Podcasts about nmo

Play Episode Listen Later Apr 23, 2025 21:36

The inflammatory and infectious optic neuropathies are a broad, heterogeneous, and common group of diseases producing visual loss. Although many now-distinct syndromes have been previously combined as “typical or atypical optic neuritis,” recent developments highlight the importance of precision terminology as well as an individualized evaluation and treatment approach. In this episode, Gordon Smith, MD, FAAN speaks with Eric Eggenberger, DO, MS, FAAN, author of the article “Optic Neuritis” in the Continuum® April 2025 Neuro-ophthalmology issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Eggenberger is a professor of ophthalmology, neurology, and neurosurgery at the Mayo Clinic in Jacksonville, Florida. Additional Resources Read the article: Optic Neuritis Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @gordonsmithMD Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Smith: This is Dr Gordon Smith. Today I'm interviewing someone who really needs no introduction, Dr Eric Eggenberger, about his article on optic neuritis, which appears in the April 2025 Continuum issue on neuro-ophthalmology. Eric, welcome to the podcast, and maybe you can introduce yourself to our audience. Dr Eggenberger: Thank you. Thanks for having me. So, my name is Eric Eggenberger. I work at Mayo Clinic Florida, and I am involved exclusively in neuro-ophthalmology. Dr Smith: I just had the pleasure, Eric, of talking yesterday with Lindsey De Lott about non-optic neuritis causes of optic neuropathy. And so, I'm going to kind of reference a little bit what I learned yesterday. She was great. I wonder if you might begin by talking a little bit about nomenclature. You talk about the need for use of precise terminology in your article. And yesterday she taught me a lot about the risk of misdiagnosis and other causes of optic neuropathy, and the two seem related. So, I wonder if you can maybe lay the foundation for our conversation by talking about terminology? Dr Eggenberger: I think that's a great point. So, we are in an era now where, instead of lumping all these different diagnoses together, we have learned to split apart some of these clinical entities. And so, I think it's really important that we focus on precise terminology and recognize that all optic neuritis is not the same. And we have very different, distinct clinical pathways for these imaging pathways, treatment pathways, for these different types of optic neuritis, whether that's MS related, whether it's MOG related or aquaporin-4 related. Dr Smith: So, I wonder maybe we can begin by just, you know, giving our listeners wisdom, pearls, and pitfalls about, how do you recognize when someone with a suspected optic neuropathy has optic neuritis versus a noninflammatory optic neuropathy? Dr Eggenberger: So, that's a really important issue because there's a lot of clinical overlap in terms of exam findings. So, for instance, in any optic neuropathy, let's say it's unