating headache. And also, as you said, rechecking the eye nerves to make sure there's no papilledema. I think if you have a good examination with the direct ophthalmoscope and you determine that there's no papilledema, I would be confident to say there's no papilledema. So, I don't think they need to necessarily cry doubt. The ophthalmology offices, we certainly are having quite a few additional referrals, particularly for this, which we kind of called IIH-RAD, where patients are coming to us for this exclusion. And I think, in the intervening time, patients can get very anxious about having a sort of MRI artifact picked up that may necessarily mean a different diagnosis. So, I guess it's a little bit about reassurance, making sure we've taken the appropriate history and performed the examination. And then knowing that actually it's really a number of different signs that you need to be able to confidently diagnose raised ICP, and also the understanding that sometimes when people have these signs, if the ICP reduces, those signs remain. You know, we're learning an awful lot more about MRI imaging and what's normal, what's within normal limits. So, I think reassurance and sensible medical approach. Dr Nevel: Absolutely. In the section in your article on idiopathic intracranial hypertension, you spend a little bit of time talking about how important it is that we sensitively approach the topic of potential weight loss for those patients who are overweight. How do you approach that discussion in your clinic? Because I think it's an important part of the holistic patient care with that condition. Dr Mollan: I think this is one of the things that we've really listened to the patients about over the last number of years where we recognize that in an emergency situation, sometimes we can be quite quick to sort of say, hey, you have idiopathic endocranial hypertension and weight loss is, you know, the best treatment for the condition. And I think in those circumstances, it can be quite distressing to the patient because they feel that there's a lot of stigma attached around weight management. So, we worked with the patient group here at IIH UK to really come up with a way of a signposting to our patients that we have to be honest that there is a link, you know, a strong evidence that weight gain and body shape change can cause someone to fall into a diagnosis of IIH. And we know that weight loss is really effective with this condition. So, I think where I've learned from the patients is trying to use language that's less stigmatizing. I definitely signpost that I'm going to talk about something sensitive. So, I say I'm going to talk about something sensitive and I'm going to say, do you know that this condition is related to body shape change? And I know that if I listen to this podcast in a couple of years, I'm sure my words will have changed. And I think that's part of the process, is learning how to speak to people in an ever-changing language. And they think that sort of signpost that you're going to talk about something sensitive and you're going to talk about body shape change. And then follow up with, are you OK with me talking about this now? Is it something you want to talk about? And the vast majority of people say, yes, let's talk about it. There'll be a few people that don't want to talk about it. And I usually come in quite quickly, say, is it OK if I mention it at the next consultation? Because we have a duty of care to sort of inform our patients, but at the same time we need to take them on that journey to get them back to health, and they need to be really enlisted in that process. Dr Nevel: Yeah, I really appreciate that. These can be really difficult conversations and uncomfortable conversations to have that are really important. And you're right, we have a duty as medical providers to have these conversations or inform our patients, but the way that we approach it can really impact the way patients perceive not only their diagnosis, but the relationship that we have with our patients. And we always want that to be a positive relationship moving forward so that we can best serve our patients. Dr Mollan: I think the other thing as well is making sure that you've got good signposts to the professionals. And that's what I say, because people then say to me, well, you know, kind of what diet should I be on? What should I be doing? And I say, well, actually, I don't have professional experience with that. I'm, I'm very fortunate in my hospital, I'm able to send patients to the endocrine weight management service. I'm also able to send patients to the dietetic service. So, it's finding, really, what suits the patient. Also what's within licensing in your healthcare system to be able to provide. But not being too prescriptive, because when you spend time with weight management professionals, they'll tell you lots of different things about diets that people have championed and actually, in randomized controlled trials, they haven't been effective. I think it's that signpost really. Dr Nevel: Yeah, absolutely. So, could you talk a little bit about what's going on in research in papilledema or in this area, and what do you think is up-and-coming? Dr Mollan: I think there's so much going on. Mainly there's two parts of it. One is image analysis, and we've had some really fantastic work out of the Singapore group Bonsai looking at a machine learning decision support tool. When people take fundal pictures from a normal fundus camera, they're able to say with good certainty, is this papilledema, is this not papilledema? But more importantly, if you talk to the investigators, something that we can't tell when we look in is they're able to, with quite a high level of certainty, say, well, this is base occupying lesion, this is a venous sinus thrombosis, and this is IIH. And you know, I've looked at thousands and thousands of people's eyes and that I can't tell why that is. So, I think the area of research that is most exciting, that will help us all, is this idea about decision support tools. Where, in your emergency pathway, you're putting a fundal camera in that helps you be able to run the image, the retina, and also to try and work out possibly what's going on. I think that's where the future will go. I think we've got many sort of regulatory steps and validation and appropriate location of a learning to go on in that area. So, that's one side of the imaging. I think the other side that I'm really excited about, particularly with some of the work that we've been doing in Birmingham, is about treatment. The surgical treatments, as I talked about earlier… really, there's no high-class evidence. There's a number of different groups that have been trying to do randomized trials, looking at stenting versus shunting. They're so difficult to recruit to in terms of trials. And so, looking at other treatments that can reduce intracranial pressure. We published a small phase two study looking at exenatide, which is a glucagon-like peptide receptor agonist, and it showed in a small group of patients living with IIH that it could reduce the intracranial pressure two and a half hours, twenty-four hours, and also out to three months. And the reason why this is exciting is we would have a really good acute therapy---if it's proven in Phase III trials---for other diseases, so, traumatic brain injury where you have problems controlling ICP. And to be able to do that medically would be a huge breakthrough, I think, for patient care. Dr Nevel: Yeah, really exciting. Looking forward to seeing what comes in the future then. Wonderful. Well, thank you so much for chatting with me today about your article. I really enjoyed learning more from you during our conversation today and from your article, which I encourage all of our listeners to please read. Lots of good information in that article. So again, today I've been interviewing Dr Susie Mollan about her article Papilledema Diagnosis and Management, which appears in the most recent issue of Continuum on neuro-ophthalmology.Please be sure to check out Continuum episodes from this and other issues. And thank you to our listeners for joining us today. Thank you, Susie. Dr Mollan: Thank you so much. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

A podcast epizódban Dr. Szőke-Milinte Enikő, az Eszterházy Károly Katolikus Egyetem Neveléstudományi Intézetének tanszékvezetője és a Neveléstudományi Doktori Program igazgatója, Dr. Fodor Richárd, a Tanuláskutató Intézet kutatásvezetője, valamint Dr. Fekete Áron, az intézet projektmenedzsere beszélgetnek az információs és médiaműveltség 21. századi kihívásairól és lehetőségeiről.A beszélgetés során hazai és nemzetközi tapasztalatok megosztása mellett szó esik a szaktárgyi megközelítések szerepéről, valamint azokról a készségekről és pedagógiai eszközökről, amelyek hozzájárulhatnak a tanulók információs és médiaműveltségének fejlesztéséhez. A résztvevők a jövőbe tekintve azokat a kihívásokat is körbejárják, amelyekkel ezen a területen a következő évtizedben szembesülhetünk.Résztvevők:Dr. Szőke-Milinte Enikő - Eszterházy Károly Katolikus Egyetem Neveléstudományi Intézetének tanszékvezetője és a Neveléstudományi Doktori Program igazgatójaFekete Áron – Tanuláskutató Intézet projektmenedzsereFodor Richárd - Tanuláskutató Intézet kutatásvezetőjeAz MCC Podcast adásaiban érdekes emberekkel izgalmas témákról beszélgetünk. Feldolgozzuk a közélet, a gazdaság, a társadalom fontosabb aktuális történéseit, de olyan kérdéseket is napirendre veszünk, mint például a művészet, a család vagy a vallás. Vendégeink között oktatóink, kutatóink, vendégelőadóink kapnak helyet. Mindenkinek kellemes időtöltést és szellemi feltöltődést kívánunk.

A kreatív nevelés útjai

2 - Egy diákcsíny megtorlásaként megverte az egyik diákját a nevelőtanára by Balázsék

Zenei nevelés, Dr. Káel Norbert zongoraművész - Valódi Nők 2025. 03. 26. - 8 óra by MannaFM

Nonepileptic events are prevalent and highly disabling, and multiple pathophysiologic mechanisms for these events have been proposed. Multidisciplinary care teams enable the efficient use of individual expertise at different treatment stages to address presentation, risk factors, and comorbidities.   In this episode, Kait Nevel, MD, speaks with Adriana C. Bermeo-Ovalle, MD, an author of the article “A Multidisciplinary Approach to Nonepileptic Events,” in the Continuum® February 2025 Epilepsy issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Bermeo-Ovalle is a professor and vice-chair for Faculty Affairs in the Department of Neurological Sciences at Rush University Medical Center in Chicago, Illinois. Additional Resources Read the article: A Multidisciplinary Approach to Nonepileptic Events Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @IUneurodocmom 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 Nevel: Hello, this is Dr Kait Nevel. Today I'm interviewing Dr Adriana Bermeo about her article on a multidisciplinary approach to nonepileptic events, which she wrote with Dr Victor Petron. This article appears in the February 2025 Continuum issue on epilepsy. Welcome to the podcast, and please introduce yourself to our audience. Dr Bermeo-Ovalle: Hello Dr Neville, it's a pleasure to be here. Thank you very much for inviting me. My name is Adriana Bermeo and I'm an adult epileptologist at Rush University Medical Center in Chicago, and I am also the codirector of the NEST clinic, which is a treatment clinic for patients with nonepileptic seizures within our level four epilepsy center. Dr Nevel: Wonderful. Well, thank you so much for being here, and I can't wait to talk to you about your article and learn a little bit about NEST, maybe, during our conversation, and how you approach things. To start us off talking about your article today, could you share with us what you think is the most important takeaway from your article for the practicing neurologist? Dr Bermeo-Ovalle: Wonderful. There's some messages that I would like people to get from working with patients with functional neurologic disorders in general. The first one is that functional neurologic disorders are very common in presentation in the neurologic clinic, almost no matter what your practice of self-specialty care is. The second is that for people who treat patients primarily with seizures or epilepsy, they account for between 5 to 10% of our patients in the clinic, but about 30% of our patients in our epilepsy monitoring unit because the seizures typically do not respond to anti-seizure medication management. Also, that in order to diagnose them, you don't need to have a neuropsychological stress already be available for the patient or the clinician. And the most important thing is that there are available treatments for these patients and that there are options that we can offer them for them to have less seizures and to be more integrated to whatever activities they want to get integrated. Dr Nevel: Wonderful. What do you think a practicing neurologist might find surprising after reading your article? Dr Bermeo-Ovalle: I think still many neurologists feel very hopeless when they see patients with these conditions. They do not have very good answers right away for the patients, which is frustrating for the neurologist. And they don't think there's too much they can do to help them other than send them somewhere else, which is very difficult for the neurologist and is crushing to the patients to see these doctors that they're hoping to find answers to and then just find that there's not much to do. But what I want neurologists to know is that we are making strides in our understanding of the condition and that there are effective treatments available. And I hope that after reading this and engaging with this conversation, they will feel curious, even hopeful when they see the next patient in the clinic. Dr Nevel: Yeah, absolutely. I find the history of nonepileptic seizures really interesting and I enjoyed that part of your article. How has our understanding of nonepileptic seizures evolved over the centuries, and how does our current understanding of nonepileptic seizures inform the terminology that we use? Dr Bermeo-Ovalle: Yeah. The way we name things and the way we offer treatment goes along to how we understand things. So, the functional seizures and epileptic seizures were understood in ancient times as possession from the spirits or the demons or the gods, and then treatments were offered to those kind of influences and that continues to happen with functional seizures. So, we go through the era when this was thought to be a women-only condition that was stemming from their reproductive organs and then treatments accordingly were presented. And later on with Charcot and then Freud, they evolved to even conversion disorders, which is one understanding the most conversion disorders, which is one of the frameworks where this condition has been treated with psychotherapy, psychoanalytic psychotherapy. And in our current understanding, we understand functional neurologic disorders in general as a more like a connection, communication network disorder, between areas of the brain that modulate emotional processing and movement control. And therefore, our approach these days is much more geared towards rehabilitation. You know, I think that's the evolution of thinking in many different areas. And as we learn more, we will be acquiring more tools to help our patients. Dr Nevel: Yeah, great. Thanks so much for that answer. Just reading the historical information that you have in your article, you can imagine a lot of stigma with this diagnosis too over time, and that- I think that that's lessening. But I was wondering if you could talk about that a little bit. How do we approach that with our patients and loved ones, any stigma that they might feel or perceive from being diagnosed with nonepileptic seizures? Dr Bermeo-Ovalle: Thank you for asking that question. Stigma is actually an important problem even for people living with epilepsy. There's still a lot of misunderstanding of what epilepsy is and how it affects people, and that people living with epilepsy can live normal, healthy lives and do everything they want to do with appropriate treatment. And if a stigma is still a problem with epilepsy, it is a huge problem for patients living with functional neurologic symptoms in general, but particularly with functional seizures or nonepileptic seizures. Because the stigma in this population is even perpetuated by the very people who are supposed to help them: physicians, primary care doctors, emergency room doctors. Unfortunately, the new understanding of this condition has not gotten to everybody. And these patients are often even blamed for their symptoms and for the consequences of their symptoms and of their seizures in their family members, in their job environment, in their community. Living with that is really, really crushing, right? Even people talk about, a lot about malingering. They come back about secondary gain. I can tell you the patients I see with functional seizures gain nothing from having this condition. They lose, often, a lot. They lose employment, they lose ability to drive. They lose their agency and their ability to function normally in society. I do think that the fight- the fighting of stigma is one that we should do starting from within, starting from the healthcare community into our understanding of what these patients go through and what is causing their symptoms and what can we do to help them. So there's a lot of good work to be done. Dr Nevel: Absolutely. And it starts, like you said, with educating everybody more about nonepileptic seizures and why this happens. The neurobiology, neurophysiology of it that you outlined so nicely in your article, I'm going to encourage the listeners to look at Figure 1 and 4 for some really nice visualization of these really complex things that we're learning a lot about now. And so, if you don't mind for our listeners, kind of going over some of the neurobiology and neurophysiology of nonepileptic seizures and what we're learning about it. Dr Bermeo-Ovalle: Our understanding of the pathophysiology of functional neurologic seizure disorder is in its infancy at this point. The neurobiological processes that integrate emotional regulation and our responses to it, both to internal stimuli and to external stimuli and how they affect our ability to have control over our movement---it's actually amazing that we as neurologists know so little about these very complex processes that the brain do, right? And for many of us this is the reason why we're in neurology, right, to be at the forefront of this understanding of our brain. So, this is in that realm. It is interesting what we have learned, but it's amazing all that we have to learn. There is the clear relationship between risk factors. So, we know patients with functional neurologic symptom disorder and with functional seizures, particularly in many different places in the world with many different beliefs, relationship to their body, to their expression of their body, have this condition no matter how different they are. And also, we know that they have commonalities. For example, traumatic experiences that are usually either very strong traumatic experiences or very pervasive traumatic experiences or recurrent over time of different quality. So, we are in the process of understanding how these traumatic experiences actually inform brain connectivity and brain development that result in this lack of connections between brain areas and the expression of them, and that result in this kind of disorder. I wish I can tell you more about it or that I would understand more about it, but I am just grateful for the work that has been done so that we can understand more and therefore have more to offer to these patients and their families and their communities that are support. Dr Nevel: Yeah, absolutely. That's always the key, and just really exciting that we're starting to understand this better so that we can hopefully treat it better and inform our patients better---and ourselves. Can you talk to us a little bit about the multidisciplinary team approach and taking care of patients with nonepileptic seizures? Who's involved, what does best practice model look like? You have a clinic there, obviously; if you could share with us how your clinic runs in the multidisciplinary approach for care of these patients? Dr Bermeo-Ovalle: The usual experience of patients dealing with functional seizures, because this is a condition that has neurological symptoms and psychiatric symptoms, is that they go to the neurologist and the neurologist does not feel sufficiently able to manage all the psychiatric comorbidities of the condition. So, the patient is sent to psychiatry. The psychiatry really finds themselves very hopeless into handling seizures, which is definitely not their area of expertise, and these patients then being- “ping-ponging” from one to the other, or they are eventually sent to psychotherapy and the psychotherapist doesn't know what they're dealing with. So, we have found with- and we didn't come up with this. We had wonderful support from other institutions who have done- been doing this for a longer time. That bringing all of this specialty together and kind of situating ourselves around the patient so that we can communicate our questions and our discrepancies and our decision between who takes care of what without putting that burden on the patient is the best treatment not only for the patient, who finally feels welcome and not burden, but actually for the team. So that the psychiatrist and the neurologist support the psychotherapist who does the psychotherapy, rehabilitation, mind the program. And we also have the support and the involvement of neuropsychology. So, we have a psychiatrist, a neurologist, social worker, psychotherapist and neuropsychology colleagues. And together we look at the patient from everywhere and we support each other in the treatment of the patient, keeping the patient in the middle and the interest of the patient in the middle. And we have found that that approach has helped our patients the best, but more importantly, makes our job sustainable so that none of us is overburdened with one aspect of the care of the patient and we feel supported from the instances that is not our most comfortable area. So that is one model to do it. There's other models how to do it, but definitely the interdisciplinary care is the way to go so far for the care of patients with functional neurologic symptom disorders and with functional seizures or nonepileptic seizures in particular. Dr Nevel: Yeah, I can see that, that everybody brings their unique expertise and then doesn't feel like they're practicing outside their, like you said, comfort zone or scope of practice. In these clinics---or maybe this happens before the patient gets to this multidisciplinary team---when you've established a diagnosis of nonepileptic seizures, what's your personal approach or style in terms of how you communicate that with the patient and their loved ones? Dr Bermeo-Ovalle: It is important to bring this diagnosis in a positive term. You know, unfortunately the terminology question is still out and there's a lot of teams very invested into how to better characterize this condition and how to- being told that you don't have something is maybe not that satisfying for patients. So, we are still working on that, but we do deliver the diagnosis in positive terms. Like, this is what you have. It's a common condition. It's shared by this many other people in the world. It's a neuropsychiatric disorder and that's why we need the joint or collaborative care from neurology and psychiatry. We know the risk factors and these are the risk factors. You don't have to have all of them in order to have this condition. These are the reasons why we think this is the condition you have. There is coexisting epilepsy and functional seizures as well. We will explore that possibility and if we get to that conclusion, we will treat these two conditions independently and we- our team is able to treat both of them. And we give them the numbers of our own clinic and other similar clinics. And with that we hope that they will be able to get the seizures under better control and back to whatever is important to them. I tell my trainees and my patients that my goals of care for patients with functional seizures are the same as my patients with epileptic seizures, meaning less seizures, less disability, less medications, less side effects, less burden of the disease. And when we communicate it in that way, patients are very, very open and receptive. Dr Nevel: Right. What do you think is a mistake to avoid? I don't know if “mistake” is necessarily the right word, but what's something that we should avoid when evaluating or managing patients with nonepileptic seizures? What's something that you see sometimes, maybe, that you think, we should do that differently? Dr Bermeo-Ovalle: I think the opportunity of engaging with these patients is probably the hardest one. Because neurologists have the credibility, they have the relationship, they have- even if they don't have a multi-disciplinary team all sitting in one room, they probably have some of the pieces of this puzzle that they can bring together by collaborating. So, I think that missing the opportunity, telling the patient, this is not what I do or this is not something that belongs to me, you need to go to a mental health provider only, I think is the hardest one and the most disheartening for patients because our patients come to us just like all patients, with hopes and with some information to share with us so that we can help them make sense of it and have a better way forward. We as neurologists know very well that we don't have an answer to all our patients, and we don't offer zero seizures to any of our patients, right? We offer our collaborative work to understand what is going on and a commitment to walk in the right direction so that we are better every day. And I do think wholeheartedly that that is something that we can offer to patients with functional seizures almost in any environment. Dr Nevel: Yeah, absolutely. And using that multidisciplinary approach and being there with your patient, moving forward in a longitudinal fashion, I can see how that's so important. What do you find most challenging and what do you find most rewarding about caring for patients with nonepileptic seizures? Dr Bermeo-Ovalle: The thing that I find more challenging are the systemic barriers that the system still places. We discuss with the patients, what is the right time to go to the emergency room or not? Because the emergency room may be a triggering environment for patients with functional seizures and it may be a place where not everybody is necessarily attuned to have this conversation. Having said that, I never tell any of my patients not to go to the emergency room because I don't know what's happening with them. As a matter of fact, we're getting a lot of information on high mortality rates in patients with functional seizures, and it's not because of suicide and is probably not related to the seizure. Maybe this is---you know, this is speculation on my part---that is because they get to more severe conditions in other things that are not the functional seizures because they just experienced the healthcare system as very hostile because we are very in many instances. So, navigating that is a little bit difficult, and I try to tell them to have the doctors call me so that I can frame it in a different way and still be there for them. But I can tell you this clinic is the most rewarding clinic of all my clinical activities. And I love with all my heart being an epileptologist and seeing my patients with epilepsy. But the number of times my patients with functional seizures say, nobody had ever explained this to me, nobody had ever validated my experience in front of my family so that I'm not- like, feel guilty myself for having this episode, I can't tell you how many times. And obviously patients who come to the nonepileptic seizure clinic already know that they come to the nonepileptic seizure clinic, so that- you can say it's a selection of patients that are already educated in this condition to come to the clinic. But I would love everybody to know managing this population can be enormously, enormously satisfying and rewarding. Dr Nevel: Especially for, I imagine, patients who have been in and out of the ER, in and out of the hospital, or seen multiple providers and make their way to you. And you're able to explain it in a way that makes sense and hopefully reduces some of that stigma maybe that they have been feeling. Dr Bermeo-Ovalle: And along with that, iatrogenic interventions, unnecessary intubations, unnecessary ICUs; like, so much. And I think, I have no superpower to do that other than understanding this condition in a different way. And by I, I mean all the providers, because I'm not alone in this. There's many, many people doing excellent work in this state. And we just need to be more. Dr Nevel: Yeah, sure. Absolutely. So, on that note, what's next in research, or what do you think will be the next big thing? What's on the horizon in this area? Dr Bermeo-Ovalle: I think the community in the functional neurologic disorder community is really hopeful that more understanding into the neurobiology of this condition will bring more people over and more neurologists willing to take it on. There was an invitation from the NIH, I think, about four or five years ago to submit proposals for research in this area in particular. So, all of those studies must be ongoing. I'm much more a clinician than a researcher myself, but I am looking forward to what all of that is going to mean for our patients. And for- I think there's other opportunities in that further understanding of the clinical manifestations of many other conditions, and for our understanding of our relationship with our patients. I feel we are more attuned to align with a disease that, when the experience of the patient- and with a disease like this, a condition like this one, we have to engage with the personal experience of the patient. What I mean by that is that we are more likely to say,  I'm an epileptologist, I'm an MS doctor, you know, and we engage with that condition. This condition, like, just makes us engaging with the symptom and with the experience of the person. And I think that's a different frame that is real and rounded into the relationship with our patients. So, I think there's so much that we can learn that can change practice in the future. Dr Nevel: Yeah. And as your article, you know, outlines, and you've outlined today during our discussion, that- how important this is for the future, that we treat these patients and help them as much as we can, that comes with understanding the condition better, because wow, I was really surprised reading your article. The mortality associated with this, the healthcare costs, how many people it affects, was just very shocking to me. So, I mean, this is a really important topic, obviously, and something that we can continue to do better in. Wonderful. Well, thank you so much. It's been really great talking to you today. Dr Bermeo-Ovalle: Thank you, Katie, I appreciate it too. Dr Nevel: So again, today I've been interviewing Dr Adriana Bermeo about her article on a multidisciplinary approach to nonepileptic events, which she wrote with Dr Victor Petron. This article 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 to our listeners for joining today.  Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Milyen férfiakat és nőket nevelünk a gyerekeinkből? - Lélekszörf 2025. 01. 25. by MannaFM

Although Alzheimer disease (AD) is the most common neurodegenerative cause of dementia, other etiologies can mimic the typical amnestic-predominant syndrome and medial temporal brain involvement. Neurologists should recognize potential mimics of AD for clinical decision-making and patient counseling. In this episode, Kait Nevel, MD, speaks with Vijay K. Ramanan, MD, PhD, an author of the article “LATE, Hippocampal Sclerosis, and Primary Age-related Tauopathy,” in the Continuum December 2024 Dementia issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Ramanan is a consultant and assistant professor of neurology in the Division of Behavioral Neurology at Mayo Clinic College of Medicine and Science in Rochester, Minnesota. Additional Resources Read the article: LATE, Hippocampal Sclerosis, and Primary Age-related Tauopathy 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 Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: IUneurodocmom Guest: @vijaykramanan Full episode transcript available here Dr Jones: This is Dr Lyle 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 Nevel: This is Dr Kait Nevel. Today I'm interviewing Dr Vijay Ramanan about his article he wrote with Dr Jonathan Graff-Radford on LATE hippocampal sclerosis and primary age-related tauopathy, which appears in the December 2024 Continuum issue on dementia. Welcome to the podcast. Vijay, can you please introduce yourself to the audience? Dr Ramanan: Thanks so much, Kait. I'm delighted to be here. So, I am a cognitive neurologist and neuroscientist at the Mayo Clinic in Rochester, Minnesota. I have roles in practice, education and research, but amongst those I see patients with cognitive disorders in the clinic. I help direct our Alzheimer's disease treatment clinic and also do research, including clinical trial involvement and some observational research on genetics and biomarkers related to Alzheimer's and similar disorders. Dr Nevel: Great, thanks for that. So, I'd like to start off by talking about why is LATE hippocampal sclerosis, why is this important for the neurologist practicing in clinic to know about these things? Dr Ramanan: That's a great question. So, if we take a step back, we know that degenerative diseases of the brain are really, really common, and they get more and more common as we get older. I think all neurologists, and in fact most clinicians and large swaths of the general public, are well aware of Alzheimer's disease, which is the most common degenerative cause of cognitive impairment in the population. But there are non-Alzheimer's degenerative diseases which can produce cognitive difficulties as well. And it's important to be aware of those disorders, of their specific presentations and their implications, in part because it's always a healthy thing when we can be as precise and confident about diagnosis and expectation with our patients as possible. I'll look to the analogy of a patient presenting with a myelopathy. As neurologists, we would all find it critical to clarify, is that myelopathy the result of a compressive spondylotic change? The result of an inflammatory disorder, of a neoplastic disorder, of an infectious disorder? It's critical to guide the patient and choose appropriate management options based on the cause of their syndrome. It would potentially harm the patient if you treated an infectious myelopathy with steroids or other immune-suppressant drugs. So, a similar principle holds in cognitive neurology. I accept with humility that we can never be 100% crystal clear certain about things in medicine, just because when you think you got it all figured out there's a curveball. But I want to get as close to that 100% as possible. And recognizing that disorders like LATE or PART can mimic the symptoms, sometimes even the imaging features of Alzheimer's disease. I think it's critical to have heightened awareness of those disorders, how they look, to be able to apply appropriate counseling and management options to patients. I think this becomes particularly critical as we move into an era of disease-specific, and sometimes disease-modifying, therapies, where applying a choice of a treatment option could have significant consequences to a patient if the thing you're treating isn't the thing that the drug is trying to accomplish. So, having awareness and spreading awareness about some of these non-AD causes of cognitive difficulty, I think, is a big mission in the field.  Dr Nevel: Yeah, that makes total sense. And kind of leaning into this, you know, trying to differentiate between these different causes of late-life amnestic cognitive impairment. You know, I'll point out to the listeners today to please read your article, but in addition to reading your article, I'd like to note that there's a really nice table in your article, Table 6-1, where you kind of go through the different causes of amnestic cognitive impairment and the different features that better fit with diagnosis X, Y, or Z, because I think it's a really nice table to reference and really easy to look at and reference back to. But on that note, what is your typical approach when you're seeing a patient in clinic, have a new referral for an older patient presenting with a predominantly progressive amnestic-type features? Dr Ramanan: Excellent question. And this is one that I think has relevance not just in a subspecialty memory clinic, but to all the clinicians who help to diagnose and manage cognitive disorders, including in primary care and general neurology and others. One principle that I think it's helpful to keep in our minds is that in cognitive neurology, no one data point takes precedence over all the others. We have a variety of information that we can gather from history, from exam, from imaging, from fluid biomarkers. And really the fun, the challenge, the reward is in piercing together that information. It's almost like being a lawyer and compiling the evidence, having possibilities on your list and raising and lowering those possibilities to get as close to the truth as you can. So, for patients with a cognitive syndrome, I think the first plank is in defining that syndrome. As you mentioned, if I'm seeing someone with a progressive amnestic-predominant syndrome, I first want to make sure, are we talking about the same thing, the patient, the care partner, and I?  Can often be helpful to ask them for some examples of what they see, because sometimes what patients may report as memory troubles may in fact reflect cognitive difficult in other parts of our mental functioning. For example, executive functioning or naming of objects. And so helpful to clarify that in the history to get a sense of the intensity and the pace of change over time, and then to pair that with a good general neurologic exam and some type of standardized assessment of their cognitive functioning. At the Mayo Clinic, where partial to the short test of mental status. There are other ways to accomplish that, such as with an MMSE or a MoCA. If I understand that the syndrome is a progressive amnestic disorder, Alzheimer's disease is the most common cause of that presentation in older adults, it deserves to be on my differential diagnosis. But there might be some other features in the story that could raise or lower those mimics on my list. So, in patients who are, say, older than the age of seventy five, disorders like LATE or PART start to rise higher on the likelihood for me, in particular if I know that their clinical course has been more slow brewing, gradually evolving. And again, most degenerative disorders we expect to evolve not over days or weeks, but over many months to many years. But in comparison with Alzheimer's disease, patients with LATE or with PART would be expected to have a little more slow change where maybe year over year they or their care partners really aren't noticing big declines. Their daily function is relatively spare. There might not be as much involvement into other non-memory cognitive domains. So, these are some of the pieces of the story that can help to perhaps isolate those other non-AD disorders on the list as being more likely and then integrating, as a next level, diagnostic testing, which helps you to rule in and rule out or support those different causes. So, for example, with LATE there can be often out of proportion to the clinical picture, out of proportion to what you see on the rest of their imaging or other profiles, very predominant hippocampal and medial temporal volume loss. And so that can be a clue in the right setting that you may not be dealing with Alzheimer's disease or pure Alzheimer's disease, but that this other entity is there. So, in the big picture, I would say being systematic, recognizing that multiple data points being put together helps you get to that confident cause or etiology of the syndrome. And in particular, taking a step back and thinking about big picture factors like age and course to help you order those elements of the differential, whether AD or otherwise. Dr Nevel: Great, thanks. In your article, you talk about different imaging modalities that can be used, as you mentioned, you know, just another piece of the puzzle, if you will, to try and put together what may be going on with the patient, and recognizing that some of these imaging techniques are imaging is special imaging, not available in a lot of places.  You know, and maybe other diagnostic type tests that could be helpful in differentiating between these different disorders may not be available, you know, for the general neurologist practicing in the community. So, what do you suggest to the general neurologist maybe practicing somewhere where they don't have access to some of these ancillary tests that could assist with a diagnosis?  Dr Ramanan: Critical question. And here I think there's not likely to be one single answer. As with most things, awareness and recognition is a good place to start. So, some of those clues that I mentioned earlier about the clinical course, about the age, the- we're talking about clinical setting there. So, comfort with and understanding that the clinical setting can help you to be more confident about, for example, LATE or PART being present in contrast to AD. That's important information. It deserves to be part of the discussion. It doesn't necessarily need other tests to have value on its own. A second piece is that tests help, in some cases, to rule in and rule out causes for cognitive difficulty. As part of a standard cognitive evaluation, we would all be interested in getting some blood tests to look for thyroid dysfunction or vitamin deficiencies. Some type of structural head imaging to rule out big strokes, tumors, bleeds. Head CT can accomplish some of that perspective. It's ideal if a brain MRI can be obtained, but again, keeping in mind, what's the primary goal of that assessment? It's to assess structure. Occasionally you can get even deeper clues into a syndrome from the MRI. For example, that very profound hippocampal or medial temporal atrophy. So, increasing awareness amongst clinicians throughout our communities to be able to recognize that change and put it in the context of what they see in other brain regions that can be affected by Alzheimer's or related disorders. For example, the parietal regions can be helpful. And recall that MRI can also be helpful in assessing for chronic cerebrovascular disease changes. This is another mimic that shows up in that table that you mentioned. And so multiple purposes can be satisfied by single tests. Now, you're absolutely right that there are additional test modalities that, perhaps in a subspecialty clinic at an academic medical center, we're very used to relying on and finding great value on; for example, glucose PET scans or sometimes fluid biomarkers from the blood or from the spinal fluid. And these are not always as widely available throughout our communities. Part of the challenge for all of us as a field is therefore to take the expertise that we have gathered in more subspecialty settings and tertiary care settings and translate and disseminate that out into our communities where we need to take care of patients. That's part of the challenge. The other challenge is in continued tool and technological development. There's a lot of optimism in our field that the availability of blood-based biomarkers relevant for Alzheimer's disease may play a part in helping to address some of the disparities in resource and access to care. You can imagine that doing a blood test to give you some high-quality information, there are going to be less barriers to doing that in many settings compared to thinking about a lumbar puncture or a PET scan, both in terms of cost to the patient as well as infrastructure to the clinicians and the care team. So I'm optimistic about a lot of those changes. In the meantime, I think there are, through both clinical evaluation and some basic testing including structural head imaging, there are clues that can help navigate these possibilities. Dr Nevel: So, let's say you have your patient in clinic, you've done your evaluation, maybe gotten some ancillary testing, and you highly suspect either LATE or PART. How do you counsel those patients and their families? How do you manage those patients moving forward who you really suspect don't have, you know, some sort of co-pathology? Dr Ramanan: So, it's- I think it's helpful to remember when patients are coming to see us, either they or the people around them have noticed an issue. And very likely it's an issue that's been brewing for a little while. I think it can be very valuable, very helpful for patients to have answers. What's the cause for the issue? Once you have answers, even if sometimes those answers are not the most welcome things or the things that you'd be looking forward to, answers give you an opportunity to grab hold of what's going on, to define a game plan. So, understanding there is a degenerative disease there, it sheds light on why that individual had had memory symptoms over the years. And it gives them a general expectation that over time on an individualized basis, but generally expecting gradually over many months to many years, there may be some worsening in some of those symptoms helps them to plan and helps them to make the adaptations that are a-ok and great to make to just help you to do the things you want to do. As much as I can, I try to put the focus here closer to how we would view things like high blood pressure or high cholesterol. Those are also chronic issues that tend to be more common as we get older, tend to get more troublesome as we get older. The goal is, know what you're dealing with and take the combination of lifestyle modifications, adaptations in your day-to-day and maybe medications to keep them as mild and as slow-changing as possible. With something like LATE, we don't have specific medication therapies to help support cognitive functioning at this time. There's a lot of hope that with additional research we will have those therapies. But even so, I think it's an important moment to emphasize some of those good healthy lifestyle habits. Staying mentally, socially and physically active, getting a good night's sleep, eating a healthy, balanced diet, keeping good control of vascular risk factors, all of that is critical to keeping the brain healthy, keeping the degenerative disease as mild and slow-brewing as possible. And understanding what some of the symptoms to expect could be. So, with LATE the syndrome tends to be very memory-predominant. There may be some trouble with maybe naming of objects or perhaps recall of emotionally salient historical knowledge, world events, but you're not expecting, at least over the short to medium term, huge intervening on other cognitive functioning. And so that can be helpful for patients to understand. So, the hope is once you know what what you're dealing with, you understand that the disease can look different from person to person. Having a general map of what to expect and what you can do to keep it in check, I think, is the goal. Dr Nevel: I agree with you 100% that it really can be helpful even if we can't, quote unquote, fix it, that for people, family, the patient have a name for what they have and kind of have some sort of idea of what to expect in the future. And they may come in thinking that they have Alzheimer's or something like that. And then, so, to get that information that this is going to be a little different, we expect this to go a little bit differently then it would if you had a diagnosis of Alzheimer's, I can see how that would be really helpful for people.  Dr Ramanan: I completely agree. And here's another challenge for us in the field when most patients have heard about Alzheimer's disease and many have perhaps even heard of dementia with Lewy bodies or frontotemporal dementia, but may not have heard of things like LATE. And they're not always easy to go online or find books that talk about these things. Having a name for it and being able to pair that with patient-friendly information is really critical. I see our appointments where we're sharing those diagnosis and making initial game plans as an initial foray into that process.  Dr Nevel: Yeah, absolutely. What is the greatest inequity or disparity that you see in taking care of patients with progressive amnestic cognitive impairment? Dr Ramanan: Yeah, great question. I think two big things come to mind. The first, you hinted at very well earlier that there are disparities in access to care, access to diagnostic testing, access to specialists and expertise throughout our communities. If we want diagnostics and therapeutics to be broadly applicable, they do need to be broadly available. And that's a big challenge for us as a field to work to address those disparities. There's not going to be one single cause or contributor to those iniquities, but as a field, I'm heartened to see thought and investment into trying to better address those. Another big weakness, and this is not just limited to cognitive neurology, it's a challenge throughout neurology, is that too many of our research studies are lacking in diversity. And that impacts our biological and pathophysiological understanding of these disorders. It also impacts our counseling and management. Again, if we want a new drug treatment to be broadly applicable throughout all of the patients that we take care of, we need to have data which guides how we apply those treatments. And so again, I'm heartened. This is a big challenge. It's a long standing challenge. It will take deep and long standing committed efforts to reverse. But I'm heartened that there are efforts in the field to broaden clinical trial enrollment, broaden observational research enrollment, and again, broaden access to tools and expertise. As a neurologist, I got into this field because I want to help people, use my expertise and my training to help people. These are steps that we can take to make sure that that help is broadly applicable throughout everybody in our communities. Dr Nevel: Yeah, absolutely. So, kind of segueing from you mentioning research and how we can better include patients in research. What do you think the next breakthrough is going to be? What do you think the next big thing is going to be in these disorders? What do we still need to learn? Dr Ramanan: There's a lot. I think for LATE and PART, the development of specific biomarkers would be top of the agenda. Now, biomarkers are by their nature imperfect. Even with Alzheimer's disease, where in comparison, we know quite a lot. We have a variety of imaging and fluid biomarkers that we can use to support or rule out a diagnosis. There are nuances in how you interpret those biomarkers. Patients can have signs of amyloid plaques in their brain and have completely normal cognition. They may be at risk for developing cognitive trouble due to Alzheimer's disease in the future, but it's one piece of the puzzle. Patients can have the changes of Alzheimer's disease amyloid plaques and tau tangles in the brain. We can confirm that through biomarkers. But at the end of the day, their cognitive syndrome might be driven by something else. Maybe it's Lewy body disease, maybe it's LATE, maybe it's a combination of factors. So, integrating and interpreting those biomarkers is challenging. But I do think, again, from the standpoint of giving patients answers with a diagnosis, having those biomarkers is really critical to just kind of closing the loop. It will also be critical to have those biomarkers as we're assessing for treatment response. So, for example, patients who may have coexistent Alzheimer's disease and LATE, I don't think we know the answer fully as to how likely they are to benefit from, say, newer antiamyloid monoclonal antibodies for Alzheimer's disease in the setting of that second pathology. So, wouldn't it be great if, similar to an oncologic setting where you engage in a treatment and then you're tracking two or three or four plasma measures and you're tracking tumor size with imaging, if we had this multimodal ability to track neurodegenerative pathology through biomarkers? I think that'll be a critical next step. And so, filling out that for non-Alzheimer's diseases, including LATE and PART, I think is item number one on the agenda. Dr Nevel: Wonderful, thank you so much. I really appreciate you taking the time to chat with me today about your article. I really enjoyed our conversation, certainly learned a lot. Dr Ramanan: Thank you so much, Kait. Love talking with you. And again, it was an honor to write this article. I hope it's helpful to many out in the field who take care of patients with cognitive issues.  Dr Nevel: Yeah, I think it will be. So again, today I'm interviewing Dr Vijay Ramanan about his article that he wrote with Dr Jonathan Graff-Radford on LATE hippocampal sclerosis and primary age-related tauopathy, which 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, Vijay, and thank you to our listeners for joining us today. Dr Monteith: This is Dr Teshamae Monteith, associate editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use 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.

A szerzővel Visky András beszélget „Különös testi szenzációk találták meg saját nyelvüket Mátyus Melinda sodró erejű prózájában. Nevelődési regénnyé összeálló elbeszélései egy mindeddig teljességgel ismeretlen nézőponttal teszik finomabbá világunk nyelvi érzékelését, jelesül a lelkésznő látásmódjával. Történetei csaknem észrevétlenül űznek ki az irodalomból, önmagunk felismerésének irányába. Mondjuk talán lelkésznőregénynek. Mondjuk talán irodalomtörténeti eseménynek.” Visky András Mátyus Melinda (1970) író, református lelkész. Szovátán született, Temesváron él. 2019 óta publikál. 2020-ban Látó-nívódíjat kapott. A Jelenkor Kiadóval közös program. A Program a Liszt Ünnep Nemzetközi Kulturális Fesztivál keretében a Müpa szervezésében valósul meg. A programok a Bookline és a Volvo támogatásával valósulnak meg. Az esemény médiapartnere a Könyves Magazin és a We Love Budapest. A beszélgetés a 2024-es Őszi Margó Irodalmi Fesztiválon hangzott el.

Móré András V1tamin a Happy Gang együttes alapítója immáron egy különleges jótékonysági misszió résztvevőjeként is példát mutat. András a Magyar Vakok és Gyengénlátók Országos Szövetsége „Kölyöknevelő” programjához csatlakozott, amelynek keretében vakvezető kutyák nevelésében vállal aktív szerepet. Mesél arról, hogyan vált egy labrador kölyök, „Álom” a mindennapjai részévé, és milyen kihívásokat rejt az egyéves, fegyelmet és elkötelezettséget igénylő nevelési időszak.Milyen érzés egy kutyát úgy nevelni, hogy tudja, végül egy látássérült ember társa lesz? Hogyan viseli a szoros kötődés és az elválás gondolatát? A zenész megosztja velünk, hogy miként szocializálják a kutyákat a városi közlekedéstől a különböző felületek használatáig, és hogyan talál időt erre a misszióra a zenészélet mellett. A beszélgetés során kiderül, miért tekinti ezt a programot élete egyik legfontosabb kihívásának, amely annyi örömöt és tanulságot ad számára, mint amennyi nehézséget rejt. Az interjúba egy rövid időre bekapcsolódik Klébesz Kinga, az MVGYOSZ Vakvezetőkutya-Kiképző Központjának kölyöknevelő referense is.Íme egy érzelmekkel és tanulságokkal teli történet!A Sláger FM-en minden este 22 órakor a kultúráé a főszerep S. Miller András az egyik oldalon, a másikon pedig a térség kiemelkedő színházi kulturális, zenei szcena résztvevői Egy óra Budapest és Pest megye aktuális kult történeteivel. Sláger KULT – A természetes emberi hangok műsora.

Musikchefin Ursula Magnes hat Intendant Matthias Naske in seinem Büro im Wiener Konzerthaus besucht und mit ihm auch über das Konzert am 18. Dezember mit dem Huelgas Ensemble unter Paul van Nevel gesprochen. Ähnlich wie John Eliot Gardiner ein treuer Gast im Wiener Konzerthaus.

Deze aflevering wil Juan het hebben over statiegeld. Een van de vele lasten die zwaar drukken op de schouders van de gewone burger. En blijkbaar extra zwaar op die van Juan.Marc wil brouwerij Nevel eren. Één van de vele Nederlandse brouwerijen die de laatste tijd het loodje heeft gelegd. Daarom drinken we een Nevel Dwaal.In deze 2-wekelijkse podcast praten Juan en Marc kort bij. De één zorgt voor het bier en de ander voor het onderwerp.   Muziek Stan Erbrink

Today's song is from the Agur , not a well-known word. We're working with the explanation that it's a crane , which is a type of bird, and he says הוֹדוּ לַיי בְּכִנּוֹר בְּנֵבֶל עָשׂוֹר זַמְּרוּ לוֹ: ( Tehilim 33,2) / Thank Hashem with a kinor/harp, with the nevel-asor (an instrument with 10 strings), sing to him. The pasuk that follows this one in tehilim, continues, שִֽׁירוּ־ל֭וֹ שִׁ֣יר חָדָ֑שׁ הֵיטִ֥יבוּ נַ֝גֵּ֗ן בִּתְרוּעָֽה׃ / Sing a new song to Him, play well with a trumpet. Why exactly does the crane sing this? The Mabit tells us something very interesting about the crane. The crane has a tremendous power of tsifsuf / chirping or noises, and is able to sing in a very powerful way. There is a pasuk in Yeshaya 38,14 where Hizkiyah Hamelech says, כְּס֤וּס עָגוּר֙ כֵּ֣ן אֲצַפְצֵ֔ף I'm going to make noise like a crane. The crane was created in a certain way to, to communicate. It has a very long trachea and its mouth is different than other type of birds. It's able to make a call that can be heard for several miles. So, the crane is known as a very powerful, loud bird and therefore, says the Mabit, the crane tells us, ' You might not have my abilities, but you have your own abilities. You can use your kenor/harp . Why does he say Hodu L'Hashem b'kinor/ Thank Hashem with the harp? He answers that a harp is something that is quite simple to play. This Hodu/ Thanks to Hashem is directed to the four people that have to say Gomel . The word Hodu is the term used in the prayer of HaGomel , which is said after surviving a situation of danger, whether crossing the ocean or desert, being released from captivity or recovering from an illness. And since these are common events, the crane says, I can't ask you to do something complicated . It needs to be a common thing. Everyone has their kinor/harp, the standard way of saying thank you. And the people that are on a higher level, whom he calls the Benei Aliya , won't simply do a Hodu they'll do Zamru/ a song , and they will use this Nevel-asor , which is a more complex instrument. The commentaries discuss about the Asor and ask, why a 10 string harp? The Gemara in Masechet Arechim 13B quotes a pasuk and tells us that the harp of the Bet Hamikdash had seven strings When a Mashiach comes, it's going to have eight strings, and LaAtid Lavo when it comes to Olam Haba , the highest level, it's going to have 10 strings. And that's actually our pasuk, where it says a 10 -stringed Nevel, and then the next pasuk says, a new song-which is the song of Olam Haba. What exactly does that mean? The Ramban explains in Shaar Hagemul letter 144 that this symbolizes the forces and energies that we have. The is the world of seven, and there are seven different Middot that are revealed to us, which are the seven Ushpizin . So we can sing to God with the harp of seven . But that's for the common folk. Then we go on to a higher level of eight, which is Olam Haba , and then finally we go on to 10. This means different people have different energies and different abilities, but whatever your ability is, you have to use it to praise, to sing, and to give over what you can and sing your song. So the crane is saying to everyone, You don't have to be like me. Rav Wolbe was once sitting with a student by the beach when they saw a beautiful bird landing in the most elegant and graceful way. The student commented, " Wow. Look how elegant and beautiful that bird is as it lands." Rav Wolbe replied, " You too can be elegant and graceful if you use your talents to do what you have to do." That's really the message of the crane. He's saying, ' You might not have my voice, but Hodu LHashem b'kinor-You can use your kinor or your nevel or whatever your instrument is.' The bottom line is this beautiful message, the song of the agur הוֹדוּ לַיי בְּכִנּוֹר בְּנֵבֶל עָשׂוֹר זַמְּרוּ לוֹ:

A Budapesti Longitudinális Vizsgálat (BLS) kutatás eredményeit a kutatók a 2023-as Országos Neveléstudományi Konferencia egyik

A Budapesti Longitudinális Vizsgálat (BLS) kutatás eredményeit a kutatók a 2023-as Országos Neveléstudományi Konferencia egyik

Peripheral neuropathic pain is primarily influenced by the biology and pathophysiology of the underlying structures, peripheral sensory nerves, and their central pathways. In this episode, Kait Nevel, MD speaks with Miroslav Bačkonja, MD, an author of the article “Peripheral Neuropathic Pain,” in the Continuum October 2024 Pain Management in Neurology issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Bačkonja is the clinical director in the Division of Intramural Research at the National Institutes of Health in Bethesda, Maryland. Additional Resources Read the article: Peripheral Neuropathic Pain Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @IUneurodocmom 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 Nevel: Hello, this is Dr Kait Nevel. Today I'm interviewing Dr Miroslav Backonja about his article on peripheral neuropathic pain, which appears in the October 2024 Continuum issue on pain management and neurology. Welcome to the podcast.  Dr Backonja: Thank you.  Dr Nevel: Misha, can you please introduce yourself to the audience? Dr Backonja: Yes, I'm Miroslav Backonja, but everybody calls me Misha. So everybody knows me by that. I'm a training neurologist, and I also have training as well as certification in pain management. And most of my practice has been where neurology meets the pain, which is neuropathic pain. I spend some time basic science lab and then transition into clinical research. And I was in academia for a couple of decades and was most recently recruited by NCCIH National Center for Complementary and Integrated Health and have been there for two and a half years now.  Dr Nevel: That's wonderful. I would love to hear more about your career at the NCCIH, a little bit and what you do in your role now, and how that came to be. Dr Backonja: Yeah, I was recruited to help and provide clinical support to efforts at NCCIH in the phenotyping of pain and neurologists who've done research in quantitative sensory assessment and other quantitative means of assessment of pain. Coming to NIH was very rewarding and quite of a learning experience. After six months being there, I've discovered that NIH is the biggest secret in plain sight. They say in the plain sight because it's public institution and everything is open to public and it's a secret because we don't think about it. This is in particular in reference to biomedical research training, including clinical trainings. So, I would encourage everybody to think of NIH as a place to spend some time and learn. There are wonderful research opportunities as well as educational opportunities. Vast library of presentations, green rounds and different other types of courses - some of them open to public, and some of them are up to FAS, which is a foundation of advances in science education by discovering. I feel like being back in school and having fun.  Dr Nevel: That's wonderful. Can you share with us a little bit about how you became interested in peripheral neuropathy and pain management of peripheral neuropathic pain?  Dr Backonja: It actually goes back to my residency and fellowship. And actually, you know, I had the luck of being exposed to a couple of clinicians who actually became my mentors. First was Jose Ochoa, who was one of the first people to quote from a small fiber, C fiber specifically, and he also was pioneered in quantitative sensory testing. And the other one was Charles Cleland, who was a psychologist and who pioneered assessment of patient symptoms, developing the Brief Pain Inventory is one of the tools. That actually peaked my interest in the topic of pain and once when I started learning about pain, what is the kind of mysterious experience of humans' pain, turns out that we have learned a lot of science about the pain and can make the pain very accessible. And I hope some of this will come to the chapter that we've provided.  Dr Nevel: Thank you for sharing that. I think of peripheral neuropathy and I think most neurologists think of peripheral neuropathy as one of the bread-and-butter diagnosis within our field. For the practicing neurologist out there who might be listening, what do you think is the most important takeaway from your article that maybe they don't already know about peripheral neuropathic pain? Dr Backonja: When it comes to peripheral neuropathy and peripheral neuropathic pain, it goes back to my early experience and still holds the truth. Neuropathies don't kill people, they just maim them. They create- cause lots of disability and if you add a pain to it, it can be quite disabling. In some regards, it has been neglected the area of development in neurology in terms of scientific discoveries, although things are changing quite rapidly as of recently. Main take home messages, and especially when it comes to a sensory neuropathies and painful neuropathies, is that it's one of the skills that has not been well researched and then not well communicated to the vaccine neurologist in terms of what to do with it. But most neurologist sensory symptoms are just like a noise because, especially when it comes to pain and prosthesias and allodynia and hyperalgesias, like, what is that like? It's just not knowing what to make of it. Frequently associated also with emotional components in terms of the people are either depressed because of persistence of pain or anxious, not knowing what's going on. And that really can create quite a bit of a challenge in terms of what to do with it. But once anybody who's interested learns the fact that sensory neuropathies and fever neuropathies as well could be as well and is easily diagnosed by a neurologist who pays a little bit of attention and gains some skills in assessing not only negative sensory phenomena, because that's what he as a neurologist get trained to detect and quantify sensory deficits as well as motor deficits and loss reflexes. Also, if you pay attention to positive sensory phenomena, which is part of the repertoire of symptoms that patients with neuropathic pain experience, it's not whether patients would have either positive sensory phenomena like prosthesia and pain or negative sensory phenomena. Actually, they have all of them. And that's kind of puzzling for many patients. And lots of times, very patients say, like, how can I hurt when I don't feel like, let's say, like most commonly it's lower extremities. Like I don't feel my feet, but it hurts. I mean, how come? Oh, that's a cardinal feature of neuropathic pain, neuropathic painful neuropathy. Dr Nevel: Yeah, thanks for that. You know, I really thought that your Table 3-1 was really nice. It kind of lists through the common causes of peripheral neuropathic pain and just demonstrates the diversity of the different etiologies or other conditions that can cause neuropathic pain. And so, I encourage the listeners to review that table. But, on that topic, can you share with us what you think are the most important components of evaluating patients with neuropathic pain to maybe come to a diagnosis, to find what the underlying etiology or driver is?  Dr Backonja: When it comes to painful neuropathies, there are actually two problems you have to solve. So, don't forget that part. The first one is finding a pathological theology. Why a person has a neuropathy, what kind of neuropathy. And then second is, what's the nature of the sensory problems? What's the nature of the sensory symptoms, specifically pain, levodenia and hypogesia. So, figuring out the theology of the B12 deficiency or diabetic painful neuropathy, you can relatively quickly or hopefully one would relatively quickly come to that at theological diagnosis. But then the second part is the diagnosis of symptoms. What's the underlying metaphysiology of that. And again, just reminding colleagues that the specific sensory phenomena such as thermal hyperalgesia is now well established to be due to what's called peripheral sensitization of C fibers, which are the small unmyelinated fibers, expressed TP 1 receptors. So, patients who will report that taking a hot shower is very painful. An example of that or when conducting sensory exam and applying if you come to the point of examining the perception of warm and hot and patient affords the pain. That's just the hallmark of the C hurtful sensitizations to C fibrous sensitization. On the other hand, if somebody has mechanical ordinia like putting the shirt on hurts, putting the socks hurts. Well, that's evident to central sensitization. These are the simple, relatively simple but symptoms or signs that could have implication if those patients with central sensitization are more than likely to benefit from medications that restore descending inhibition, such as tricyclic antidepressants or SNRI's. And so just paying attention to that, it gives a clinician being a clinician or a neurologist, like, let me consider prescribing medication that have central A acting properties. Or if it's purpose sensitization, something we have like a sodium channel blocking property, things of that sort. Actually, there are some other strategies such as antagonist TRPV1receptors, the capsaicin base. Those are the kind of things that can help a neurologist kind of take the evaluation of painful neuropathies to the next level. Dr Nevel: Yeah, the- by getting a careful history and exam, that can influence what treatment you prescribe to patients. Understanding whether it's central or peripheral. On the topic of treating patients and talking with patients and evaluating them, what do you think is most important to counsel our patients about who we are treating for neuropathic pain? Dr Backonja: Number one: by getting good history and exam. Well, really in the coming to specific diagnosis is huge relief to the patients who thinks many themselves that they're just going nuts are crazy because nobody else understands these symptoms. So, validation in terms they have a real problem. Second important step is that for the most patients, there is probably reasonable degree of therapeutic interventions that can lead to relief of pain. And also, with applying the integrative approaches with complementary medicine is that patients are given tools to deal with what is otherwise underlying problem. Those two steps make a huge difference.  Dr Nevel: Absolutely. What's the most challenging aspect about managing patients with peripheral neuropathic pain? Dr Backonja: Actually, there are a couple. Number one thus far: we do not have a cure for any other neuropathies or painful neuropathies. So that's one of the big disappointing things one would need to communicate to the patient. The second challenge is actually the therapies that actually for neuropathic pain. There's a half a dozen- yeah, half a dozen FDA approved treatment. One thing that's interesting characteristic that all of them prove proven efficacy in clinical trials. If you scratch the surface, you find out that only 40% of patients obtain 30% pain relief. So, it's a rare patient that gets 100% pain relief, and even those, too, get what we call clinically significant, and then in studies, basically significant benefit. It's only partial penalty. But for the most those who do get the benefit, pain goes down probably enough for them to get some a semblance of normality in terms of having some control over the symptoms and their function. It's then the third challenge is really working through those available therapies to find what works for individual patients because we're not at the point yet where for example, other fields like oncology, you can quickly through the means of biomedical and other evaluation come to the patient specific therapy. So, at this point in time you're far from that. What we end up doing with when it comes to management for painful neuropathies is a trial. Sometimes patients say, well, trial and error. I would say, well, it's a treatment trials. We try one thing at a time, assess the risks and benefits and then there was many treatments that carry the benefit. If you carry it on when once, when they don't or if there's adverse events, side effects, we discontinue them. And then most of the patients end up with a combination of pharmacological and now pharmacological treatments and most of them can get some semblance of symptoms control. Dr Nevel: I really appreciate your point on preparing our patients and you know, expectations and things like that and working with them and looking for things that may help. But also having an understanding that the likelihood of complete pain relief is maybe not a super high chance of complete pain relief.  Dr Backonja: But if you're going back to the kind of preparing patients, it's a good to acknowledge or give a chance to express themselves because many times they patients are confused because they have symptoms that are confusing to them. And so just to have them express it. And for example, my alma mater, we developed the color paint drawing where the different sensory qualities are presented by different colors. And then on the body diagram, patients draw where they have symptoms. And this is probably one of the rare examples where you can literally see a pain because these neurologists can recognize the patterns. You can see the pattern of the motor, right, is multiplex or radiculopathy or the list goes on and on. So, this is one of the kind of tools that's very simple, but gives the patients another way to communicate because lots of times they really have difficulties expressing themselves. Dr Nevel: Right. So, the opposite of the most challenging, can you share with the listeners what you find the most rewarding about taking care of patients with peripheral neuropathic pain? Dr Backonja: What is rewarding is that with some work- and again, it's not easy work because it does require multiple visits and multiple assessments and the reassessments, most patients can get control over their symptoms to the point of coming to beginning some of the functional improvement and aspects of quality of life like sleep and work, they are definitely rewarding and most of the time it's fairly obvious. And again, pain management is definitely a team sport where really, it's important to gauge colleagues. Most of the places don't have what I have had when I was in academic institutions, easy access to health psychologist or physical therapist. Most communities do have those specialties. And many patients actually benefit from things that are what's considered a complementary medicine, such as Tai chi or yoga. And actually, in my practice, Tai chi was probably most common prescription for my patients because, as I tell them, there are multiple benefits. Number one: one of the risks of patients, especially prophyl neuropathies and lower extremities, is a loss of proprioception. Again, even those who have a reasonable preserved proprioception over welding, noise of pain actually makes the problem walking the at risk of falling. Actually, Tai chi one gets improvement in balance. There's also medicating component to it. So, mindfulness medication is kind of built in it and that all kind of gives the patients a better control of symptoms. So, some of those interventions are easily accessible in community. So, it's, again, it's a patient education that really takes important part. Dr Nevel: Yeah. And that Tai chi is maybe one of the answers to the next question that I have for you. But as the clinical director of the Division of Intramural Research at the National Center for Complementary and Integrative Health, I have to ask you, Misha, what sort of integrative and complementary type interventions do you counsel your patients about, maybe beyond Tai chi, and which ones do you think are the most helpful? Dr Backonja: To clarify, the NIH patients I see are all admitted per protocol. Actually, NIH has the largest research hospitals called clinical NIH Clinical Centre, which has a hospital and clinics. All the patients that come to our program, they come per protocol for the most part. They come for specific investigations. At the moment, we do not have intramural treatment protocols, although in near future one of my goals is to establish that. The NIH funds- 90% of funding from NIH goes extramurally to academic institutions and other healthcare organizations and so on, and only 10% goes for intermural research. So, what we do is much smaller in scope, much more focused. So, what do we support NCCIH actually support extramurally full range of anything from probiotics, research in microbiome related to health and pain all the way to interventions such as mindfulness meditation? Intramurally, once when patients come for protocol, we evaluated and it's unavoidable to be a question. So, what do we do now? What recommendations do we make? Again, we don't- with the present time, we have treatment protocols and then, most of the time, what I can do is provide recommendations to the patients when they go back to the treating community, to the treating providers. It's usually a fairly comprehensive list including pharmacological and non-pharmacological accommodations for those who have had experience with pharmacology. Sometimes I can just say yes, continue or change or whatever. But then when it comes to additional complementary accommodations, they always provide information. For example, why do I recommend Tai chi? Or, what's the benefit of yoga and why would one want to try to learn trying to behavioral therapy or mindfulness meditation? What's the benefit of turmeric and some other components of what's called anti-inflammatory diet and what's the rationale behind all of that? So rather than just giving a list of recommendations and leaving it that, I try to engage patients in terms of having to understand why something is recommended, whether the fits with their expectations and what fits with their lifestyle and so on. Dr Nevel: Yeah. So, what's coming up, what's next in painful peripheral neuropathy? What do you think is exciting? Where do you foresee some breakthroughs in this field? Dr Backonja: Probably what will make the most difference is application of some of the really molecular biology tools that are being applied to peripheral neuropathy. So hopefully one of these days you'll have a cure for neuropathy and pain and anything would come to that will be probably interaction between a nervous system and an immune system, in particular neuroinflammation. That's kind of my bias. They're probably that's- well, the answer will be, but many painful neuropathies - actually every painful neuropathy, because they come from, as a result, specific pathologies - are different in a sense of trajectory natural course that will have to be first addressed. And again, depending on the underlying disease and molecular biology of that and genetics of it will determine that. But on the other hand, there are some common denominators, as we talked, when it comes to painful neuropathies, which is drivers of peripheral and central sensitization. And maybe one of these days, we'll find what are those drivers and how to change the system so it does not produce pain and other associated symptoms. Dr Nevel: So once again, today I've been interviewing Dr Miroslav Misha Backonja, whose article on peripheral neuropathic pain appears in the most recent issue of Continuum on pain management in neurology. Be sure to check out Continuum Audio episodes from this and other issues. And thank you to our listeners for joining us today. And thank you, Misha, so much for talking with me today about your article. I encourage all of the listeners to read it. It was very comprehensive and just really wonderful to read. Dr Backonja: Thank you. Enjoyed it. 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.

4 - Háromszor annyi elhagyott csecsemő vár nevelőszülőkre a kórházakban, mint tavaly by Balázsék

Basic knowledge of the common CNS manifestations of rheumatologic diseases and sarcoidosis is important. In the context of many systemic inflammatory diseases, CNS disease may be a presenting feature or occur without systemic manifestations of the disease, making familiarity with these diseases even more important. In this episode, Kait Nevel, MD speaks with Jennifer A. McCombe, MD, author of the article “Neurologic Manifestations of Rheumatologic Disorders,” in the Continuum® August 2024 Autoimmune Neurology issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. McCombe is an associate professor in the Division of Neurology, Department of Medicine at the University of Alberta, Edmonton in Alberta, Canada. Additional Resources Read the article: Neurologic Manifestations of Rheumatologic Disorders Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @headacheMD Guest: @Div_Dubey Transcript 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 Nevel: Hello. This is Dr Kait Nevel. Today, I'm interviewing Dr Jennifer McCombe about her article on neurosarcoidosis and neurologic involvement of rheumatological disorders, which appears in the August 2024 Continuum issue on autoimmune neurology. Welcome to the podcast, and I would love to have you introduce yourself to the audience.   Dr McCombe: Well, thank you, and thank you for having me. As you said, my name is Jen McCombe. I'm a neurologist in Edmonton, Alberta, Canada, where I spend kind of a third of my time in teaching roles (I coordinate the undergraduate block for our medical school there), I spend about a third of my time in a neuroinflammatory clinic in Edmonton, Alberta, and then about a third of my time doing clinical research.   Dr Nevel: Wonderful. Well, thank you so much for being here today and for chatting with me about your article on this topic.   Dr McCombe: Thank you for having me.   Dr Nevel: To start off, can you share with the listeners a little bit about your career path?   Dr McCombe: Absolutely. Yeah. So, I've had, uh, a bit of a circuitous career path. I did my medical school in Queens (which is in Eastern Canada, in Kingston, Ontario) and then went back to Edmonton, Alberta, for my residency (in Canada, we have a five-year residency program, so a little bit different than the US), but finished my residency and then did a master's degree in Public Health at Johns Hopkins while completing clinical research in HIV, actually, and did this thing we call the Clinical Scholar Training Program – so, kind of like a fellowship, but a little bit more, you know, research and academic-based. So, when I first started, I was focused more on neuroinfectious diseases, and that's kind of what my career path looked like at the time - but, actually, shortly after I finished my residency program, I also had my first child, and he, unfortunately, developed opsoclonus-myoclonus syndrome, and at the time (this was in 2010), it was a rather rare condition, so, I ended up finding myself having to become a bit of a neuroinflammatory disease specialist at the same time. So, at that point, I transitioned into working in the neuroinflammatory clinic with some mentorship but was getting all of the kind of weird and wonderful referrals and diagnostic dilemmas from my colleagues who recognized I kind of developed some expertise, and so decided (actually, mid-career) to take a sabbatical, and in 2021, completed a fellowship in autoimmune neurology at the Mayo Clinic. So, I finished that quite recently and then went back, and now I'm feeling much more, I guess, confident, too. Sometimes, you wonder about, you know, the choices you're making. I recognize most of the conditions I'm dealing with don't have, in fact, any evidence for their treatment, and that was confirmed when I went to the Mayo Clinic and found that, really, it was just trying to gain an understanding of the disease process to make a rational choice to medications and treatments. So, now, I'm back and kind of trying to focus a little bit more on some clinical research in that area since I've kind of solidified that expertise.   Dr Nevel: Wow. Well, thank you for sharing with us your career path and how, you know, unexpected life events kind of changed your interests or molded your interests (changed kind of the things that you became expert in, you know), and being fluid in your career path and willing to kind of take a break and reassess and get additional training. That's really inspiring to, I think, to me, and probably to a lot of listeners, that you can always, you know, develop more expertise in the more niche area or additional area no matter where you are in your stage of life or career path.   Dr McCombe: Yeah.   Dr Nevel: So, can you tell us a little bit more about - you know, you shared with us kind of autoimmune inflammatory disorders and how you became interested in that, neurosarcoidosis, specifically (you know the article focuses on that), and what's your background in neurosarcoidosis, how you became interested in that specifically and in neurologic manifestations of rheumatologic disorders?   Dr McCombe: I started in our neuroinflammatory clinic over a decade ago, and, you know, at the time, a lot of the expertise in any of these neuroinflammatory disorders was quite spread out over the country, and so, as I kind to alluded to before, often some of the more complicated patients where there wasn't necessarily clear-cut evidence or even, you know, a fellowship path to get there, I would end up getting referrals for - and so, I developed quite a cohort of patients with central nervous system primarily, but other types of neuroinflammatory and autoimmune neurologic diseases, and part of that cohort was a rather large (and still growing) group of patients with neurosarcoidosis. And so, I kind of developed some practical expertise, although, as you can see in the article (and as I'm sure you all know), the approach to the treatment is extremely variable. One of the most telling things is when we were at the Mayo Clinic, one of my co-fellows actually pulled all of the neurologists in neuroinflammation at all of the Mayo Clinic sites and asked them, you know, what is your treatment approach to a patient with neurosarcoidosis, and I think got twelve completely different responses as to the medications chosen and the length of time for the tapers and things like that. So, you know, it is very much a part of neurologic disease treatment that we still really don't have great evidence for, and although we do have some kind of rational choices that we can make based on other types of evidence, so -   Dr Nevel: Yeah.   Dr McCombe: And I enjoy working with patients with these types of diseases where we can kind of work together to come up with a treatment plan that makes sense for them and also makes sense based on whatever evidence we do have at this time.   Dr Nevel: Yeah. So, moving on to the article a little bit, knowing that this is a area of neurology where there's a lot of, you know, maybe personal expertise and experience but not a ton of data or evidence to necessarily guide our standardization to our treatments and approach, what do you think is the most important clinical takeaway from your article for our listeners?   Dr McCombe: Well, I mentioned before I coordinate the neuro block for our undergraduate program here, so I've developed over the years (I've been doing that for a number of years) a curriculum that's all based on, kind of, that approach to - and I like to do it that way because it's very practical. I like the students to be able to basically take their class notes and then go to the emergency department on their first shift as a clerk and, you know, use their approach to headache that I've developed for them to kind of take a clinical history and examine a patient with that sort of problem. And so, similar to that, I tried to do an approach to, you know, a couple of the more common presentations that would make you think of a rheumatologic condition or neurosarcoidosis in looking at the approach to CNS vasculitis and the approach to, uh, pachymeningitis - and these are difficult differentials for lots of neurologists, because it really relies on a lot of medicine knowledge, and we graduate from our residencies slightly more confident in our medicine knowledge, because we get a lot of that in our residencies. But as neurologists, as we go through our careers, we get much more confident in our areas of specialty, and at least for myself and many of my colleagues, much less confident in other things like general medicine. And so, it's difficult, because you have to face your areas of potentially less confident knowledge and really think about that in the differential - and so, I think, you know, I put those two big “approach to” sections in there, because they're the most relevant for the conditions that I was covering. But, I think also what I would say to a learner or a more experienced neurologist who might be reading the article, kind of pick out the little things that you might add to your own kind of approach to - you know, when you see that person with an ataxia, remember that Sjogren syndrome is one of the things you might consider that could be a treatable cause, or you want to see a sensory neuronopathy, don't just think paraneoplastic – again, Sjogren syndrome. So, kind of pick out those little pearls and add them to your approach to that patient that we all see, and I think that would be my biggest takeaway.   Dr Nevel: Yeah. Thank you. So, kind of like, keep this information from the article in mind so that you keep rheumatologic disorders in mind as a possibility when you're approaching a patient with whatever neurologic symptoms they're presenting with. So, what do you think is challenging? You kind of already mentioned a little bit, you know, just that it stretches us maybe into the medicine arena and so maybe stretches our medical knowledge, especially as we become more subspecialized or focused in neurology - but what is challenging about identifying, diagnosing neurologic symptoms as being related or due to an underlying rheumatologic disorder?   Dr McCombe: Absolutely. Yeah. Well, as you said, you know, it forces us to kind of face that medicine stuff that we might not be as comfortable with, but I think what else is challenging is that, sometimes, those medical clues aren't there. For the rheumatologic disorders for the most part, they are. Sjogren's is potentially a little bit different in that, potentially, the symptoms are less obvious or a little bit more subtle. But, in particular, with neurosarcoidosis, there's a distinct proportion of the patients that won't, in fact, have any systemic complications of their underlying disease, and so, you have to think about it even when the clues aren't there. That's why you have to add it to those kind of differential diagnoses where it might be considered, because those systemic clues that we all rely on when we do our review of systems and we ask about rashes and joint pain and lung issues, and these sorts of things may not be there - and so, you still have to think about it even when it might be completely isolated to the central nervous system.   Dr Nevel: What is our understanding of why some patients with rheumatologic disorders develop neurologic involvement? Do we have an understanding? Do we know why some patients do and some patients don't? I know that's, you know, kind of, uh - that's a tough question, but that was something that I thought of as I was reading your article, like, why does this happen to some people?   Dr McCombe: Absolutely. I mean, I think, potentially, it's a little bit more clear for some of them, like rheumatoid arthritis, because, typically, if you develop a CNS complication of this, it's, in fact, just because you've had the disease for a very long time, and often, it's uncontrolled, and so you think about the disease “spreading” now to the central nervous system - but for other conditions, like neurosarcoidosis, it is much less clear, and even if you look at the epidemiologic patterns for that, it makes it even more muddied in that in some populations, it appears that they develop more central nervous system disease, whereas in others, less. And so, why that is the case and why certain individuals might develop this complication of these diseases I think is yet to be seen.   Dr Nevel: Yeah, that's always the crux of things if we can figure out the why, then maybe we could prevent it, right?   Dr McCombe: Million-dollar question always.   Dr Nevel: Always. So, what do you find the most intriguing about neurologic involvement of rheumatologic disorders?   Dr McCombe: Well, I think one of the things that, really, I mean, for neurosarcoidosis in particular, so many patients do so well, and that's what I really like about it. You know, you see patients who present with an incredible burden of disease radiologically, and yet, don't look nearly as sick as they should when they're sitting in front of you. And then, you start them on therapies and some of them do so well, and even those with relatively devastating deficits, or moderate disease who do have neurologic symptoms, have a remarkable improvement in their neurologic symptoms with treatment. And so, that's always something that's quite rewarding when you get to see these patients in follow-up, and they're generally quite thankful because they're doing so well. And it's different from many of the neurologic diseases that we treat. I mean, in autoimmune neurology, we're lucky because we do have a number of diseases that are quite treatable and patients can have wonderful outcomes. But, you know, it's always scary when we see patients with devastating neurologic signs and it's great to see improvement with treatment. And so, that really draws me to it.   Dr Nevel: Yeah, absolutely. That's really rewarding when you're able to help somebody get better in such a profound way.   Dr McCombe: Mm hmm.   Dr Nevel: What is one common misconception about neurologic manifestations of rheumatologic disorders? Or what do you think is not well understood by treating clinicians?   Dr McCombe: I think probably one of the things I see the most is, sometimes, an undertreatment of the patient. And so, I see patients who, you know, other clinicians may have seen and have made the diagnosis, and perhaps it's a lack of confidence in the diagnosis and so they kind of want somebody else with a subspecialty to kind of confirm the diagnosis, but that treatment hasn't been initiated despite pathological confirmation on biopsy of another tissue. And these patients, like I alluded to before, they do well, but you need to treat them and you need to treat them adequately, and when their symptoms are quite impairing, you need to treat them adequately now. And so I think, sometimes, that delay in starting a second-line therapy and relying on steroids for too long - those sorts of things can really expose a patient to a lot of different side effects and to a lot of different complications that they may not have had, too. So, that's why I spent some time focusing on the treatment, because I think just gaining a little bit of comfort with some of these more common second-line medications is a good thing, because starting those early, I think, makes sense because you can really save the patient a lot. And then, the other thing, too, is that when you're using steroids, think about all of the systemic things that you're causing - think about the increased risk of infection and the fact that you need to prophylax for certain infections, think about bone health, think about protecting the lining of someone's stomach - so not only kind of thinking about your disease in isolation and what you need to do for treatment, but that you need to ensure that you're appropriately prescribing the patient all of the things they need to do to protect themselves during these times.   Dr Nevel: Yeah. I think that's so important. And I'm glad that you brought that up, because I think, unfortunately, many of us have seen a patient who ended up having PJP pneumonia (or something like that) because they weren't put on antibiotic coverage for prolonged steroid use or, you know, bone health - all of that is really important to think about. So, this may be entering a territory where there's no, you know, great evidence, but you mentioned, you know, starting kind of that maintenance or second-line agent - when do you decide to do that in patients? And maybe we can focus (since it gets a little broad), but, you know, in a patient with neurosarcoidosis, let's say - when you're starting the steroids, when do you decide, okay, this person is also going to need a maintenance therapy? Is that something that you do at the beginning when you're starting the steroids, or is that something that you think about later on depending on how their course goes?   Dr McCombe: Yeah. In my practice, I do it at the outset - again, because I'm quite focused on, you know, as soon as I get them on it, getting people off steroids - and so I start essentially almost all of my patients on it unless there's some other contraindication or complication to their disease. And because I deal with central nervous system complications in the vast majority of my patients, I'm starting a TNF-a inhibitor as well as methotrexate, and that's because I see a lot of patients with cord disease and significant brain disease, and so I want to treat them kind of more aggressively from the outset. And so, typically, they'll be on steroids, um, a TNF-a inhibitor, as well as methotrexate, and then I just back off, actually, as they do well. And so, I try to taper the steroids quite quickly over the course of just a number of weeks, or kind of two to three months at most. I maintain the TNF-a inhibitor, and then in some patients, depending on how they're doing, I might eventually stop the methotrexate. Some patients tolerate it so well that we don't for a number of months - other patients want to try to minimize their medications as quick as they can. So, that's my personal practice. In the province where I live, we don't have to worry about access to these medications, and so I understand that that might be an issue in some centers where people practice and have different access and different funding. Of course, I live in a country where we have universal healthcare, and in our province, I have very good access to these medications and they're funded from my patients regardless of socioeconomic status, and so I have the luxury of making these choices and I understand that other people might not, but that's my personal practice and I find it works quite well in the vast majority of patients.   Dr Nevel: Yeah. And you bring up a really good point that, you know, access to some of these medications for patients with CNS manifestations of sarcoidosis, neurosarcoidosis, sometimes can be challenging to treating the patient with medications that you feel like would be best for them. But that's wonderful that you don't have those access issues where you live. How long do you typically continue the TNF-a inhibitor in patients, since you mentioned, you know, tapering off the steroids, tapering off the methotrexate, potentially depending on patient tolerance and course. What's your approach to the TNF-a inhibitor?   Dr McCombe: Yeah, so, of course I follow them clinically, and then radiologically as well, and it's really satisfying if you can see the resolution of their symptoms as well as resolution of the abnormalities and the MRI, so I let that guide me a little bit. But, in most patients, I keep them on therapy for about one to two years, and then at that point, see if I can cease it in some patients. And I, again, continue to follow them radiologically and clinically after I cease it so that I can ensure that I'm catching their disease more quickly if it does come back and then can just reinitiate therapy, but in lots of patients you're able to stop the medication and they have persisting, kind of, disease freedom after that, and so they don't need to be on anything.   Dr Nevel: Yeah, great. And I'm almost hesitant to focus so much on neurosarcoidosis. (It was the rheumatologic manifestation that you talked about the most in your article.) I'm going to put in a plug for everybody to read your article so that they can read about neurologic manifestations of rheumatoid arthritis, Sjogren's, lupus, Behcet's - many more things. But focusing on neurosarcoidosis, it can be difficult in my experience to definitively diagnose, and people who have neurosarcoidosis particularly, and people who don't seem to have any systemic manifestations or, you know, imaging findings consistent with sarcoidosis - can you share your approach with us? And you outlined this in your article nicely, too, but your personal approach to patients with suspected neurosarcoidosis, and how you make that clinical decision to treat somebody with possible neurosarcoidosis, somebody who maybe you're not able to get pathologic evidence on?   Dr McCombe: Absolutely. Yeah, those ones are difficult. And, you know, whenever possible (as I mentioned in my article), I think pathological evidence of a diagnosis is important, because then when you find yourself a year down the road and a treatment path and you have uncertainty, it's much more difficult to consider continuing medications that can have quite a number of side effects when you're not absolutely certain about that diagnosis. But, in some patients, you know, I've had patients who might have nondiagnostic biopsies (if you attempt to do a biopsy), or they have disease in a site that really just isn't amenable to biopsy, or they have some other reason they can't have a biopsy. So, how I approach that is that, you know, if you think about possible neurosarcoidosis similar to any other nondiagnosed, you know, blow out-like lesion (for lack of a better term) in the CNS, if it's steroid-responsive, I think that kind of going down a path of treating it as a steroid-responsive lesion is kind of the approach that I take - so the diagnosis in the chart might be possible neurosarcoidosis, but in the back of my mind, I'm just thinking of kind of a steroid-responsive nondiagnostic or idiopathic lesion. So, I then follow that up typically with something like methotrexate (so, a more broader- spectrum immunosuppressant-type medication), and if the methotrexate is able to maintain the response that the steroids initiated, then eventually get them off the steroids. And so, you know, if I think about my patients that I've treated in the past, if they have a diagnosis of possible neurosarcoidosis, I probably don't start a TNF-a inhibitor as quickly in them, because in the back of my mind, I'm always wondering what type of inflammatory lesion this is, but that steroid responsiveness really helps me decide to start a second-line or maintenance therapy and then, typically, in those patients, as I mentioned, I'll start something like methotrexate a little bit more soon.   Dr Nevel: Yeah, great. Thanks for sharing that with us. So, what do you think comes next in this field? What excites you? Where do you think our next kind of development or understanding or breakthrough, whether it's diagnostic or treatment-wise?   Dr McCombe: I think, in the field, you know, any immunologic diseases, we've been really gaining a much better understanding of pathophysiology, and that's honestly what excites me the most, when you can know precisely what part of the immune system is at play here (whether it's, you know, complement-mediated or antibody-mediated) and then being able to then rationally choose medications based on a really clear understanding of the disease is something that I think is kind of novel in a way. For so many years, we would use kind of big broad-spectrum immunosuppression - even in multiple sclerosis, still, we use medications that, historically, we've found to be helpful - but we don't have a great understanding sometimes of why the medicines work. So, kind of going at it from the other way, where we're actually determining what is the exact pathophysiology of disease and then making a rational approach to a therapy, or choosing a therapy based on that, I think is what excites me the most, and I think we'll gain a better understanding of even a broader swath of diseases and be able to make those choices more often. That's what I like about this field.   Dr Nevel: Great. Well, thank you so much for sharing that - and looking forward to the future in this area of neurology. And thanks so much for talking with me today and sharing your story and your expertise and knowledge.   Dr McCombe: Well, thank you for having me. It's been fun.   Dr Nevel: And I encourage all the listeners to read your article. Again, today, I've been interviewing Dr Jennifer McCombe, whose article on neurosarcoidosis and neurologic involvement of rheumatologic disorders appears in the most recent issue of Continuum on autoimmune neurology. Be sure to check out Continuum Audio episodes from this and other issues, and thank you to our listeners for joining today.   Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use 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.

A lány egy éjjel arra riadt, hogy a szobájában két idegen férfi áll. A férfiak közölték, hogy azonnal velük kell mennie és kirángatták az ágyból. A lány segítségért kiabált, de hiába: az idegenek magukkal vonszolták, le a lépcsőn. A bejárati ajtóban a lány megpillantotta a szüleit - de ők nem szóltak semmit. Később megtudta: mindez a szülei kérésére történt. A férfiak egy bentlakásos magatartásjavító-intézetbe vitték a lányt, ahol hosszú hónapokon keresztül testi-lelki megalázásnak és bántalmazásnak volt kitéve a “nevelők” részéről. Ez a lány Paris Hilton volt - de ez nem csak az ő története. Ez sok ezer tinédzser története: az 1950-es évektől napjainkig(!) működtek és működnek olyan intézmények, szervezetek, táborok, ahol azt ígérik a szülőknek, hogy segítenek megoldani gyermekük viselkedési problémáit - ehelyett a kamaszok a legrosszabb rémálmaikat élik át.  Adásunkban a “Troubled Teen Industry”, vagyis a “zűrös tinédzser iparág” hátterének néztünk utána. Egy túlélő történetén keresztül bepillantunk a zárt falak mögé, és azokra a kérdésekre keressük a választ, hogy honnan származnak ezek a programok, miért indították őket, hogyan terjedtek el az Államokban és mi a helyzet napjainkban.  Források:  Könyv: Liz Ianelli - I See You Survivor Netflix: Hell Camp: Teen Nightmare c. dokumentumfilm MAX: Tinik tortúrája c. dokumentumfilm-sorozat https://drogriporter.444.hu/2024/03/14/synanon-a-szigoru-szeretet-tundoklese-es-bukasa https://hu.wikipedia.org/wiki/Anonim_Alkoholist%C3%A1k https://medicalonline.hu/gyogyitas/cikk/anonim_alkoholistak https://www.dea.gov/sites/default/files/2018-05/Early%20Years%20p%2012-29.pdf https://www.huffpost.com/entry/nancy-reagan-drug-treatment-straight-inc_n_56ddda84e4b03a405679693e https://en.wikipedia.org/wiki/The_Seed_(organization) https://survivingstraightinc.com/ https://www.motherjones.com/politics/2007/08/cult-spawned-tough-love-teen-industry https://parishilton.com/paris-impact-work/ https://survivingstraightinc.com/home The Real Story of Paris Hilton | This Is Paris Official Documentary | Paris Hilton https://www.michiganpublic.org/families-community/2021-04-30/one-year-later-whats-changed-and-what-hasnt-since-the-killing-of-cornelius-fredrick https://www.nbcnews.com/news/us-news/video-shows-fatal-restraint-cornelius-fredericks-16-michigan-foster-facility-n1233122 Ha szeretnél havi extra tartalmakat kapni tőlünk, akkor gyere a Patreon oldalunkra és válaszd ki a neked megfelelő támogatói szintet. https://www.patreon.com/hihetetlentortenelem Kiemelt Patreon támogatóink: Busa-Fekete Róbert, Lovas Gabriella, Rója Gergő Elérhetőségek: E-mail cím: hihetetlentori@gmail.com Facebook oldalunk linkje Spotify linkünk . Hirdetés és együttműködés: hallgatom@betonenetwork.hu www.betonenetwork.hu Learn more about your ad choices. Visit megaphone.fm/adchoices

Juniális – erre a névre keresztelték azt rendezvényt, melyet a Szent Miklós Gyermekvédelmi Intézményben évről évre júniusban, a tanévzárók után rendeznek meg különféle helyszíneken a nevelőszülői hálózatban nevelkedő gyermekek számára. A majális és a gyermeknap ezen keveréke egyfajta ajándék a hosszú iskolai hónapok után, ugyanakkor lehetőség arra is, hogy a vármegyeszerte sokfelé tevékenykedő nevelőszülők közösségként együtt legyenek, megismerjék egymást. Helyszíni riportunkban az esemény főszervezőit, Petneháziné Pócsfalvi Erika és Bene Dóra fejlesztőpedagógusokat, valamint az intézmény vezetőjét, Erdei Sándort kérdeztük.

The critical care management of spontaneous subarachnoid hemorrhage (SAH) is similar to that of other acute brain injuries, with the addition of detecting and treating delayed cerebral ischemia. Recent trials are influencing practice and providing guidance for standardizing management. In this episode, Kait Nevel, MD speaks with Soojin Park, MD, FAHA, FNCS, author of the article “Emergent Management of Spontaneous Subarachnoid Hemorrhage,” in the Continuum June 2024 Neurocritical Care issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Park is an associate professor of neurology (in biomedical informatics) at Vagelos College of Physicians and Surgeons, Columbia University in New York, New York and medical director of critical care data science and artificial intelligence at NewYork-Presbyterian Hospital in New York, New York. Additional Resources Read the article: Emergent Management of Spontaneous Subarachnoid Hemorrhage Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @IUneurodocmom Guest: @soojin_soojin Full episode transcript   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, a companion podcast to the journal. Continuum Audio features conversations with the guest editors and authors of Continuum, 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 by visiting the link in the show notes. Subscribers also have access to exclusive audio content not featured on the podcast. As an ad-free journal entirely supported by subscriptions, if you're not already a subscriber, we encourage you to become one. For more information on subscribing, please visit the link in the show notes. AAN members, stay tuned after the episode to hear how you can get CME for listening.   Dr Nevel: This is Dr Kait Nevel. Today, I'm interviewing Dr Soojin Park about her article on emergent management of spontaneous subarachnoid hemorrhage, which is part of the June 2024 Continuum issue on neurocritical care. Welcome to the podcast. It's so great to be talking to you today.   Dr Park: Thank you so much, Kait. Nice to be here.   Dr Nevel: Before we get started, could you introduce yourself for the audience?   Dr Park: Sure. So, I am an Associate Professor of Neurology - also in Biomedical Informatics - at Columbia University here in New York City. I trained in vascular neurology and neurocritical care.   Dr Nevel: Great. And so, I always like to ask at the beginning of these interviews, you know, if we could take away one thing from your article — and this is specifically (I'll direct this) towards the neurologists out there that are covering inpatient consults and ER consults — and so, for our clinical neurologists listening out there, what is the most important thing that you think that they should take away from your article?   Dr Park: So, I guess the most important thing for the general neurologists out there is that it may have been a while since they were aware of some updates that have occurred. There are some recent trials that are influencing practice and will potentially influence practice in the next few years that readers should really know about, and it provides a little bit stronger guidance to drive more standardized management. There have been two recent guidelines published this year. But there remain several gray areas for management where you need to be a bit more nuanced, and so I'm hoping the article gives the readers a framework to deliver more expert care.   Dr Nevel: Yeah, and I really, of course, always urge the listeners to go back and read the article and reference the article, because I do think that you do that really nicely and are clear when there are things where there's more higher-level, evidence-based reasons for things and where there's, kind of, just more expertise and guidelines on certain things. So, could you tell the listeners a little bit more about yourself, what interests you about subarachnoid hemorrhage specifically, and how you approach that interest and clinical background in writing this article?   Dr Park: So, I mentioned that I trained in both vascular neurology and neurocritical care back when many people used to do that. As a result, I've trained or practiced in four different academic medical centers who have specialized neurointensive care units. And the patients with subarachnoid hemorrhage tend to have a substantial ICU length of stay, and the neurointensive care that we provide can have a very large impact on patient outcome. And what I saw, though (practicing across four different centers), was that the management of patients with subarach can be quite variable across institutions and across patients within institutions, and it's reflective of a couple of things. One, there's, like, complexity in detecting ischemia, even when your patient is a captive audience in their ICU room. Second, there's many clinical mimics that occur (the patients with subarachnoid hemorrhage, they have a risk for), such as hydrocephalus, seizure, and things like delirium. And then, finally, there's limitations in the technology that we even have available in terms of monitoring these patients. But, for me, it was this complexity and the variability of management that kind of posed an opportunity, and it really sparked my curiosity early on and has sustained me. So, I'm particularly interested in the role that, kind of, the complex analysis of existing monitoring technologies can play to improve outcome for patients with subarachnoid hemorrhage, and that's where the marriage of both being a neurointensive care physician and a biomedical informatics person comes in.   Dr Nevel: Yeah. That's really interesting, and I could see that, because I always felt, even during my training, that some of the management and, you know, what diagnostics were even ordered to follow patients throughout the ICU was expertise based and seemed to vary without a lot of really solid, again, high-level studies, guiding what was done. So how do you marry the bioinformatics with your interest in SAH?   Dr Park: Right. So, I have two grants on - basically, I guess you would say AI, but really data science - on how we can manage patients with bleeds, specifically ICH and subarachnoid hemorrhage and hydrocephalus. So, we use data that comes from the monitors and we process that in a multimodal fashion and apply signal processing and machine learning and we build predictive analytic tools. So, I'm very interested in this pipeline of developing clinical decision support (information that we don't really have), and we're trying to glean from all the data and turn it into information that clinicians might use. The problem in subarachnoid hemorrhage patients is that a lot of what we're looking for is subclinical - so, it's not quite obvious, either because you can't possibly be in the room to be constantly monitoring for it (and, currently, the best monitor is the human, is examination), but, specifically in patients who have disordered consciousness, even the examination can be somewhat limited, and that's where we rely upon some of our neuromonitors. So, my interest has come in taking those multimodal monitors - but even nonneurologic monitors (stuff about your physiology, like your heart rate and blood pressure, et cetera) - and able to find signals that might tell us that a patient is getting into a dangerous zone. So, that's what my research portfolio has been 100% about - it's about subarachnoid hemorrhage patients and trying to optimize management, both for prevention and intervening in a timely fashion.   Dr Nevel: Wow. That's really interesting and would be so wonderful, it sounds like, for this patient population, if, you know, something was able to be identified that you could easily monitor to kind of predict or catch things early. So, kind of segueing from that, what do you think are the most — and you outline these nicely in your article, and I'm going to reference the listeners to, I believe it's the first table (table 5-1) - but what are, just like in general, the most important initial steps a clinician should take when managing somebody with an aneurysmal subarachnoid hemorrhage?   Dr Park: So, I think it's sort of along the timeline. So, at the time of presentation of a patient with subarachnoid hemorrhage, the focus you should have should be really on differentiating the etiology of the subarachnoid hemorrhage. At the same time, if the patient has any coagulopathies, you should manage that coagulopathy reversal, blood pressure management, and then detection and management and treatment of hydrocephalus. That's first and foremost. But then there is a longer timeline of neurocritical care management, and that's really centered on prevention, detection, and treatment of delayed cerebral ischemia, and that can occur anytime from onset of subarachnoid hemorrhage to two to three weeks out. And then that period of neurocritical care is made challenging because you have early brain injury (which is the period of seventy-two hours after onset), cerebral edema, and then, like we talked about, disordered consciousness. This kind of knowing how to augment your management strategies with monitoring or imaging is really key.   Dr Nevel: Yeah. And you, you know, spend some time in your article really going through delayed cerebral ischemia really nicely. And I would love to hear your take on what is the most challenging aspects of delayed cerebral ischemia in both, you know, diagnosis and management - and you alluded to it a little bit earlier, I think, with some of your research, but I would love to hear you talk about that.   Dr Park: Yeah. And actually, this is probably one of - if there was a controversial area in this topic, it would be about this - because there does not seem to be one best way to operationalize how you either survey for, or monitor for, delayed cerebral ischemia. There has been, historically, a merging of these definitions of vasospasm and delayed cerebral ischemia, which are not the same thing.  And so, if you were to draw a Venn diagram, not all patients who have cerebral vasospasm end up having symptomatic or delayed cerebral ischemia, and not all patients who have delayed cerebral ischemia have any discernable vasospasm - and, so, to use the terms interchangeably leads to a little bit of confusion. I mentioned the clinical mimics - you know, the causes of which are myriad (could be delirium, or hydrocephalus, or early brain injury) - and so that also poses another challenge. And, so, what I always say is that delayed cerebral ischemia, sometimes - when you're thinking about it in the context of subarachnoid hemorrhage - is sometimes a retrospective diagnosis. And it really kind of came from a really earnest attempt to standardize what the community is talking about, so that we can better understand how to define (if you understand how to define it better, then you can tailor treatments, study treatments, you're talking about the same disease) - but we're still not there, and I think that's where a lot of the controversy or confusion comes from. My personal approach is really to focus on the symptomatology, so, if a patient has vasospasm - whether that is, you know, screened for with a transcranial Doppler (if your institution does use transcranial Dopplers, it might be a nice screening tool) - but the fact of the matter is that not all patients can get a transcranial Doppler every single day. You know, most of the institutions that I have worked in offer that technology Monday through Friday and not on holidays, not on weekends, and so you can't fully rely upon something like that. The advantage of it is that it has pretty high sensitivity but it does have a lower specificity (so it overcalls vasospasms), so to treat just based on a TCD would probably be erroneous. Not all people agree, but I think that's the majority of the sentiment - is that you should then be triggered to go look for confirmation with some neuroimaging and really potentially wait for symptoms so that it might be a trigger to optimize the patient in terms of volume and blood pressure, but not necessarily to treat. So, yeah, operationalizing that workflow of how do you trigger, you know, confirmatory neuroimaging, what type of neuroimaging you should then choose? This is where the variability exists. But, in general, I focus on symptomatology. The extra challenge comes in the patients who have disordered consciousness. And so, at an institution like mine, we do rely upon invasive neuromonitoring, and that's now called for in the guidelines as well.   Dr Nevel: And I imagine these are high-intensity situations where also I would suspect decisions, you know, need to be made quickly on some of these things that you're talking about, too.   Dr Park: That's right.   Dr Nevel: What do you think is a misconception - or maybe (I hate to call it a mistake, but for lack of a better term) like an easy mistake that one can make - when treating patients with aneurysmal subarachnoid hemorrhage?   Dr Park: Hmm, an easy mistake. I guess, you know, time is brain, so it's an opportunity to miss ischemia - or actually attribute everything to ischemia and ignore the possibility for things like seizure (so nonconvulsive seizures), a resurgence of more of a delayed hydrocephalus - and so, I think it's important as you're managing a patient not to get kind of pigeonholed into looking for one particular thing (only looking for delayed cerebral ischemia), but being really vigilant that there could be lots of different reasons for a neurological change of a patient. And so, timely monitoring - kind of figuring out the etiology of a change in neurological status - is really important. And then, also, on the flip side of that, is we're really good at being aggressive in both inducing hypertension or managing a patient (trying to prevent ischemia), we're not that great about starting to pull back - and so I think being vigilant about opportunities to reassess your patient's risk for ongoing ischemia and deciding when that period of risk is over and starting to peel back on therapies, because these patients are also at risk for the down sides of inducing hypertension, which is PRES - and we have seen that in patients, and, you know, the phenotype of that will look very much like ischemia.   Dr Nevel: Yeah, it's complicated because you're taking care of patients with often impaired consciousness who have a lot of symptoms that could represent many different diagnoses that you would treat very differently, so I could see that that might be easy to do to kind of fall into the mindset of thinking that it's definitely one thing without fully evaluating for everything. So, caring for patients with aneurysmal subarachnoid hemorrhage obviously can be really, you know, challenging from the medical perspective, but also from the perspective of, you know, communication with families, and families asking questions about prognosis and things like that (and you mentioned this in your article about prognostication a little bit) - and can you talk a little bit about our ability to prognosticate long-term outcomes for patients who are in that acute phase (maybe even early first, you know, couple of days or a week) with a subarachnoid hemorrhage?   Dr Park: I think one of the most rewarding aspects of caring for patients with subarachnoid hemorrhage is that these patients can look, really, very sick in the beginning, and they're quite complex to manage, but you can see some very impressive recovery. And from a neurointensivist perspective, seeing that recovery in kind of a rapid timeline is rare - and we get to see that in subarach patients. We see patients who just have refractory recurrent vasospasm and delayed cerebral ischemia getting all of the tools thrown at them and you're really kind of, you know, concerned that there seems to be no end - but there is this peak of that injury, and then after that window of secondary brain injury risk kind of resolves, the patient can very much recover (so seeing patients who look the sickest be able to leave and go home). I think there is a hidden cost to subarachnoid hemorrhage where, maybe on our gross measures of outcome, patients look great, but there are this hidden cost of social psychological outcome that is unmeasured the way that we are currently measuring it. And I think our field is getting better at adopting some of the ability to measure those kind of hidden costs, and we're able to see that, even a year out, patients are really not back to where they were before (even though on the scales we currently have, they do look great, right, in terms of motor function, and things like that) - so, I think as clinicians, we have to be sensitive to that. So, when we talk to families, we have to remain hopeful that they are going to have a remarkable potential recovery but prepare families that they really should be on the lookout for any opportunity to rehabilitate in all aspects of function.   Dr Nevel: Yeah. And you mentioned in your article that as we're moving into the future  - and even currently - that there is some focus on gathering more patient-reported outcomes for people who are, you know, out of the ICU back in their normal lives after subarachnoid hemorrhage (which speaks to this that you're talking about, that even if their motor function is normal, they may not be back to their normal lives). So, what is something you think that's really important that we've learned in the past ten years - I'll give it ten years, you can go back further, make that time frame shorter if you want, but about the past ten years - about subarachnoid hemorrhage's impact on patient care, and then what do you think we're going to learn in the next ten years that will impact the way we care for these patients?   Dr Park: So, you know, subarach - in terms of the literature that is forming, that has formed - like I said, the guidelines had not been updated for over a decade, and we're fortunate to have not just one, but two sets of guidelines from two professional societies that were published right next to each other this past year in 2023 - but the field is fast moving, so even after the publication of those guidelines, there was one of the first randomized controlled trials in the field to be published maybe a month or two after that (that was the early lumbar drain trial). So, the key areas that I think where the literature has really helped strengthen our practice in terms of bringing standardization is in the antifibrinolytics. And so, in that space, recently, there was a very nicely performed randomized controlled trial for early administration of antifibrinolytics. It's a practice that, even when I was training, was sort of based on old literature back when we used to treat subarachnoid patients very differently - so we were really kind of extrapolating from that literature into our practice, and we were all sort of just giving it uniformly to patients early on with the good intention to try to prevent rebleeding, (which we understood, prior to aneurysm securement, was a high source of morbidity/mortality). So, in trying to reduce that risk of rebleeding (which happens very early) as much as we could, we were giving it. But the length of treatment (you know, who should we give that medication to) was really kind of uncertain - and this recent randomized controlled trial really gave a definitive answer to this, which is that it probably makes no difference. It should be seen with a caveat, though, that the trial (like any trial) was a very specific population. So, it could probably be said that for patients who are secured very early, there's no role for antifibrinolytic therapy, but, potentially, for patients who may be in a lower-middle-income environment or lower-income environment or for whatever reason can't reach aneurysm securement within that seventy two-hour period - you could consider, you know, greater than twenty-four hours you should consider the use of antifibrinolytics - but largely has brought an end to uniform administration of antifibrinolytics. This is where that expert nuanced care comes to, right?   Dr Nevel: Mm-hmm.   Dr Park: Another area is, really, kind of something as basic as blood pressure management. I think we were taught very early on that we should be very rigorous, bring that blood pressure down - and so, I think, across all types of stroke now, we're realizing there is a little bit of nuance, right? You have to think about your patient, about prior existing renal failure, about prior existing chronic hypertension that's poorly controlled - and in subarachnoid hemorrhage, the additional impact of that early brain injury. If you have cerebral edema, you should be considering, do we really want to control our blood pressure that low? Because we might be inducing secondary brain injury from our presumed protective intervention. So, these types of things are being revisited - so, the language around that in the new guidelines is a little bit softer, and it does sort of refer more to, “let's consider the whole patient”.   Dr Nevel: Yeah, rather than making a blanket statement that doesn't apply to maybe everybody.   Dr Park: Yeah. And you also asked about future.   Dr Nevel: Yeah. Where do you think things are heading in the future? What's exciting in research, and if you had a crystal ball, what do you think we're going to figure out in the next ten years that's going to impact care?   Dr Park: Well, fortunately, for patients with subarachnoid hemorrhage and for people like me who are treating patients with subarachnoid hemorrhage, there's a lot going on. So, I mentioned lumbar drainage because there was a very nice trial that was published - I think we'll see in the next few years how much of that diffusion of innovation travels across the country in the world about the usage of this. There are some who point to prior studies that may have conflicting results and so want to wait and see it be validated. Others are pretty convinced, you know, by the quality of the study that was done and are trying to incorporate it into their protocols now. I think we're going to see more usage and more study of things like intravenous milrinone, early stellate ganglion blockade, intraventricular nicardipine, and even maybe optimized goals for cerebral perfusion or blood pressure - and this is for looking at a myriad of outcomes, including the prevention and treatment of vasospasm and ischemia, improving outcomes, and preventing infarction. There's also a lot to come about early brain injury (and I kind of talked about that). It's like a seventy-two-hour period window after subarachnoid hemorrhage, and it comprises processes like microcirculatory dysfunction, blood-brain barrier breakdown, and things like oxidative cascades, et cetera. While currently, there doesn't exist any practice besides, like, the nuance and expert determination of blood pressure goals prior to aneurysm securement, I think this will be an area that hopefully will become a target for intervention, because it has an independent and influential impact on poor outcomes for subarachnoid hemorrhage patients. So, watch the space.   Dr Nevel: Yes, absolutely. Looking forward to seeing what comes. Well, thank you so much for talking to me, Dr Park, and joining me on Continuum Audio.   Dr Park: It was my pleasure.   Dr Nevel: Again, today, I've been interviewing Dr Soojin Park, whose article on emergent management of spontaneous subarachnoid hemorrhage appears in the most recent issue of Continuum in neurocritical care. Be sure to check out Continuum Audio episodes from this and other issues. And thank you to our listeners for joining today.   Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practice - and right now, during our spring special, all subscriptions are 15% off. Go to Continpub.com/Spring2024 or use the link in the episode notes to learn more and take advantage of this great discount. This offer ends June 30, 2024. AAN members, go to the link in the episode notes and complete the evaluation to get CME. Thank you for listening to Continuum Audio.

“Caddyshack” (A Mumtidimentional Mixtape) {Enter The Multiverse} From Wikipedia: Caddyshack is a 1980 American sportscomedy film directed by Harold Ramis, written by Brian Doyle-Murray, Ramis and Douglas Kenney, and starring Chevy Chase, Rodney Dangerfield, Ted Knight, Michael O'Keefe and Bill Murray with supporting roles by Sarah Holcomb, Cindy Morgan, and Doyle-Murray. It tells the story of a caddie, vying for a caddie scholarship, who becomes involved in a feud on the links between one of the country club's founders and a nouveau riche guest. A subplot involves a greenskeeper who uses extreme methods against an elusive gopher. Caddyshack was Ramis's directorial debut and boosted the career of Dangerfield, who was previously known mostly for his stand-up comedy. Grossing nearly $40 million at the domestic box office (the 17th-highest of the year),[3] it was the first of a series of similar comedies. The film has a cult following and was described by ESPN as "perhaps the funniest sports movie ever made" SAUCE (IN CASE YOU MISSED IT) —- AHAHA. ITS ME AGAIN. OH SHIT! Oh shit, i guess it's Jimmy Fallon's Galaxy. Oh nooo. Oh, yes. Look at this penny. I see you. Now look into my eyes. I see you, Jesus. Ahahaha! Okay, now what? This shit is twisted I missed the shift of the dimensions— Till Jimmy walked in with his pennies For some cigarettes and swishers, Just to get the picture It's 5 AM again, And it's still Infinite, I'm disinterestedd as ever in living in LA, Or just living, period— But it is what it is, I work for my rent, I've repented for this, Used to sleep in a tent, But when I was an Infant, I instantly— Wait, a customer walked in. I better help him. Heaven help him. Another level, Call dr. Nevel, Or an Ambulance, I just can't get it Just can't get it, Wait, let's insert some of the script here, I guess. Took you long enough, didn't it? That took forever. How are you alive? Maybe I'm not. Finally, we agree on something. Oh, this guy Lol. Good to see you again. Likewise, now— Here it goes… As you promised. Working on it. As I promised. Take my heart for granted, Take my soul, If this is loveless Till the end, I just can't manage, having Thoughts of death and tragic ends I haven't Felt the same since Waking up without the day to come ahead; The day has passed again A test, No fail, or pass It's just progressive, In a trance, It's just the stress, It's just to pass the time, I guess, if this is purpose Then, we'll see if this is worth it Now, or never, then Now or never, Never had a friend, All envious at best, This is the end all, In the end, it's just Me and God, And God would want A better body, To have fun I wished it all at once, And then I watched it crumble Oh, I watched it Stumble in, again, my friend I'm different when it's wet, I might not never see the Sun again I might not ever love again Oh well “Oh well” , I said Oh, well, I guess Oh well Okay. One hour left. Okay. Who gets the gold? Hum. Honestly I didn't want to hear a thing ; I had quit music—I just wasn't cut out for the industry—I was, but not by societal standards by far; my lowly place in the smoke shop would have to do for now, and though I knew it wouldn't sustain, there wasn't much else I could do but keep showing up, for as long as it lasted—dresses in at least 2 layers and 5 pairs of socks tucked into boots two-sizes-too-big I had been forced to purchase specifically due to the frigid and painful, freezing temperatures at the locations I worked, which kept its doors open 24/7. Play Iambic. What, right now? Yeah, play Iambic. Uh… Iambic played st exactly 1 hour and 19 minutes—it's script, the transcribed rendition crafted especially for the Broadway stage, an 88-page-masterpiece collecting dust in the confines of my Google Documents, along with anything else I had written and had yet the advantage of placing anywhere besides my podcast channels, which I constantly thought about cancelling, despite its innumerous downloads—nothing really seemed to matter anymore, as I was trapped in my body, in a loveless world, in a dead-end job and though my bed was clean and comfy, sharing the room wirh 3 others became exhausting. INT. SMOKESHOP. 5:58 AM DREW BARRYMORE … SUPACREE … I'm done. I quit. QUIT?! YOU CAN'T QUIT. Nope. That's it. I quit. You can't quit. I just did. I hadn't quit the music industry—the music industry had quit me. I wasn't pretty enough, skinny enough, light skinned enough, or willing to do what any of the other girls were to get ahead. WTF is THIS. Since you like to troll so much, I just thought I'd turn you into one This is not Kosher, 199x Jimmy Fallon; Let me out of this plastic —not exactly “fireproof” — death box, before I let myself out, and I trap you in it. But oh, You already did. FIGHT. UGH OH. Ok, rotate. Who is this. Oh shit, hey dude. FUCK, what year is it? MEANWHILE, Under the bridge. …anybody seen this, uh… *Troll* Yee! *Troll* Alright. That's it. Everything checks out. The story was air tight. TIGHT, TIGHT I want you to wear this tonight “The Lady In The Red Dress” You really went all out for this I really didn't. lol Oh I see, You thought this was the matrix. MIT I WISH GOD Wish what. MIT … Mm. Did u see that. See what. ALRIGHT FUCK THIS, YA'LL IT GOT SERIOUS, WHERE'S MY CYCLOPS He called me his cyclops— —-and then he said LIKE GET OUT WHAT GET OUT OF MY HOUSE WHY CAUSE YOURE JUST A PIÑATA, MAN! And I ain't got time for that! I just got a DeLorean And a new HAT I gotta go get Oof. WRECKED. Yo, Wicked. KENDRICK (TODDLER) WIZARD. Oh my. I'm J00F'd up. | | | trance | | | Look; I gotta get out of this MOTHER OF PEARL do not beach this whale carcas on my warehouse project A what A beached whale I know You brought a beached whale to my fucking rave show Oh I get it It's Avant- Guarde No, that's just how I got here …. Trust me, it's okay that This never happened You did not see me It's because I wasn't there Is this U Ū No I wasn't there. Ü I was. Fuck. What happened. It's ok. All I remember is “The Quatardashians” Hmm Also The indigenous But that's it But mostly that was all just Jesus showing off his flexes Are u fasting? Yes, “Ū” is. So, do you need this?! TRUMPP Get rid of this recording imiidiately GOT IT. kill that bitch. SKRILLEX Yessir. —-but before all that happens. …did you want fries with that?! Why are we boycotting McDonald's —for poisoning —the allies —our enemies. Wait, you're eating this? Yes. Like, for fun, or like? No. This is what I'm feeding my children Why Cause they hungry. Uh, ok— —and there's six of them. Aight, ya'll can each have one nugget with your— I wanted a cheese burger! You git hamburgers. Ham. Cheese costs CENTS; And you know your momma If I ain't about a dollar - A dollop of Daisy You really are Ashamed of his Alright, you evil bastards. I see you want to Cause suffering Correct For which you will eternally recurve damnnation and all of the pain you've caused Karmas a bitch It's lonely at the top Not when you're GOD Get off my rock Did you miss an appointment? Nah, can't do it Why what happened Too high up. Whatchu mean So what, it's just like Done. Well, this is it, huh guys. Oh, yeah, it's that, alright This is the longest ride we ever took.d This is the ONLY ride we ever took. I WANNA GET OFF THIS RIDE. I AM REALLY HIGH UP. JUST LET GO. NO. NO. NO. Put me down, kite!!! KITE wtf do you want me to do. I'm a KITE. I'm YOU FUCKIN KIKE NOOOOOOOOOOOOOOOOOOOOOOOOOO—- Well, I'll be honest, man, this sets you back, some How far back GET GONE, But? We're dinosaurs. Why would something with razor sharp teeth be so— —peaceful, and friendly?? T-REX …cuddles. I just can't fake the feeling( I can't pretend to cry It just comes, when it does But when the well runs dry That's when the the world will end That's when the world will end After this movie, I guarantee we will no longer need the Wilhelm scream AGGGGGHHHHHHH!!! YAHHHHHHHHHHH!!!! AAAAAAIIIIIIIIIIGGGHHHHHHH UUUUUUUUUUUUU This movie broke the world record for the amount of times the word “No” was screamed NO NOH. NO. ‘No! NOOOOOOOOOOO! NONONO. NOOOOOOOAAAAAHH …No! Here they all come for her, Defended upon New York In order of important, or appearance? One doesn't wonder, At al, of what's to come Uncommon, we are The call has come TRACY My tummy hurts. That's probably because you've been drinking straight tequila for the last hour and a half. No I haven't! This is water! Tequila is YELLOW, Liz Lemon! No, Tracy—that's silver tequila, And regular tequila is, You know what? Nevermind. Alright, who's got the night shift? [nobody raises their hand, at all] Seriously guys?! Come on! COME ON! Look up WHAM! For some reason, idk. Can we just— not do this? No. Out of my mind a bit Speaking in tongues, In total silence Guess it's the times, I guess that's just who I am And who I am is I said I was Sam I'm the same, I said, “Say Uncle” I guess it's a game, we're playing I don't want to be played with At all I just want to feel loved again By someone else Superb, like him I just want to be felt, I guess By someone else That's “Different” I just want to be kissed on the lips A splendid blend of Twisted trysts Let's not pretend It hasn't ended yet Until you've finished it Class dismissed again Let me off of it I just want it to stop Keep rolling Keep rolling your eyes in the back of your head Like you did just morning Just go for a walk Just stop for a moment Run a bath And just keep running Cause here something comes, Of course, It's all your callings Neatly rolling into one, They said But I Just want to be loved again And who doesn't That's the fucked up part I just want to be loved again But nobody ever Just comes up I just want to be loved again It's a walk in the park Don't follow the dog Even if he barks at you It's time to start again I wonder what comes after this part You are the gleaning in the shadows, The reckoning in my eye, The siren in my silence; The green in all the lights, I am a shamed to have just been One of your many One of your many Images, You still have me twisted, I miss you, It's just you, at the end, Again I left you where you left me Solid on solid Sounds are invalid now How are you so Swore by your awesome No more songs, I said No more songs, he's dead to me No more songs! She's inlisted He's uninterested, Isn't this interesting The problem is: I'm still in love with Everyone i've ever been in love with (And I love him) But he doesn't remember my Name And he's famous And she's crazy And he hates her But he made me hate him The day I became you The day I became So famous, I finally made it I'm dead It smells like dill in here At least it doesn't smell like dead mouse. Aha. Youre Hellen. Keller or Mirin How would you be Hellen Miren Cause I'm the Queen. posh. You want to die Well, you better do it quick Better get your shit toggether, paint a l Bigger, better picture Bitter Betty gliching steady Just remember when you're ready Ever steady still forgetting dinner Dessert was already Forget this significance Remind me why I'm on this speeding bullet to nowhere Had no other options but to go under for something Shy, sickness it's a secret Just kill me already Semi robotic, Something like a magnet, attracted, Simply symphonies And soulless bodies, tied to money Wonder what was in the vaccum cleaner meaning What did you suck up, dude Who do you suck up to. When nobody loves you But your own son And the audience is robots Nothing really works more than once, if it's really magic Sit and do nothing would you Like you're supposed to Fall over like the mannequin you are Just a body in my count A mattress without a bespost, if it matters If it matters Doesn't really matter But hey, you know We all go downtown every once or twice a note For Hanukkah I could try to be nice But there's no sense in it, Is there If everything and everyone else is just as nasty As the rest of it Just is just a test, again A doctors office visit. Simple robotics, Or already stocked up for Hanukkah, Hollywood Where's your homeland deposit box Closet full of robots Closest to the moon, I wrote another poem for you Sorry that I wasn't on the offering table The parakeet, pigeon and pirated Slattery, Damages, damages, All with the Amazon packages, Now we're all robots, Aren't we What corporation to you belong to! Something corporate , or say anything Whose to say Jeff Besoz won't replace us With m robots with thought processes, If once such could project as such presence As an AI freestyle Meanwhile, I've got a butload of buckets and bunts, Bullletwounds, eyes on Manhattan and happens to wish something bad upon me When all I wanted is Somebody to love me And someone to love him, If that's what he wanted (But who knows if what he wanted was all of the bodies opposite of him) I don't belong on this planet I belong in the garbage Put me on mars, mom Stop it, You're almost a robot, get out of my peripheral With your mental illness Geez, I must really want a menorah This is the animal house There's no one alive here Set to be slaughters. Honor the box of offerings as Thoughtful words And parallels What could be under your tongue Is the surface of love Just to touch with the battery acid or chemical trails You have left in your axis Nobody knows better than this How close it is to touching Without being loved But nobody loves you Psychotron, sure we're all robots now Nobody loves anymore {Previously, On…} L E G E N D S The Secret Life of Sunnï Blū {Enter The Multiverse} Ascension What the FUCK did you DO? What did I do?! You know what you did! I didn't do anything! Oh yeah? No! Not on purpose! GODDAMMIT, YOU SON OF A— Where's Jimmy Fallon?! What?! I don't know! Oh no. Oh shit, run. Oh no. What in the FUCK— I am “the fuck” You know what. I'm gonna sue the everliving shit out of you. For WHAT. We'll see. Fuck. Uh oh. FUCK. What now? What this time? Apparently, Jimmy Fallon is missing. What the fuck does that got to do with me. We'll see. Okay, great, Now finish that chapter. What fucking chapter?! All of it. That's—a lot. I want all of it. By my desk, by noon tomorrow. “By” your desk?! Yes, BY. Not ON. I've got too much stuff on my desk— …but it's…like 9 o clock. Should be easy, given your natural talents. What natural talents. PEACOCK. AHAHAHAHA. Okay. Well. Well what. This sucks. I lost all my coins. Hey. Ugh. You dropped this. So how was Los Angeles. What the fuck. You fucking DICK. I told you, I own shares in this. So what's the plan for this, exactly. I dunno, Harry. I got a book of stamps, And a yellow envelope marked “Jimmy Fallon” I will hate you forever. Well, that's retarded. I haven't even smited you yet. I will annihilate you, human. WHERE'S MY SHIT. Who the fuck are you, anyway? Nobody! No one. No one cares about this series, yo. I'l seriously doubt that, Jesse Pinkman. What is this stuff. It's your stuff. This is not what I ordered— Hey— Why is it BLUE Cause it is. So. WHY IN THE— Mischief managed. Alright. This should be good for the night, but we gotta get out of here by morning; I thought your parents owned this place. It's a time share! So? So it's like only —part of the time. That is stupid. No! You're stupid! You're the one who got us into this mess. It's your mess, I was just cleaning it up! Whatever! Stop trippin. Nobody's “tripping.” That's it. I'll be a stripper. Straight outta hell, that kid. Don't I know it. Alright, fine. I said, whatever you do— DONT watch this show. Stuff it, J. Slatts. I'll kill you with my eyeballs Sounds like a threat. Put on a lawsuit, then. Maybe I oughtta… —with a bow tie. You'll look so pretty. I thought I was already pretty. Uh huh. Yeah, look, so honestly I don't know if I'll ever be on the same vibration as like, Jimmy Fallon and them, ok? I don't know how I did it; I don't know what did it, It just happened and then— And then WHAT. It just—ended. Just like that. I'm not trying to offend anybody here. Just like that. Now, I ask: What are we going to do to sell you this dream? Doesnt matter what you do, I'll never believe it. Sure, fine; Don't believe it— We're gonna make you live it. Who the hell us “we” anyway? Now you're speaking in my cadence— Don't flatter yourself I like it. Too late, I guess. So, you see We're building Power triangles And love squares Power triangles And love squares Don't let it scare you, There's love there Don't let it scare you, There's love there Never fear where love has dared To call you up there Corrupt file—no fair. Don't be suprised even the odds seem to turn in your favor, I promise you; Nobody's ever ready For what has just happened here. WAKE UP, FUCKER. Ugh, I can't go through this again. So, I guess I'll have to erase, Or just secretly publish Everything I've ever written About my actual experience as a color, Just so that I can earn money As anything other than A slave— A maid, A housekeeper, A dog walker Or servitor So far under her, That I can't see far enough up to just Scratch the surface Her birthright: The entire network And mine, To sit under her, Wondering what the world would be like At the other end of the spectrum The word form of the White woman The wicked witch of all directions, In which I stand in; I'm at her mercy I've been abandoned before But this disservice, is, I'm afraid The best advice I can take is just To go straight to the bank with my angst and my hatred And shove it So here comes the nameless Face I love, Yet, The faceless God, Was Intoxicated, at best— Manipulation of the Mass Media I'm so Seriously jaded In this torture chamber In my corner office In this hall of racists, I claim, but if all is One in the same Then It's one in the same And I'm mainstream I'm famous If it's One in the same Then It's one in the same If it's One in the same Then I'm mainstream I'm so famous In a whole room full of humans I'm groomed to be useful for something, But what? It just hasn't come yet. I could sit down with a paper and pen, But I'm filling up all of my documents With hollandaise and God For what? It's just another song, or something Or something. It's just another — Goddamnit it, more coughs again. I told you not to watch this. Why do I taste pancakes? Maybe you're having a stroke again. Chyeah, a stroke of genius. I'll show you a stroke. Or don't. Well, there goes the captain. where is that scene, anyway? I don't know, I just wrote it. Great, she left the door open. She's got no furniture! It's a “dance floor” It's “the black box” she called it “the black box” Goddamn, do you listen to all her stuff? “Fear stimulates my imagination” Pilot ASOT Fuck man, What is a woman to a man, And an androgynous genius to The industry, or anyone at all If all are foes ans frauds All else is toxic! I woke up with one hand tucked behind my back Feeling dead drunk, I just woke up again But never fell asleep What world am I in? The end of the Dream sequence The end of the energy keeping me between three things: My past, My future And these prequels, Sequels And seeing arrangements And She's going crazy But nobody quite understands That these demons are chasing me saying “You deserved those hands in your face” The scratches on Kayla's back should have had me but I was too fat To find love again And still have something Wonderfully, undone And wrong with me Wrong with me enough to slam poetry So I'm guessing the white women I love beyond words and bounds are— In charge of whatever happens At the top of the rock; So I jumped off. I want to see someone suffer for all that I've done; No, that's dark, and karmic, you know— To go on like that; The confusions and refusal to accept that The album is called ChaosMagick, But the cover is more Urgent, A prose or a pawn of protection Against all the coughs And the reckless mismanagement The hands in my head And the eye on my scar And the lies on my heart So tell me, What happens When you're flying a kite with your heart, And it's broken? What happens to the kite , When you fly it with your heart And your art up in bundles— heartbroken, heartbroken So what come of Miss May, Come January? What come of Miss April By Next December what comes of the words I was saying For no one But everyone heard them And I've been gone Much longer than months, But still stocked up on all that I've wanted Or all that I got Or just, all that I love But got no undercovers to acknowledge no more How right I was Or how wrong I am What come of Miss June, when Miss January comes around? what come now, around August, When March is long forgotten? What comes of the drugs, Of the come ups, and come downs What comes of the process When nothing is served But the surf has come up Somewhere And I just can't love enough To go there I want to go to there I want to be that girl I want to sit at the top of the rock Writing songs, and sipping mock cocktails I want to Don't you know I just want to get back to Where I belong I'm so out of money and love That I want to be Under the train, When it's coming (Sometimes it's just the impulse that says “GO” Then the train starts to slow And my pain bubbles up into a numb, Dumb, crumbling cluster of poetry You know? Or you don't Cause you're all just on your phones Scrolling Some black man stands over me, Reminding me of why I never trust the ones Who want me most, Or just assume, By color code, That I belong to them I'm sorry, I just can't write with your arms around my neck like this Your heart around my arms like this It's so wholesome I had other verses but forgot them They took away my movies for the curses And the hexes That they put on me I said don't. And the king said “Heads will roll” Cause, you know; I've got parts for all of them now, The ones I'd forgotten But come from the catacombs, Back from the conduit You know, This is awful I had another one, But lost it. The king?! Which one. Teas I! No, it wasn't, It was Gían's father, From further off Should I call John back? Which one? Turns out, I love all of them— Turns out, I've got all of them In my college I taught them all to be someone Becoming of acknowledgement With nombres most common Juan, in subcultures, but Beyond that (Or above them) It's John, Or just Jonathan, Watch the ones who drop the consanant; They're always so troublesome, But I took them all up As understudies, Social Studies and some theatrics, Joan of Ark said Two more moments (Two more weeks in) I could have a body worthy Of a Grammy award, but — Would I be a writer then? Probably not, hon— Writers are Off a bit. If you were pretty, ever at all— would you have written this?! If I were pretty at all would there be reason to be this Conflicted? Some of those old New York hallways Haven't been painted In ages Since they made them Don't make that face at me I only dropped my key once On the fourth floor —they're horrible, you know To us, The “brothers” know no love They are destruction, speaking Of this, I got a cold heart. Cold like the robber Cold like the calling I've done in my corner office cold, like the jello mold forming a thought process Worthy enough I might love it like a husband We're re-evaluating your circumstances. Whatever the fuck that's supposed to mean. I've got friends at USPS What the fuck could that even account to. Look, I'm gonna have to give this some serious considerations. It's not that serious. It's not that serious. Of course it is! I'm up to my knees in investments! So?! I wade a waiste deep, Surely you can get by “Up to your knees” What exactly do you need? Money. And lots of it. I mean, from me. Money. Really? Leave me alone. I told you not to write this. You're a voice in my head; No, I'm the hand in your mailbox. What in the fuck do you believe in. I believe in everything! They said you were a genius; I didn't expect you to be —at the very least, lucid— *squints* learn some new vocabulary, okay? For what? Dinner. Maybe. We're still in the process of voting. She's crazy. We'd be crazy not to actually hire her. Her accounts are all practically open; We could just take it. Yeah, and when she kills herself, and there's no blood on our hands— There's nothing that can be done about the amount of this stuff that's already printed! Printed?! What?! You mean— She's published? Self-published. My, what a beautiful happenstance To have already had you And awakened atop mattresses Marked for my assassins hand— Polite, I lost you All of us, Atop the rock We stood and suffered Months beyond a montage, Undercover Love was lost, And all's uncertain The interception of God, At the cost of What terror and cutbacks Have caused us all What you lost was $50, a Hallmark Card, an Academy award, a long lost star's phone number, And all that you wanted, The cock of the gun Was the sound that you wondered What was called , then ran off into wonder. How am I gonna make money And become an award winning songwriter Music producer And multidisciplinary artist, Without all the funding it takes to get noviced Without taking clothes off Wake up 10 years younger I'm suffering My stomach was a rubber band My stomach was a rubber band My only song was Water I forgot to stop For the applause I drowned in all the love; right then and there I died of Lovenessness [The Festival Project] The sound and laughter of children play A baby in a basket The basket case at Trader Joe's Who know what happens It just doesn't pull my heartstrings any longer That my son belongs without his mother So I'd better have another This is us, come on. Don't do this to me. Don't do this, Timmy, you'll be sorry. Come on! We're not even in that movie! We are, though; it's still Listen, you've got the right guy for this. Are you sure. Yeah, I promise. Officers, Stop for a *movement [hot cops flash dance number] Fuck, well, that was all wrong. But worth it! What I meant was— God, this show gets good at 31, But I'm only 22, So I guess I'll know how wrong the war was Once we've lost it, Cause imm a man now The episode is over, Soon comes the next episode With snoop dogg, Or not That was our wedding album. Scatterbrained, and pregnant— There she was just putting all the things together That she needed to be Needed To be needed. There she was, All on 4/20 Trying not to do the wrong thing, But what was it? To be loved. Then, There she was at 21 just going off again At some event— A friend, and her Back then could not imagine They'd become him To be someone. Not as one, But of entirely another World apart, aside from Cyclones into snow cones Turns the watchers into artists All their own, And off my own accord Or own account Or done with boredom Dove soap Open doors And clocks that turn the other hand away, Each day you love Manhattan But can't have that. That's it— This is just Season 1 of Mad Men WHERE THE FUCK IS— [she throws her hands above her head in surrender] I don't KNOW! Oh, you're a girl now?! I guess! What's with those pants, then? To hide the assets! What assets?! You look tragic. I'm going for ‘skeleton' to match all your wives and everybody else on the red carpet Who said you get the red carpet? Manhattan. That guy lies! Well how about this: The walk of stars were carved out in blocks of marble All in my honor. 1000/1 You're our God, now. What! I don't want to be God! SUCK IT UP. YOU WON. I don't wanna! Yaaaaaaayyy. You got the award! All the awards! Speech! Speech! SUNNI BLŪ Uh—- I'm drunk, And there's nothing on the teleprompter [a man in the audience coughs] A-HEM. [Sunni Blū immidiateky shoots the coughing man] [multi-camera shots of celebrity audience reactions; laughing, clapping in hilarity as if someone hasn't just died] TAYLOR SWIFT (unmoved at all) SUNNÏ BLŪ I don't know why you're laughing. That was awful. That guy died [audience is insane, super fake as usual] [more cut takes] SUNNÏ BLŪ It should have been you, Taylor. TAYLOR SWIFT (Still unaffected) SUNNI BLU Anyway. I'd like to thank the academy… Cause I am the academy [Audience is celebrities being celebrities] SUNNI BLU You guys are all idiots: I'm a go f*ck myself— And anyone else who wants to show up At my afterparty. Whatever. Peace. [cheesy academy award music plays—Sunnï knocks over the mic, peaces out obnoxiously; the audience cheers wildly and the host returns to the stage.] Who's the host? Whatever. Hey, better than nothin. You're telling me. yeah. I know: Oh, she's a comic? Yeah. I got it. BOB SAGET Ooh, that's good. Ū No—no my God. No Bob Saget, stop it! Wait, Bob Saget is dead right? Last I recall: Fuck—FUCK! Dammit. Dammit, dammit. Okay, Rue— you're up. Rue, what in the— Shhhh, don't let them know I'm in here! Oh, wait— It's me, Blanche. That's hot. I'm a debutant. My god, you're so young. Here, take this, What's that, You'll need that. V.O. I'm being hunted by the ghost of Bob Saget. *haunted. No, hunted! There she is! Grab her! Ooh, Bob Saget. Why, yes. How old are you? Not dead yet! You don't have to kidnap me, I'll happily go with you, sir. Really? Yes. GET IN THE— NOH, GET IN THE VAN. INT. IN THE VAN. [a bunch of hot male celebrities are in the van] Oh. Okay. Wow. That was easy. What is it, Friday. It's Friday and a half. Friday.5 What. There's a Friday movie between 1 and 2 So I guess this is season 8.5 I guess this is season 8.5 HEY, GET BACK HERE. What is this. It's your lunch. I don't want this. Well, okay. What— is this strange music— They call it dubstep Come on, Jimmy, you're slipping Kimmel, cause Fallon is dead or presumed missing Probably Skrillex Probably a bounty on his head, Dog willing The Festival Priojects Inclement Infinite Is coming up next, on Legends Come on Jim, KEEP UP. Nobody can know about this, okay? Wait, where's Kimmel Okay, I got O'Brien— Black Irish Bastard… Alright, Alec Baldwin is a little tied up, right now, but LEMON, Fuck. That's l—future me. What?! I gotta go, okay?! What? Go where. Let's get DRUNK. No, That's—I got a show tonight What?! Look at my lexicon. Your—what, Meet me on Lexington. Oh, this pussy is finished! I got it, I got it! He's LENNONNNNN!! JOHN LENNON Fuck. Look, I gotta go. John Lennon?! You're dead! Funny, I thought not. Watch this. MOOOOOOOOOOOM. Fuck, What, It's my kid. I gotta go. Wait, you have kids?! Well, I just had you, didn't I? “The mayor” is a secret underground rap star lol #trappin Okay, What's else happened Idk hold on Okay, So whats the sauce on this sandwich. Oh. Jeez, this again. That *sandwhich? Hah. There's no sauce on that sandwhich. —there's not!? No: You see. It's very simple. WAKE UP, YOU'RE A ROCKSTAR. we gotta take the train. The train?! NO. NOTTHETRAIN. NO. Man, fuck the train! [SUNNI BLŪ wakes up on the train.] What's this, the train? [is the train] (Angrily, tossing newspaper) Man, FUCK the train! Other hobo: Aww, thanks, I need that for my— [s/he snatches back the paper]. Wait! I need that back—what day is it? [drunkenly illegible gibberish turns into perfect Hebrew] GODDAMMIT, it's Shabbat; I gotta get to Temple. [s/he shoves the newspaper back into the hobo's lap] Here. Oh no, I thought I couldn't forget RABI FUCK _]€_# WHAT WAS IT GODDAMIT IT WAS SO CLEVER. God So it was… What did you do with it? Do with what My idea what idea My—my rabbi joke— What rabbi joke you know what rabbi joke! You were the one who gave it to me. Oh, did I? YES, SATAN, JESUS. GOD Ohh, Satan-Jesus. I like that one. NO— it was— It was much better than that, it was— It was funny. Oh, it was? YES. —did you write it down? Fuck, I realize I just opened a A FUCK PORTAL. OHH, GET IN IT, GET INSIDE. I had an Artemis in my pocket But I lost him Walked away from the cornermarker And the cornerstone, for the sunset I wonder if songs always come When I'm walking, Or God makes us promises, For world of I'm not JB, I'm KG, Can you see me now? If you could see what I see, We'd be even wtf did I just write this And not realize I just wrote this Yeah. That shit happens to me all the time. WHAT. ALL THE TKMEx Shut up, THE ANDRE3K CHARADES GAME is getting intense. What in the FUCK is that. *flutes* Ohh. And KITES. yyyyyYYYYYYYAAAAAHHH—— GODDAMMIT. I can't see really, I just dream I'm not thinking, I'm dancing This is what you asked for Exactly what you asked for For once, I'm finally glad I have your eyes on My friend I can see you all on the horizon, Singing NO, NO MORE MUSICALS!! Jimmy, what did you do?! I don't know what I did! You lyin bastard. I'm not lying! So, where ya from? —I don't know where I'm from. Listen, I'm gonna need you SHUT UP, JUST SHUT UP. It seems like these scenes are getting shorter. I'm bored with this. Ok. Let's do something else. I fuckin hate you. I hate you. I fuckin hate you. 88. Oh no: 8 Wait, what the— *dolphin* WOAH, okay: Oh, no. No, No, no OHNONO. I told you I'd find him. Anyway. Seems like there's something more important I should be doing. Are you sure this is the right place. Right place. Right time. Fuck— FUCK. What, what happened. I lost my— SKRILLEX! No. SKRILLEX. NO, NO— SKR— I swear to God, Google knows everything. Google don't know shit about SHIT. I gotta lose m 39 lbs. For what. MADONNA DO IT FOR THE BANANAS. I hate— you. COME ON, MISTER. Fuck off, Madonna, I'M A GOD. I miss Beyoncé. That's not relevant. Beyoncé is relevant to everything. *smacks* QUIT FANGIRLING. Trust me, I hate you. I don't trust you, but I believe you. I got it. I hate this place. Holy shit. What. I developed a new phobia. What's that mean?! I don't know, I can probably use it in a fight or something. For what. SPECIAL ABILITY UNLOCKED. I see you looking over my shoulder I see the shadows, I try not to jump at em. I spent six months in a coffin, you know I spent my life a sarcophagus (Wow, I got it right.) Try not to mutter those haunts in a hospital Try to recover from trauma Uncovered post traumatics, Anxiety attacks and a lot of those— What do you call them? A flashback. Here goes one: SONNY MOORE aka SKRILLEX appears. I told you not to— But I did! I didn't mean to! But you did! This is ludachris! Oh look, it's— Fuck. God dammit. Come on! What's his name!? What's his name?! I'll think abo it it. Are you serious? Another shapeshifter? Yes, I guess welll just have to kill them all, then. I just want to go home. You don't have one. …oh. So here we have. Okay, wait a second. I wasn't faking my symptoms at all, actually. My heart had dropped, and been pounding and fluttering insessantly— It had been a hard week, but especially the last three days; The coughing—. Everyone seemed to be wearing clothing with stars or bears on it, Champion sportswear. I fucking hate champion sportswear. But the palpitations were real as ever— and now— On a Saturday night in the Jamaica, Queens medical center emergency room, There they were again. Only this time I knew exactly why. ‘Too Bizzare' by Skrillex begins to play, via Complications 003- The Trauma Method. Irony. It was ironic, but still startling, Started with some nostalgic traumas, Every other time I saw an ER doctor (Why I don't go) Fuck, I just realized I have to airdrop myself 880 times. That fucking sucks. Did you say you were a doctor? I was, once. When is “once” At some point. Listen, I'm gonna need you to backtrack to get to the bottom of this. I'm innocent, I promise! We caught you at 27 different angles doing this. Oh. [beat] I plead the 5th. Ohh. Cerulean. My favorite. c R A Y On Oh, I get it, I L L U M I N A T U S. Nice, it worked. I know everything about you. So you do. [beat] You're a God. What the fuck do you want from me. Listen. I. Am not. A God, Right. That's exactly what a God would say. No they wouldn't! Because a God wouldn't say anything! AHA. Don't ‘AHA' ME. I don't mind, at all It don't matter— to me I don't mind, at all It don't matter—to me Might as well not think about it The space between us Might as well just stay awake then No sense in leaving Just to come back It don't matter to me, now Now and again I go crazy just making arrangements, But besides that, If you like it, you should have it It's a long road, As Kaskade says, And a short dance, With the right one And time goes by I would call it mild, But actually I'm in a wild panic It might be a heart attack I just might even Die right here But I don't mind, at all It don't matter—to me I don't mind—at all It don't matter to me, I said I don't mind, at all, now It really don't matter to me I said, I don't mind, at all It really don't matter to anyone Now does it (Not it doesn') I don't mind, at all It don't matter— to me I don't mind, at all It don't matter—to me Might as well not think about it The space between us Might as well just stay awake then No sense in leaving Just to come back Palpitations and precipitations at the pulpit Preacher, please don't make me a culprit I been prayin— I been paying my tithes, 10% Even, Now 25, Almost half of me is not mine! Why try? I've been walking out, in straight lines I been crying silently It ain't right I been making most of my nights Sometimes I see sun come up twice Up, down up 10 degrees, It ain't right Up down up 33, it ain't right Up, down, up I've been spending my time Down, up, down Riding round, Trying not to down in my mind Up, down up What is this. It's my project. What is it? The Festival Project. Yeah but—what— What. Is it? …it's my project. *painfully infuriated* Okay, enter here. EXAM ROOM 10 Why exam room 10? Because. Where are the other nine? Just—get in. I'm not going in there! JUST GET IN. UGH. DEADMAU5 (head and all) stands at a tall podium in the center of the room) What is this, This is deadmau5. I know that. —-!!! —?!? What. !!! What? This is the exam? Yes! NO. What is “no”. I'm not playing for deadmau5. That's the exam. Then I fail! Automatic Fail? yes. Automatic fail. Then you win. What. *slams gavel* Congratulations—you're the next superstar DJ. WhY. . What. Woohoo! I just retired! DEADMAU5 exits. … … After a few moments of comic tension, the Deadmau5 head rolls back in through the exit which he has taken. Ugh. Fuck this. No matter what you do, you're a superstar DJ. What. No! Yes. The answer is yes. NO. Fuck. What the FUCK. No matter what you do. You want to go, Go, you want to die, Die, you want to try, try You want to cry, cry Do what you want; As so will I, Demand is demand— Supply is supply. EDX So then, I followed this long hallway under the stage deck. Uh huh. And it led to a door— Uhhuh, where'd the door lead? To a portal. Woah. Pasqualle! You made it! I—yes. Congratulations! *blows party horn* *Daisies/ confetti* You're like 25! I'll be 25 forever. Nice! Yeah. I guess that's why it's called ‘music'—a musician without muses is just useless. ‘Well, whose next?' I wondered. All of my muses were not just so wonderful to me, but adored by many—and perhaps this is what allured me most—befuddled ans confounded me; once my mind was set on something, there was nothing else its eye could see—and for how long one God could only know, how deep the love would go and that the blood would run deep, and the scars to show for it, only upon my heart and never by soul—for a love was a love, and even once came and gone, to the end of my life I knew I would still ponder upon them, at one time or another, my muses—star studded lovers, rather than crossed, shiny and golden like all diamond and trophies so treasured and thought of as precious. ‘Yes, you are—precious.' Another tongue in cheek thought, for the other that I was, and also was not, as summer drew onward as short as it would come and go—a reminder to leave the apartment more often, and to mind my manners, to find the upper echelon wherever it was and come quietly into its doors, to open my world and wordform of thought, into a place where my heart always was; then, and only then, would I be home. Amongst the men and women of the uppercut and classy, luxurious big fishing ponds and flocks of doves upon olive branches—the peaceful world long parted from where mine was, by only the fault of my own. What had been done just certainly was, and yet, what was to come was an open poem, not of mine, but Godform in thought. ‘I wonder what's at the top of Rockefeller Plaza.' —perhaps, a gander at the bottom of an even larger entertainment complex. Then, again, only God would know what was beyond all that I wanted; a job—and not just any job at all— the one that I had always wanted. Mmm. Birthday cake. Suddenly the taste of a white confetti crème filled my mouth with a delicious remnince of what it might be like to taste a confectionary sugar again—but i couldn't imagine ever making it just on talent and charisma alone—no. Indeed, it seemed something had damaged my charm, and perhaps it was just the swarms and droves of phone controlled masses that saw me as nothing more than dust, I had started to surrender my desire to perform, and the quality of my music—along with my ability to make it, suffered with the awful thing that had been crowding my soul at all—whatever it was, evil and dark in nature, sure saw to it that it wanted to hurt me in all the ways that it could—and in all the ways it could not, I stayed away from most others, favoring my delusions of love. ‘Nobody seems to understand that the pain they cause will only harm themselves.', I thought Younger souls, however, they were—and they would be kept in the pain that I was in one way or another until eventual death, far behind me on the infinite road to the source. Far enough behind, that it seeked to destroy my progress, and for all that it could, it also couldn't. The infliction of pain would simply not act as a measure for control any longer. Off into my own world, where I was at least free from the thoughts and judgement of others. She's the most beautiful girl, And I'm the most beautiful boy; So naturally, we belong together, don't we? I see a pretty picture, Picket fences and a family Golden Retrievers Someone relieve her; She doesn't believe me TV dreams and exquisite pretty people Burning candles, fire flames and frequent figures, Guest characters and cameos, Repeat offenders, multiple appearances Suddenly, really, it's another need People, people pleasers Audience affection, Tragic endings, Butterflies and new beginnings Gun under my tongue, Rubber like a frog My mind is in a fog Haven't bothered going on a walk To Trader Joe's but The anthem of my youth, A lost soul Another form of my love So what I wonder Put the gun up under my chin Rubber like a frog Blow my head off Just cause I didn't blow up Selfish cunt Big brother, Another hypnotist Little brother, Gotta love him Gotta love em For the Love of God I could stop for a moment Wash my mind out with soap Like I'm ten years younger, even Seriously 20 years between us, You can't even hide underwater In a bathtub Seriously, Someone help us For the love of God, for the love of Hollywood Seriously, Someone love us, For the love of God, For the love of Rockefeller Plaza Someone help us Another possible walk of stars A little shop of horrors Another whole story I get rid of my demons The hoes screamin I put semen in her Permanent like semen, Just keep dreamin I'mma just keep preaching SaMo, Brooklyn Europe Next I keep scheming Whoever you are; If you're a wreck— You need a check No respect, neglect Just cover your neck (I'm blind to my own design, sometimes) That's what the eye is Try this: Close your eyes and say thrice, kids I am the God of the eye, Osiris I am the God of the Eye, I'm Osiris I am the God, I walk amongst the highest Thoth, You lost Better just die and keep trying I am the God of the eye, I am (Try this) I am the God of the eye (I never die) I am the God of the eye (That's right, three times) I am the God of the eye No black and white television, In my dimension we pay attention to centrifugal, The mission isn't in materialism, Whatever youre spending If money the God, l of your eye, Realize, I am higher My gunfire, Is right on the back of The one dollar I am the God of the eye I Am Your money is nothin to us We come in peace, To end suffering Pretty little nigga Look just like Kendrick Kickin it with jigga I'm the new higs boson Part of me never left Boston (Fuck Starr!) Part of me never left homeless This ain't my home It's my office You never heard this song You don't notice I'm an ugly kid, you don't notice me Rooftop smells like soy sauce On god I am ugly You don't notice -Atari the God Can we get back to this, please? Damn. She really whooped her ass, though. Janet, can I borrow you for a second? No. Please. [Whoopi Goldberg appears in the doorway, gesturing “c'mon”] …alright. I got convictions on my lips, I took a picture Turn the page The worst of all was, it really did seem like they were racists— INSOMNIAC EVENTS Not just racists— the most deadly kind of racists. WHITE SUPREMACISTS You really want it this way, don't you? No! I LOVE you! Oh, do you? If there's a mile in here, I swear to god.. Are you high enough yet? I thought so HIGHER! hire star* What. Just do it. You remember these guys, right? GOOD CANNABIS, FAIRBANKS, ALASKA No. Why are we back here. Alright, we might have fucked up. Why. This guy sucks. HEY. What. COME BACK TO ALASKA never that. WHAT, WHY NOT! GOD HATES FAGS!!! Well, you're wrong! WHITE POWER. Nah. ALL LIVES MATTER O rly? Even this guy? Literally every “NO” …so, “all lives.” Look, I don't care what color it is; I want that book in my library. GO TO THE LIVRARY. NO. GET IN HERE. NO AUBREY. STAY DEAD. She's dead, right? YOU CALLED ME HERE. I didn't! You Did. I did not, all i said was *swoons* …I love her. (I really do) WHAT?! “I Love you?!” It was more the *swoon* that did it. Disconnect. Fuck, I lost deadmau5 again What'd you do to him? Nothing! Put him back! He's still there! He's right there, you see him? No! This isn't deadmau5. We want deadmau5. bring him BACK. Fuck, I fucked up. What'd you do? …nothing? Pick up the phone Pick up the phone …hello? Who IS this? Fuck it, I quit. Man, God never puts my dishes back in the right place, like ever. I told you, I don't live here, I'm just… Babysitting. CC! What! CC! What? CC WHAT. Fuck, man. That was wild. Where the fuck have you been? I don't know. You don't know—you smell funny. “Funny” is that what that smell is? No. When were you? When? Ha. Did you—- Did I what? —did you go to a party without me? Lmfao fuck these niggaz. Why, what happened. What's this. Where was it?! Idlewild. “IdLeWiLd”?!?!? You. Old. One here and die, you know, l. It's cattle call for curtain calls guy Where did this go— What was this, once? It's the return Welcome to Oz This is the Tower of Babel Remember; I wrote that Better than the bottom, Still not the top —it's not as fast, when it's not going all the way up Did you jump yet Come around more Keep coughing Are you sure this is where it was or—? Somewhere else I stayed Back when I was homeless It's hopeless! We lost her Antenna, antenna SUPERMARKET I loved her —she was undercover —I'm still in your stirrups I'm lost in New York, then BACKFIRE Adele remix is on [have a seat] Can I go now? I still need a hat, a half dollar and an alter cloth You could win an award for this; I don't want an award, I just want my son back Motherhood, motherhood Brotherhood, brotherhood This isn't one of us! No one was No one was Can I go now? Where to? Home! Nope, that's just the office, I'm still homeless, unless I They got cabanas on top of offices! (The rich and the famous) Networking and brunches— _this looks fun, doesn't it? I altered the course of history In brief exchanges and Various social atrocities This is hypocrisy! lol rly This is hypocrisy!! Hyper awareness and, psychic inclinations… You realize the more low quality people you let in The more low quality this country becomes, don't you? I put a roll in the back of the chosen ones. Used to be cast more, Now something seldom ever happens Such as this— A fun Fortune 500 What does that even mean Forbes. Look it up. What if the policy is Foreign; Look it up. I know enough about the girl next door to know Something is horrible, Something inside of her Rots at the core, Her obsession; My undeservedness of such, What she must, I mustn't, just Unjustice Broski, okay I got to discard All the pichardo Besides just this one (I'm standing on top of you) Put somebody worthy on the fourth floor Worse off, I was done for Before I got to New York What's her for?! I know enough about the man upstairs to know All these glares and “How dare you's” and Hatred says Why would you wait 30 years Until today, I guess Something is certainly off about her. I said yes. It was more probably something like “SUCK MY DICK” What. “YOU HEARD ME” Oh yes, I did. From 1990 to 1993 From 1990 To 1993 From 1990 To 1993 Stop breeding these things, “Love is familiarity” No Love is what you make it But you can't Because of slavery They don't make music —they don't make love either Well, look where your lust took you! Nowhere! Exactly! Look where your love took you: Vegas, Los Angeles, South of the Border Above it a New Yorker— Under budget, Celibate and My arms are too short to jump the turnstyle, Meanwhile My ex husband left permanent scars on My face My lips My arms My hands And my heart. Did you bite him? Of course I bit him, he was strangling me. You definitely won this fight. I know. Look, if I don't call for security, This bitch is gonna make me kill her. OCTOPUSSY NO. What. NO. Stankass. I will KILL this bitch. Look, I gotta get ahead in this. I need a WIN. These are customs. Trash. Wash your pussy. Send her back. Nah, you know what. Remove that hex. Wait, what, really?! Yeah, like; Reverse it. Woah. That's crazy. They got like….white slaves now. That's not right. What do you mean. That's not it. You said “reverse it” This is what the white supremacy just did to everyone else: [world in crisis except for for people who look like Kayla Lauren, to whom EVERYTHING is a fucking crisis, that isn't] BECKY/KAREN/WICKED WITCH OF WHITE AMERICA I AM OFFENDED I'm offended that you signed your like 12 year old daughter up to pose nearly nude, but— Hey look, it's us now; is this freedom?! Uh…. Why are all the female models like 12 and all the male models are fully grown men— Or women. Right. Idk. Wait, I do. You do?! Wait. Something tells me all the pedophiles and all the white supremacists are in the same group… Run the same businesses— Have the same families. This is disgusting Okay, this is gross That's not right ! That's not my job! Oh, it's not!!? NO. Who should I call That guy. So you want this? Oh, it's a death curse?! It will NEVER end. Wanna bet. I'll kill you and take the whole world with me. Now that's a threat. Thing is, I'm actually making it. I'm telling on you! Ok. Wait 30 years though so you look and sound REALLY fucking stupid. Ok. 30 YEARS. Doesn't make sense. What's the statute of limitations for— Hm. Depends. Depends on what. Who are you?! WHO ARE YOU?! NOBODY YOU SHOULD KNOW ABOUT. THEN WHY DO I? wtf is this? This is Texas being petty. Ok, fuck ya‘lol YAW. I'm serious, wtf is wrong with you. Something. What. Fix me. Fix you. Hm. Ok. *COUGHING* Somethings wrong here. Yep, it's definitely some kind of FIX IT. Where's this ROCK? At the ROCK. Like, where tho?! Ur gonna need this. What. They r crucifying u. Noted. Hunts Point Food Distribution Center Lmfao I need this word hold on “eliminating redundancies, setting strict timelines, and allowing cases to proceed contemporaneously” [ Finally, recognizing the danger that social media poses to young people and mental health, New York City Department of Health and Mental Hygiene Commissioner Dr. Ashwin Vasan today issued a Health Commissioner's Advisory identifying unfettered access to and use of social media as a public health hazard, just as past U.S. surgeons general have done with tobacco and firearms.] A win. I don't play dead. What do you call this: DIE! DIE, BITCH! Corrections. I still don't understand how this— ACID HAPPENS. Out of sight Out of mind So why these guys Tryna waste my time Tryna fuck with my mind with All these lights OH MY GOD I ain't got time for that Well, Maybe I do— I just Don't like NIGGAZ LIKE YOU. (Say what) I don't like Niggaz like U! I'm Sunnï Blū! You're stupid Oh, so he put a curse on sunni blu, too? Ok. Cool. When all my aliases come up This dumb motherfucking drunk Is gonna get stuck In his own woods He'll bury himself In the words that he left With the scars In the words that he left With the scars Sunni blu Is the sayer of stars I slaughtered them all Swallowed them whole Like a big black hole I'm a big black god I'm a big black God Fuck Twinkle that broad One punch girl One punch girl 5 punch faggot I'll unwrap flags on your Goddamn Fuck that Put a curse on my alter ego Lucky he's a he, tho I blow holes in em I blow smoke And love sausage I'm a hedon And he not a Hero He broke He lost I'm open Shirts vs skins I got 666 Curses to show you What your words did IM RA I'm a big black God You're at home with the young apostle Let's be honest He never even liked his father So turned him to a mother, Told his mother to ‘run far, And bring back The life that I want' I'm a big black God In light skinned clothing You don't know to explode Or explode on me Cause my mommy's a Dark skinned icon That my God Find something to pass the time, God Sunni with I, huh I won Fuck a pedophile wifebeater Bury him in the woods with his fury Fear me, now I'm coming up with reverse curses And cures Cause my words Bought the whole world Buried you in the woods I'll bury you in the woods, Bitch Very good I'm a big black God -Blū. GOD is the GOAT I just became god I do what I want I get what I want when I want it I don't want no problems Me myself and God only I buy everything I used to steal These tears in my heart say I'm healing What's the difference, anyway? I've never been fit for your interests, or industry Add insult to injury Add everything to my Amazon cart, then My sympathies Nothing is greater in heaven As it is in hell, for this industry Turned on its head And turned over from 7 to ten Check your messages, then Shut up kid, this doesn't involve you You're not included in the package Michael c hall and John c Riley reprise Mr. Cellophane in the style of DEXTER MORGAN. HA. Classic. GOT EM. V.O. I met her at The Jumping Point {Coming Up…} INT. THE JUMPING POINT POP-UP NIGHTCLUB LOUNGE & BAR. NIGHT “A Long Day's Night” / “A Hard Day's Night” C {CONFUSION SPELL, SUCCESSFUL} [Sequence Initiated.] {Enter The Multiverse} [The Festival Project.™] COPYRIGHT © THE FESTIVAL PROJECT 2019-2024 | THE COMPLEX COLLECTIVE. © ALL RIGHTS RESERVED. © -Ū. {

Puzsér Róbert, Horváth Oszkár, Kovács 4 Zoli

Puzsér Róbert, Horváth Oszkár, Kovács 4 Zoli

Change happens through time, it unfolds within the rhythmic inhale and exhale, it expresses through lunar and solar cycles, it follows the arc of development, fruition, and decline. There are recognizable pathways and markers that arise within what is mostly a non-linear experience of life.Daniel Atchison-Nevel used to skip school and hang out at the library where he found himself in the company of old Russian Jewish mystics, their stories and tattered copies of the Dao De Jing. Not a bad place to begin, if your destiny holds the potential to include the practice of Chinese medicine.Listen into this discussion of how undifferentiated wholeness ratchets down into the world of yin and yang, the constant interplay of fate and destiny, the vital importance of of being able to recognize the impulse towards healing within dysfunction, and how the most profound learning he received on the Extraordinary Vessels came from a man with whom he shared no common language.

Us chiropractors have some hard and fast beliefs and opinions that while rooted in truth and good intentions can at times create unrealistic standards that we hold ourselves to and unnecessary mindset burdens when things don't go exactly the “right” way. The topic and act of giving birth is one area where these mental gymnastics come into play more often than not. For today's episode, Dr. Lauryn starts by coining the idea of the “girl scout badges of chiropractic,” before welcoming on Dr. Lacey Nevel to discuss one of the most noteworthy of those badges: having a natural home birth. Dr. Lacey shares her own birthing story, and the two discuss ideas around what is “right” or “necessary” and how to live congruent with your beliefs while being ok with any positive outcomes. Dr. Lacey Nevel is a true wellness visionary wearing multiple hats. She's the co-owner of Free Spirit Chiropractic with her husband, Dr. Colton Nevel. Along with running the practice, Dr. Lacey is the founder of The Start Up Lab for Chiropractors, where she and her team do coaching and workshops for chiropractors in their early days of opening their practices. And finally she is also the founder of Free Spirit Social for Chiropractors, where she provides social media coaching and tools to other chiropractors. Overall, Dr. Lacey is on a mission to elevate consciousness and authenticity for others inside and outside the chiropractic community!The conversation kicks off with some podcasters talking podcasting chat, burnout in chiropractic, and how to build up associates, before diving into Dr. Lacey's background in the birthing community and her entire personal birthing story, and then close out with discussion on postpartum grief, making congruent decisions, why needing a specific outcome can backfire, and a whole bunch more related to the mindset around birthing for female chiropractors.New chiropractor at the beginning of your journey? Check out The Start Up Lab for Chiropractors to see if one of their programs may be right for you!Listen to Free Your Frequency podcast: Apple | Spotify Are you a chiropractor in need of some social media help? Check out Free Spirit Chiropractic Social!Follow Dr. Lacey: InstagramFollow Free Spirit Chiropractic: Instagram– – – – – Sign up here to receive our monthly associate job postings email.Rate & subscribe wherever you get your podcasts!Join the Weekly Slay mailing list HEREIf you want to submit a question or have feedback, make sure to tell us:Website | Instagram | FacebookMentioned in this episode:Learn more about Sunlighten Saunas and get your She Slays discount by clicking the link below!

The explosion in diagnostic tools to identify immune-mediated myelopathies has led to much more precise diagnosis and treatment of these patients, but also created gaps in knowledge. In this episode, Kait Nevel, MD speaks with Michael Levy, MD, PhD, FAAN author of the article “Immune-Mediated Myelopathies,” in the Continuum February 2024 Spinal Cord Disorders issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Levy is an associate professor at Massachusetts General Hospital and Harvard Medical School in Boston, Massachusetts.  Additional Resources Read the article: Immune-Mediated Myelopathies Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @IUneurodocmom Guest: @mlevy18 Transcript  Full transcript available on Libsyn 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, a companion podcast to the journal. Continuum Audio features conversations with the guest editors and authors of Continuum, 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 by visiting the link in the show notes. Subscribers also have access to exclusive audio content not featured on the podcast. As an ad-free journal entirely supported by subscriptions, if you're not already a subscriber, we encourage you to become one. For more information on subscribing, please visit the link in the episode notes. AAN members, stay tuned after the episode to hear how you can get CME for listening. Dr Nevel: This is Dr Kait Nevel. Today, I'm interviewing Dr Michael Levy on immune-mediated myelopathies, which is part of the February 2024 Continuum issue on spinal cord disorders. Dr Levy is an Associate Professor at Massachusetts General Hospital in Harvard Medical School in Boston, Massachusetts. Welcome to the podcast. Thank you so much for being here today and chatting with me about your article. I really enjoyed reading your article. I read through it, and it felt like, you know, just really enjoyable. I had no concept of time when I was reading it. I encourage all of the listeners to read the article, too. I'll start with just a really broad question, with - what is the most important, clinically relevant thing from your article that you'd like the neurologist listening today to know? Dr Levy: I would say that the group of conditions in which the immune system can attack the spinal cord are growing. We're getting better at identifying the specific antigens, like in the case of NMO neuromyelitis optica and in MOG antibody disease. We're getting better at identifying targets for treatment, like with neurosarcoidosis - identifying those biologics that seem to help. And then, we're even beginning to characterize some of the idiopathic forms, some of which follow covid, or vaccines, or other conditions. I think the message is that we're getting a lot better out there, and if you have a case of inflammation in the spinal cord, then this is something that has a good workup now (and people should be paying attention to articles like this that give them an idea for how to work this up), and then the most appropriate treatment. Dr Nevel: Right. And not to get too much “in the weeds,” but in your article, you really outlined very nicely an algorithm or stepwise approach in evaluating patients with suspected immune-mediated myelopathies. Could you just briefly go through the general principles of that evaluation and stepwise approach, and what you would consider really necessary tests to order for these patients? Dr Levy: Sure. I would say that the first thing that you want to do is to make sure that it's inflammatory. And to do that, we have – the blood tests are few and far in between. If you're dealing with inflammation in the spinal cord, the few ways that we have to convince ourselves that there's truly inflammation - there are MRI and spinal fluid - and those objective tests need to be considered in the appropriate clinical context. The order of events is: patient comes in, reports certain neurological functions that localize to the spinal cord - that's step one, Step two, neurological exam that confirms that there's a neurological problem that localizes to the spinal cord. And then, numbers three, four, five are objective workups, including MRI of the spinal cord and other parts of the neuraxis, CSF testing, and blood testing, all of which then support your differential diagnosis. For each diagnosis, that order is the same, and it should always result in an answer for you, which ultimately may all be negative (and then we have a plan for that, too). If all your workup is negative, you don't know what caused it - at least a plan to deal with that as well. Dr Nevel: Building off of that - in your article, you mentioned that there are shared features between the different immune-mediated myelopathies. We have some tests that can help us differentiate, but what are some of the limitations or strengths of our currently available diagnostic evaluations - our clinical clues to help us differentiate between the different types? Dr Levy: The biggest limitation, of course, is that it's hard to access the spinal cord. We're not going to biopsy almost any patient unless we really have to rule out cancer. Otherwise, we don't want to take a punch out of a very small spinal cord that's carrying a bunch of fibers going in and out of the brain. So, that is our biggest limitation. We can't physically see it under the microscope, so we have to infer what's going on with MRIs and spinal fluid. And of course, spinal fluid isn't necessarily directly in touch with the inflammation - it could just be around it and bathing it. But we're hoping that there are clues from the spinal cord that shed into the spinal fluid that we can detect by lumbar puncture. I do think that we're getting better and also we're identifying things in the bloodstream that could also impact the spinal cord. And of course, blood tests are much easier to do, and some of these blood tests look for antibodies, which we know last for months and months. So, even if a person is having trouble getting their workup done on time, these antibody tests are still useful, even months after onset. Dr Nevel: Yeah. In your opinion, what have been some of the bigger breakthroughs? And I know there's been a lot in immune-mediated myelopathies over, let's say, the past five to ten years. That's a long timeframe, and I know a lot of things have happened during that timeframe – but what do you think has made the biggest impact in either evaluation and/or treatment for these patients? Dr Levy: When I was training, everything in the spinal cord was always MS. It was just - everything was multiple sclerosis in this big bucket of MS that we thought was heterogeneous. Now we're identifying the biomarkers that actually are distinguishing these patients from MS. We know what the immune system is targeting now in many of these conditions. Then, based on that immunological pathway, there are drug targets that have been developed. So, for even a very small disease, with 20,000 people in the US (one in 100,000) who have neuromyelitis optica, we now have three FDA-approved drugs because the science is so well worked out. And now there are two trials in MOG antibody disease, for example. As we identify new biomarkers based on the antigen specificity of the disease, I think we're going to have more and more specific therapies for each of these conditions, even if they're rare diseases. Dr Nevel: Yeah, that's great. Thanks for mentioning those, and I urge the listeners to check out the article to read a little bit more about some of those treatments for NMO spectrum disorder and MOG antibody disease that are in trials. What's the most common mistake that clinicians can make when evaluating or treating patients with immune-mediated myelopathies. What should we watch out for or to try to avoid doing? Dr Levy: I would say, at the beginning, there might be an urge to overtreat because we know that “time is spinal cord” - we don't want to waste time; we don't want to lose time. Some clinicians might just be inclined to give high doses of steroids, even in cases that they're not sure are inflammatory. The big overlap here is especially in older people who might have vascular myelopathy, where steroids might make things worse and it might delay their care. So that's the first problem – is, when physicians rush to judgment. Then the other big problem is when they take their time, and they say, “Well, this is just multiple sclerosis, probably. And we know that, in the end, MS patients do the same whether they're treated or not treated, and so we can take our time with this.” Whereas if we know that this is actually NMOSD, time is spinal cord and destruction is ongoing and potentially irreversible. I would say that there's problems on both sides of the time window. My approach is to be aggressive very early on and try to identify whether or not it's inflammatory. And then if it's not, then you can take a step back and go to the other chapters in this continuum - try to figure out what this is – and if it is inflammatory, then you definitely want to get on top of the treatment. Dr Nevel: Yeah, finding that sweet spot; making sure that you're not waiting too long but that you're not treating inappropriately or the wrong thing. So, what do you think - let's say you have a patient with an immune-mediated myelopathy; you've diagnosed them, they're undergoing treatment. What's the most challenging part of ongoing management of a person who has an immune-mediated myelopathy? Dr Levy: I would say that one of the most satisfying parts of my career lately has been that we're good at preventing the next attack once we know what the disease is. So, for NMO and for MOG and MS, we're good at that. We can suppress the immune system or modulate it in a way that we're preventing the next attack from occurring, and patients are excited about that. But when they come into clinic and I say, “Great job, no new attacks,” then they look at me and they go, “But how do I get out of my wheelchair now?” Because the damage done from prior attacks is not touched by any of these meds. So, there's a huge unmet need in that area of regeneration and recovery of function because, while it's all great that we can prevent the next attack and with all these great drugs that are approved, patients are still suffering. They have mobility problems, bowel/bladder problems, and pain, especially neuropathic pain, that really causes a lot of disability, and that's from damage that's already done. It's the same as spinal cord injury from trauma or from tumors or whatever - the spinal cord injury is the same and there's still a huge unmet need in that area. Dr Nevel: On that note, who else do you usually consider part of the team, if you will - who else should be involved in the management of these patients? Dr Levy: A lot of people. We have urologists involved for bladder, we have physical therapists involved for mobility, and occupational therapy for things related to hand and hand function. We have psychiatrists related to mental illness and also just dealing with these issues, because even if you don't have clinical depression, you still have an adjustment from the disease process and from all the treatments. Social workers, because this is a huge financial burden for a lot of people. An often rheumatologists, because NMO, for example, has about 25 percent overlap with other diseases. We don't want to double treat - we'll often choose a treatment that's applicable to both the rheumatologic disease and the neurological disease. So, I'd say that we don't work alone in almost any case; it's usually quite a big team involved. Dr Nevel: One of the questions that I always like to ask is, what do you think the next big breakthrough is going to be in immune-mediated myelopathies? What's most exciting to you - what do you think is on the horizon here? Dr Levy: I think probably the most exciting area is in multiple sclerosis, where we're starting to understand the role of the Epstein-Barr virus in triggering the disease, and potentially, even in driving the disease. Up to now, we've been suppressing immune systems in people with MS. But maybe we should be looking more at how can we prevent MS from occurring in the first place. And in cases where MS has already started, how does the virus play a role, and can we potentially modulate the outcome of disease with something like antivirals against EBV? So, I think that's the huge, exciting area. It's dominating a lot of the conversations at neuroimmunology conferences. But I think it's well worth the investigation because if MS turns out to be just an Epstein-Barr virus infection, I think a lot of what we've been doing up to now might not be as relevant. So, this is something that's very important. Dr Nevel: Yeah - to have a way to prevent disease rather than treating it after, too, would be a super powerful thing. Dr. Levy: And there are lots of Epstein-Barr virus vaccines that are being developed. But then the question comes up, “Well, are we going to prevent one in a thousand people from getting MS by vaccinating all thousand kids?” Is that really worth it? Can we pick out the ones who are more high risk for developing MS and just vaccinate those kids? A lot of ethical questions involved in that, too. Then what happens if we don't let our population get infected with EBV? We've evolved with that virus for hundreds of thousands of years. What if we abolish it all of a sudden - what does that do? Does it have any implications? I don't know. Dr Nevel: Yeah, lots of really complicated things to think through, with exciting potential but a lot of unknowns. Dr Levy: A lot of unknowns. Dr. Nevel: Talking about patients with seronegative relapsing transverse myelitis - what's your general approach to those patients? When you feel like you've exhausted the extent of your workup but they have a relapsing transverse myelitis, how do we approach those patients and take care of them? Dr Levy: “Seronegative” refers to patients who test negative for aquaporin-4, which is NMO, and test negative for MOG antibody disease (so they are double seronegative), but they have a recurring disease that looks an awful lot like one of the two. We generally stratify these patients into the “aquaporin-4-like,” “MOG-like” or “MS- like.” So, we try to put them into a category even if they're seronegative because we think that the treatments would be the same. So, for the MOG-like, for example: these are patients who have recurring attacks; they're not necessarily all long, but they do tend to remyelinate, and they can be severe at first but then they do get better over time. That's “MOG-ish,” so we treat those people with MOG treatments. Whereas people who have this sort of aquaporin-4 type, they have severe attacks and they really don't get better, and they have a lot of necrosis if you look at it under the microscope. And those people we tend to treat with aquaporin-4 NMO drugs. And then we have the MS type that kind of lingers or is more focal white matter lesions. Even if they don't have a lot of brain lesions, they might be oligoclonal band-positive; we put them in the category of MS. But we have a very active research effort to identify new antibodies in case any of these diseases that are seronegative and don't fit into any category - it's certainly possible that there's an antigen of their own that they're attacking, so we'd like to try to identify that in these novel assays that we're doing in the lab. Dr Nevel: How do you counsel patients on what to expect in the future, who you're seeing in the hospital with their first episode of transverse myelitis, for whatever the cause? Because one of the biggest questions I suspect most patients ask is, “Am I going to get better? Is this going to happen to me again?” How do you navigate those tough discussions, and what do you tell patients? Dr Levy: In the hospital, it's tough, because a lot of our testing takes time - it takes ten, fourteen days. So, in the hospital, I say, “Look, we're going to focus on here and now - we're going to suppress the inflation; we're going to try to get you better from this event.” It could have been a severe optic neuritis or transverse myelitis, or brain stem injury, or whatever - we're going to try to focus on that. And then I say, “When you come back to my clinic, we'll have the results from all of your testing and we're able to talk about the future and how to prevent the next one, if we have to.” It does take time, unfortunately, to get all that data back, and it is a little bit suspenseful for patients, but that's what we have at the moment. Dr Nevel: Yeah, the most honest answer that you can give them is always the best one. And that's the scenario when you're in the hospital - that there just isn't full answers. Dr Levy: Yeah. One of the reassuring things I can say is, “We have a lot of medications that target different parts of the immune system, so no matter what you have, we can probably treat it.” Dr Nevel: Right. Obviously, really important to give people a sense of hope and reassurance that you're there and you're going to help find a treatment that's going to help them in the future. Well, thank you so much for chatting with me today. I really enjoyed our conversation and reading your article and learning more about immune-mediated myelopathies. Dr Levy: It's been a pleasure. Thank you. Dr Nevel: Thank you, Dr Levy, for joining me on Continuum Audio. Again, today we've been interviewing Dr Michael Levy, whose article on immune-mediated myelopathies appears in the most recent issue of Continuum, on spinal cord disorders. Be sure to check out Continuum Audio podcasts from this and other issues, and thank you to our listeners for joining us today. Dr. Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, please consider subscribing to the journal. There's a link in the episode notes. We'd also appreciate you following the podcast and rating or reviewing it. AAN members: go to the link in the episode notes and complete the evaluation to get CME for this episode. Thank you for listening to Continuum Audio.

While collectively uncommon, the clinical presentation of genetically-mediated spinal cord disorders frequently overlaps with other neurologic conditions. Our understanding of these disorders has grown considerably. In this episode, Kait Nevel, MD, speaks with Kara Stavros, MD, FAAN, author of the article “Genetic Myelopathies,” in the Continuum February 2024 Spinal Cord Disorders issue. Dr. Nevel is a Continuum® Audio interviewer and a neurologist and neuro-oncologist at Indiana University School of Medicine in Indianapolis, Indiana. Dr. Stavros is an associate professor of neurology and clinician educator at Warren Alpert Medical School of Brown University in Providence, Rhode Island. Additional Resources Read the article: Genetic Myelopathies Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @IUneurodocmom Guest: @StavrosKara Transcript  Full transcript available on Libsyn 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, a companion podcast of the journal. Continuum Audio features conversations with the guest editors and authors of Continuum, 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 by clicking on the link in the show notes. Subscribers also have access to exclusive audio content not featured on the podcast. As an ad-free journal entirely supported by subscriptions, if you're not already a subscriber, we encourage you to become one. For more information on subscribing, please visit the link in the episode notes. AAN members, stay tuned after the episode to hear how you can get CME for listening. Dr Nevel: This is Dr Kait Nevel. Today, I'm interviewing Dr Kara Stavros on genetic myelopathies, which is part of the February 2024 Continuum issue on spinal cord disorders. Dr Stavros is an Associate Professor of Neurology and Clinician Educator at Warren Alpert Medical School at Brown University in Providence, Rhode Island. Welcome to the podcast. What is the biggest takeaway from your article that you'd like the neurologists listening to this to know? Dr Stavros: I would have to say that there's maybe two big takeaways that I would want to highlight. One would be that, generally speaking, in a nutshell, the genetic myelopathies can present with chronic and progressive symptoms, oftentimes (but not always) a family history of similar symptoms, and involvement of other structures outside of the spinal cord. Exclusion of the more treatable causes of myelopathy is a really key and important step in the diagnostic process. And because there are many different causes of genetic myelopathies, in some cases, the symptoms can overlap. I think this really underscores the utility of doing genetic testing to really confirm the precise underlying neurologic condition. The second takeaway that I would want to highlight is that, while treatment for most of these conditions is typically supportive, there have been a number of recent therapeutic breakthroughs for treatments in ALS, spinal muscular atrophy, adrenal myeloneuropathy, and Friedreich ataxia. While these aren't cures, it's really exciting and gratifying to see new therapeutics emerge via different mechanisms for patients with conditions that we've had very little treatment options for in the past. Dr Nevel: Yeah, I really enjoyed reading that in your article - about these treatments that have been coming out over the past several years. The one with Friedreich's ataxia, too - that looked like it was really just recently approved this year. Dr Stavros: Yes. Dr Nevel: And so, kind of jumping off of that topic - there have been these exciting treatments that have been coming through. What do you think is going to be the next big thing? Or what do you think is the next thing that might come through? Or what's going on in research in genetic myelopathies that might help our patients? Dr Stavros: That's a really great question. I think that, as far as the future in this area, genetic testing has definitely grown in terms of being able to identify more genes now that are implicated in these disorders than ever before. But this is still an area where our knowledge is continuing to evolve. So, I think the future holds further advancements in our ability to successfully diagnose patients who have these conditions and provide them with the sense of closure that having a definitive diagnosis brings, as well as opening the door to potentially targeted treatment options once a specific diagnosis is made. Another thing I think the future holds is continued development of expanded treatment options for patients with these conditions, both in terms of advancing our supportive care capabilities and then also providing more disease-modifying therapies. Again, as I mentioned, in recent years, new disease-modifying treatments have actually become available for several of these conditions. And I think that's just the beginning. There's going to be more to come, for sure. Dr. Nevel: Yeah, that would be great. Going back to the genetic testing and how things are - we're finding more and more and more genes. When you decide that genetic testing is indicated, how do you counsel your patients about genetic testing and walk them through that process? Dr Stavros: Okay - I would say that it usually starts with having a conversation with the patient about whether they want to pursue genetic testing or not for the particular condition or conditions that are suspected. Genetic testing is really helpful to, again, confirm the diagnosis once the initial diagnostic workup perhaps has given you some clues as to what the underlying condition might be. Again, because sometimes the clinical symptoms can overlap in different genetic myelopathies in particular, the genetic diagnosis can be really important as far as getting a definitive, final diagnosis. Usually testing is pretty carefully considered and the risks versus the benefits are explored with the patient. Oftentimes, this is done in conjunction with a genetic counselor or with genetics clinic. So, there's a lot of teamwork there in working with the genetics department, at least in my experience. There's a lot of options that might include testing a panel of genes for the suspected condition, to up to whole-exome sequencing. Again, this is really like an evolving landscape. So, we have a current understanding of the genes that are implicated in some of the genetic myelopathies, but there's still so much that we don't know. So, a lot of times, testing can result inconclusive or may be falsely negative, and it can be tough because a negative test doesn't necessarily exclude a potential genetic etiology. It becomes a very nuanced, I think, conversation and journey with the patient. Dr Nevel: Yeah, and in your article you mentioned some of the health care disparities that exist around genetic testing and access to genetic testing, specifically. How do we, as clinicians, try to mitigate inequities in regard to access, or in regards to being able to offer our patients genetic testing - is there anything that we can do? Dr Stavros: I do think there are some resources available, where free or sponsored testing can be utilized from nonprofit organizations or pharmaceutical companies. But you're right that this is a real area for potential health care disparities. And making sure that we have equitable access to genetic testing is really important. Some of the issues that come up are: limited access due to location; due to socioeconomic factors; a lack of awareness on the part of the patient or sometimes the provider about testing that's available; cost, of course, being a big issue, oftentimes; and sometimes, distrust of how the medical information, the genetic information, might be used or protected. Dr Nevel: What do you think is one of the most challenging things about managing patients with genetic myelopathies? Dr Stavros: I think one of the more challenging aspects of the care is the diagnostic journey. I think that some of these conditions - most of them are not terribly common – and they may not always be at the top of our differential diagnosis in the course of a workup for myelopathy. The first step, I think, is really continuing to be aware of these conditions and not letting them become a “blind spot” when we're formulating a differential diagnosis for a patient with myelopathic symptoms. I think it can really take some time to reach the ultimate diagnosis for most of these conditions. Another challenging aspect, which I alluded to earlier, is sometimes when genetic testing might come back inconclusive or nonrevealing, and there remains some diagnostic uncertainty despite best efforts and a thorough workup -that can be frustrating as well, sometimes. Again, our knowledge of these genetics and the genetic mutations underlying these disorders is still really evolving. But on the flip side, there's a lot of rewarding aspects as well. I think one of the most rewarding aspects is trying to help patients identify interventions that improve their quality of life, and working with the patients and their families (who oftentimes become very expert in their own rare conditions in their own right), and working amongst the interdisciplinary teams. So many of these conditions are associated with extraneurologic manifestations, and so patients need coordination of care with other specialists. Hereditary spastic paraplegia is a great example, as well as Friedreich ataxia, where you often work closely with the cardiologist and of course, ALS, where there are a lot of multidisciplinary needs. Dr Nevel: Yeah, I'm so glad that you mentioned that because, in neurology in general (and specifically in this area), I can imagine the benefit to patients when there are multiple specialists involved in their care who are experts in the various aspects that are impacted from their underlying condition. Shifting gears a little bit - but going back to something that you've mentioned a few times, about making sure that we don't have a blind spot to genetic myelopathies, and that we consider this in part of our differential diagnosis when we're evaluating patients - in the patient who doesn't have an extensive family history of the exact same neurological symptoms, when should we consider genetic testing for patients that we're seeing in clinic? Like, at what point should we say, “Okay, we've done the other tests and now is the time to consider genetic testing.” Because I think, unless somebody has that really strong family history, it's probably not on the top of your list to do it right away, for a variety of reasons. Dr Stavros: I think you make a great point. Family history is tricky because, typically, we use that as a really strong clue of an inherited disorder of any type. But it can be tricky because, for a variety of reasons, it might be negative. Sometimes there is a de novo mutation, or there's variable phenotypes within the family, variable penetrance within the same family. Autosomal recessive inheritance can actually be, sometimes, hard to pick out. Or sometimes, patients don't have knowledge of their family members' medical histories. For all of these reasons, there may be information lacking in the family history. But I would say one of the most important things to exclude when you're working up patients initially is, of course, acquired causes of myelopathy, because you wouldn't want to miss a more treatable cause. And so, things like structural causes, nutritional, vascular or demyelinating causes (things that are explored more deeply in some of the other articles in this issue) are important. But if you've excluded acquired causes despite lacking a strong family history, I think, at that point, it's worth broadening your differential diagnosis to consider whether you might have reason to suspect a genetic myelopathy, particularly if you have some extraneurologic manifestations, some systemic symptoms that might be a clue towards a more systemic process. In genetic myelopathy, sometimes imaging can actually be quite helpful. It helps you exclude - MRI of the spine can help you exclude acquired causes, but it also helps you sometimes get clues toward a genetic cause. Typically, the finding might be either normal or show some spinal cord atrophy (but typically without signal change, so that can sometimes be a clue). Dr Nevel: What's one mistake that is made in managing patients with genetic myelopathies? Maybe “mistake” is too strong a word; maybe “misconception” about treating patients with genetic myelopathies. Dr Stavros: That's a great question. I think that one of the, maybe, misconceptions might be that these are homogeneous entities, these different diseases. But one of the things that surprised me anew in going back to research this topic and prepare this article was a reminder of just how variable both the genotypes and the phenotypes are within what we consider sometimes just one diagnosis, like hereditary spastic paraplegia, for example, spinocerebellar ataxia. There's so many different presentations and genotypes associated with these. It's really a family of different conditions. You could say the same thing about ALS as well. So, the spectrum of disease, I think, is important to recognize. Dr Nevel: Yeah, and I can imagine because of that spectrum of disease, just having an open mind in considering genetic testing and not excluding a potential genetic cause because it doesn't fit into what we think is the most typical presentation of that genetic condition. Dr Stavros: Yes - I'm in total agreement. Dr Nevel: I've asked you about what some of the misconceptions are and what some of the challenges are, but what's the most rewarding part about taking care of patients with genetic myelopathies for you? Dr Stavros: I think one of the most rewarding parts has to be working with the patients and the families. Like I mentioned earlier, sometimes they become so expert in their own conditions - it's amazing. And, working with them, working with the interdisciplinary teams, is a really rewarding process. I think that the more I've encountered patients with some of these rare conditions, the more I've learned from their stories and experiences, and so, that's, I think, been the most rewarding aspect to me. Dr Nevel: You've mentioned the multidisciplinary team a couple of times that we've talked about this, but who specifically do you usually include or contributes to the care of these patients? Dr Stavros: It may depend on the condition in question. So, for example, for Friedreich ataxia, there's always going to be a cardiologist involved in the patient's care. For ALS, there's going to be a larger team. For those who are familiar with ALS multidisciplinary clinics, this often includes physical therapy, speech therapy, nursing, pulmonary, and many others. And so, it really depends. I think in most cases though, genetics evaluation and genetic counseling is a really important piece. Dr Nevel: How do you work with the genetic counselors in counseling families about testing other family members? Because that's something that's really challenging in genetic conditions, especially for people with children that may be underage, and this is a really complicated topic. But how do you approach that? Dr Stavros: I think that it may depend on your particular institution. Where I'm at, typically, that's something that our genetics department will take the lead on and they will meet with the patient first and then also meet with and bring in any interested family members who are hoping to pursue the possibility of testing themselves. There's a bit of controversy or differing opinions around genetic testing, specifically for presymptomatic individuals for inherited ALS, because - certainly, there's pros and cons for being tested for any condition, but some special considerations come into play when someone is presymptomatic. There's actually been studies done, in particular, on patients who have a family history of ALS who are presymptomatic, and generally, the studies have shown that those patients are usually - the majority - in favor of being tested. But it does certainly bring up some ethical implications. Of course, any discussion is going to be undertaken with the goal of informing the patient and discussing the risks versus the benefits in detail. There's actually recommendations on the principles and the practice of presymptomatic testing for ALS, which is available and referenced in the article. Dr Nevel: Do you think as - hopefully, in the future, as more treatments become available - that presymptomatic genetic testing could play a role in how we manage patients? Dr Stavros: I think that's a great thought. I think it may, especially as more treatments become available, I think there may be a greater interest in demand for finding out early whether you might have a likelihood of developing a certain condition so that you can plan accordingly and perhaps even pursue treatments early on. Dr Nevel: You know, you mentioned this (and this isn't maybe quite exactly the same thing), but in SMA - you mentioned newborn screening for SMA and new treatment for SMA, and that newborn screening is not always a standard, and that there's controversy around that, now that we have treatment for it. Dr Stavros: Yes. That's another area where some controversy comes up as well, as far as cost and treatment, for sure. Dr Nevel: Thank you, Dr Stavros, for joining me on Continuum Audio. Again, today we've been interviewing Dr Kara Stavros, whose article on genetic myelopathies appears in the most recent issue of Continuum on spinal cord disorders. Be sure to check out Continuum Audio podcasts from this and other issues. And thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, please consider subscribing to the journal. There's a link in the episode notes. We'd also appreciate you following the podcast and rating or reviewing it. AAN members, go to the link in the episode notes and complete the evaluation to get CME for this episode. Thank you for listening to Continuum Audio.

Idén több mint 72 ezer tanulót és családját tartja stresszben a középiskolai felvételi. Gyarmathy Éva klinikai és neveléslélektani szakpszichológussal, a Magyarországi Diszlexia Központ és az SNI tehetségeket segítő tanács megalapítójával arra keressük a választ, miért vált ki ilyen szélsőséges indulatokat a felvételi rendszer. Műsorvezető: Sashegyi Zsófia.

Interjút adott a Szabad Európának a bicskei gyermekotthon volt nevelője. Bárnai Árpád és egy kollégája lépett fel először a gyerekeket szexuálisan bántalmazó igazgatóval és az ügy eltussolásában segédkező helyettesével szemben. Az interjú készítője, Kerényi György a Sztoriban vendége.

A kegyelmi botrány kapcsán sokkal több szó esik a politikai felelősségről, mint a gyermekvédelemről, noha a szakemberek szerint ez az ügy valójában a gyermekvédelmi rendszer leggyengébb pontjait mutatja meg. Herczog Mária szociológust, gyermekvédelmi szakembert ezekről a gyenge pontokról kérdeztük.

A kormány a családok és a gyermekek támogatását, védelmét hirdeti, azonban a Szabad Európa tényfeltáró sorozatában a Szabadonban megszólalók, volt állami gondozottak, nevelők beszámolóiból kibontakozó valóság arcul csapja az embert. Podcastunkban a riport készítőjét, Bihari Ádámot kérdeztük.

Vandaag eens geen lezing uit arxiv.org of Wikipedia, maar een pleidooi voor de verwondering. Als vehikel voor de verwondering gebruiken we in deze aflevering de wonderschone Trifid nevel of M20. Maar u kunt natuurlijk iets pakken wat meer bij u past, zoals een afbeelding van Anna Kournikova, uw laatste aanwinst op het gebied van glazen vensterbank-beestjes of een catalogus van BMW.Het bezit van de zaak is het einde van het vermaak:https://www.sg.uu.nl/artikelen/2013/08/het-bezit-van-de-zaak-het-einde-van-het-vermaakTrifid nevel:https://theplanets.org/nebula-facts/trifid-nebula/HII regio:https://en.wikipedia.org/wiki/H_II_regionDe Zimmerman en Space podcast is gelicenseerd onder een Creative Commons CC0 1.0 licentie.http://creativecommons.org/publicdomain/zero/1.0

Sz. Bíró Zoltán Oroszország-kutató történésszel a putyini emlékezetpolitikáról és az oktatás egészére kiterjedő ideológiai nevelésről beszélgettünk a G7 Podcastban. The post Már az óvodákban kezdik az ideológiai nevelést, Sztálin a legnépszerűbb Oroszországban first appeared on G7 - Gazdasági sztorik érthetően.

Esta semana venimos con menos temas que tetas en los brasieres de Jenniffer González, pero sin dejarla caer neveL. La convención del PNP nos dejó muchísimas emociones, entre ellas la lucha de Rivera Schatz por el “campeonato de la fe” ante Proyecto Dignidad, los estadistas ponen la cafrería como punta de lanza de cara al 2024 con los Can-am, y la prensa decide que hay que combatir a las huestes penepés con cartas falsas y fotos viejas. En el PPD, Tatito y Jesús Manuel se agarran por lo güevos porque aún creen que tienen break de ganar las elecciones; Donald Trump estrena un hermoso mugshot, más padres brillantes deciden darle homeschooling a sus hijos genios, y sacamos un rato para hablar de un tema bien, bien serio: cómo le robaron la corona de Miss Universe PR a nuestro gallo, Miss Cabo Rojo. Recuerda: si te ofendes, eso no es problema de nosotros. ¡Desde GW-Cinco, esto es #LaHoraMachorra! PODCAST DE OSCAR DE LUCHA LIBRE: https://www.youtube.com/@LuchaLibreNewsPR USA EL CÓDIGO "20MACHORRO" PARA UN 20% DE DESCUENTO EN: https://www.manscaped.com/ LAS MEJORES ARTESANÍAS: https://prartisans.com/ LA MEJOR MARCA DE ROPA BORICUA: https://www.resistancecompany.com/ PATREON: https://www.patreon.com/lahoramachorra INSTAGRAM: https://www.instagram.com/lahoramachorra/ CANAL DE CLIPS: https://www.youtube.com/c/lahoramachorraclips EL MEJOR STUDIO DE PE ERRE: https://www.instagram.com/gw_cinco/ Hosts: Alexis 'Macetaminofén' Zárraga, José Valiente & Oscar Navarro === REDES === Maceta https://www.facebook.com/TioMacetaminofen https://twitter.com/Macetaminofen https://www.instagram.com/macetaminofen/ Valiente https://www.youtube.com/user/valiente101 https://twitter.com/JoseValiente https://www.instagram.com/josevalientepr/ Oscar https://linktr.ee/oscarnavarropr   

Amanda Nevel joined the Department of Wildlife Resources in 2016 as a Conservation Police Officer serving in the Northern Neck of Virginia. Amanda has a passion for outreach and education initiating a Women and Youth Hunter Education Class, which is going on its sixth year. The class focuses on gettingstudents out of the class and into the works for hands-on training. She won a DWR Regional Outreach award for her work with the Women's program. Amanda even started a National Night Out program in Richmond County to raise awareness for the different first responders in the area. She is passionate anddriven when it comes to natural resource protection. In a year-long investigation of a poacher, she discovered over 50 wildlife violations including over the limit, shooting from the road, trespassing, license violations, and more. She has conducted several investigations for fatal boat accidents, as well as boating and hunting accidents with injuries. Amanda won the Conservation Police Officer of the Year for the State for 2022. She is passionate about teaching the next generation of CPOs, assisting at the last two CPO academies. Amanda was recently promoted to the Basic Academy Training Sergeant in June 2023. Before DWR, Amanda spent 5 years in the United States Marine Corps as a Military Police Officer with the Presidential Helicopter Unit, HMX-1. During this time, Amanda traveled to over 21 different countries and served under two different Presidents.In her free time, she furthered her education completing two Master's Degrees in conservation. Amanda also enjoys section hiking the Appalachian Trail and currently has 350 miles completed.

Season 4 Episode 85 Accounting High is supported by our Booster Club Thank you ⁠G-ACCON⁠ Check em out, 14 day free trial go to accon.services  CLASS: #PeerReview FACULTY: John Nevel, CPA & Jason Ackerman, CPA  SPONSOR: G-ACCON TITLE: Teaching Accounting Soft Skills: From CAS to ASS About this episode: In this episode of Accounting High, Scott and Jason interview John Nevel, co-founder and CEO of Compass East. a Nashville-based accounting firm. John shares his journey to Nashville, how he founded his firm, and the challenges he faced while growing it. He also talks about the importance of bridging the GAAP and the services provided by his firm. John goes into detail about his firm's pricing strategy and how they decide on fees, including tips for raising fees. He shares what he would have done differently if he could go back in time and how he spends time training his employees. The discussion also covers topics such as vetting clients, dealing with different personality types, and managing a virtual workspace. John shares his excitement for the future of his company and offers valuable advice for firm owners. Don't miss this informative episode! --- Send in a voice message: https://podcasters.spotify.com/pod/show/accountinghigh/message

In this episode, we speak with Jesse Nevel, Chair of the Uhuru Solidarity Movement, on his history with the Solidarity Movement and his perspective on the FBI attacks on the African People's Socialist Party and the Uhuru Movement. Jesse talks about the strategic importance of the Uhuru Solidarity Movement and how the Movement has grown since these attacks. 

Néhol egy pofon sem csattanhat el, máshol pénzért árulják őket – rendkívül eltérő volt a gyerekjogok helyzete a kilencvenes évek elején, és azóta is maradt javítanivaló. A Szabad Európa Rádió műsora körképet ad arról, milyen sorsa van a családokban élő és a szülők nélkül felnövő kiskorúaknak.

Anne is so much more than a short bio, and more complex than a business summary. Whether working at her day job, volunteering with organizations she cares about, maintaining side ventures, or serving as a good friend or family member – she aims to create reliable, safe spaces for others to feel free to be themselves. Anne has held a variety of positions in various industries. Over the last 16 years, in her role in the association space, she has overseen educational activities in several different industries, primarily within trades and healthcare (her favorite was the helicopter industry). Currently, she is the Vice President of Education for the Healthcare Distribution Alliance. She is fired up by connections… connections of all types. When she talks about people or projects, she sees connections. Her combination of strengths is what drives her desire to connect the right people to each other and to the right projects. She leads with confidence in her instincts in terms of the best opportunities for individuals to truly shine in their own talents, for themselves and for the greater good. The reason people feel good around her is that she truly SEES them and knows what they need to be successful. She then presents her vision of them with so much confidence and leadership they can't help but believe her – this makes her good at getting people to do things they otherwise are unlikely to do.

Anne is so much more than a short bio, and more complex than a business summary. Whether working at her day job, volunteering with organizations she cares about, maintaining side ventures, or serving as a good friend or family member – she aims to create reliable, safe spaces for others to feel free to be themselves. Anne has held a variety of positions in various industries. Over the last 16 years, in her role in the association space, she has overseen educational activities in several different industries, primarily within trades and healthcare (her favorite was the helicopter industry). Currently, she is the Vice President of Education for the Healthcare Distribution Alliance. She is fired up by connections… connections of all types. When she talks about people or projects, she sees connections. Her combination of strengths is what drives her desire to connect the right people to each other and to the right projects. She leads with confidence in her instincts in terms of the best opportunities for individuals to truly shine in their own talents, for themselves and for the greater good. The reason people feel good around her is that she truly SEES them and knows what they need to be successful. She then presents her vision of them with so much confidence and leadership they can't help but believe her – this makes her good at getting people to do things they otherwise are unlikely to do.

Jovanni and I talk with Jesse Nevel, national chair of the Uhuru Solidarity Movement. We discuss the horrifying raid conducted by the FBI against the African People's Socialist Party (APSP) […]

4 - Egész állatkertnyi nevelési stílust létezik by Balázsék

Harrison Nevel is a content creator in the Sneaker and Clothing space. He has amassed nearly 2m subscribers on youTube and 500k followers on Instagram. _____________________________________________________________ Today… Is an episode with Harrison Nevel YouTuber, content creator, sneaker head, car nut and overall just amazing guy… We learn more about who is Harrison, a little understanding of the sneaker world, a deep dive into the creator economy, And his thoughts on recent infleuncer crypto scandals, It's another great one, so lace up your kicks, cuz we're off and running. This time, before we begin, smash that sub, like, and noti and share with your friends if you enjoy. Appreciate yall Lets go. _______________________________________________________________ 00:00:00 Introduction 00:00:37 Warmup with Fun Questions 00:03:23 What sneaker should I buy with $200-300? 00:05:00 Why the sneaker hype? 00:08:47 WhistlinDeisel 00:10:44 StockX Hack 00:15:24 Sneakers as an indicator of economy 00:17:49 Dealing with YouTuber fame 00:19:25 Handling negative comments 00:22:38 Tik Tok vs Youtube 00:28:16 Influencers responsibility for promoting scams 00:37:00 Mystery Box Scams 00:41:03 Do you feel trapped by your niche? 00:45:13 If you can make other types of content… 00:47:59 youTube for the future generation 00:55:26 When does youTube push your content? 01:00:04 Rumble 01:02:04 YT shorts 01:06:06 Are YouTubers all introverts? 01:07:26 Sneaker chat and Yeezys 01:12:07 Advice to me and podcast --- Support this podcast: https://podcasters.spotify.com/pod/show/mattkimpodcast/support

This week, the performer and author Elizabeth Wilson speaks to Artemis from the offices of Yale University Press in Bedford Square. Elizabeth tells us about the early life of a remarkable pianist, Maria Yudina, who rose to fame in Stalin's Russia. Maria Yudina was born in 1899 to a Jewish family in Nevel, a small town which now sits close to Russia's border with Belarus. Legend has it that Maria was Stalin's favourite pianist. Those who have seen Armando Iannucci's satirical film The Death of Stalin may remember the opening scene in which a pianist is forced to repeat her live performance so that a recording can be made of it and sent to Stalin. As Elizabeth explains in her new biography of the musician, Playing with Fire, the provenance of this story and whether it is about Maria is unclear. However, there is no shortage of fascinating and true stories about Maria, as Elizabeth shows us in this conversation. Maria came of age as the February revolution broke out in St Petersburg, where she was studying music. She took part briefly – even accidentally firing a rifle through a ceiling – before being questioned by a teacher from the conservatoire where she was studying. For most of her life though, Maria wasn't a revolutionary but an intellectual. Her social circle was made up of the leading figures of Russia's intelligentsia, including Boris Pasternak, Pavel Florensky, and Mikhail Bakhtin.  In this episode we visit Maria in 1921, the year she graduated from the conservatoire and was appointed as a member of staff aged just 21. It was also a year in which the relationship between Russia's new revolutionary state and the country's artists and intellectuals felt uneasy and, at times, destructive.    Show notes: Scene One: Maria's graduation ceremony. Scene Two: Maria's debut performance in Petrograd, which coincides with the poet Alexander Blok's death and funeral.  Scene Three: The end of the civil war and the introduction of NEP. Memento: A chess set which shows pieces representing 2 sides of the Russian Civil War.   People/Social Presenter: Artemis Irvine Guest: Elizabeth Wilson Production: Maria Nolan Podcast partner: Ace Cultural Tours Theme music: ‘Love Token' from the album ‘This Is Us' By Slava and Leonard Grigoryan Follow us on Twitter: @tttpodcast_ Or on Facebook See where 1921 fits on our Timeline

Reed Alexander, who played the infamous Nevel on iCarly sits down with us to discuss his life after iCarly, overcoming media bias within journalism & his struggles with mental health. Do you think people in your own life know the real you? What would you say to your younger self? What's your hottest take? Answers these questions with Reed Alexander during this episode by texting "POVZ" to 1 (877) 222-1119 to share your POVz! The Conversationalist is a non partisan platform that doesn't affiliate or identify with any viewpoints, beliefs, or opinions that may be featured throughout our content.

This week we went with exclusively new stuff released fairly recently. I can't be doing back catalogue shows every week! In both the US and Canada it s a long weekend, so I took a little time for myself this weekend and decided it was AOK to post the show a little later than usual. No more long weekends until Canada Day in July so I'd better enjoy this one! Solitary Experiments - Every Now And Then (Imperative Reaction)Fusspils 11 - Dei Drei Säulen Des WahnsinnsCubic - Impact 2023 (Nevel)Supercraft - A ForestPsy'Aviah - Can We Make It Rhyme feat. Mari Kattman (Omniks Club)Rhys Fulber - Glory To LabourBratři - BlocksTragic Impulse - Killswitch http://synthetic.org/https://www.instagram.com/djtodd242/https://twitter.com/djtoddrsahttps://www.youtube.com/c/RealSyntheticAudio

To get live links to the music we play and resources we offer, visit This show includes the following songs: Julie Nevel - Asbury Lane   Alex Bach (writer Ed Daniels) - No Greater love  Livia & the Rosebuds - Had To  Sabrina Carmen - Dreaming Wide Awake  Dierdre - Bleed for Me  Diana Kelley - Willow  One Week Later - Mars  IMAGESONG - And Was It Just Luck  Sa'ra Charismata - Life Is Not About Control  Koko Conley - I Was Coming Back Home  For Music Biz Resources Visit and Visit our Sponsor Shena! at Visit our Sponsor Rock Your Next Release at Visit our Sponsor Bandzoogle at: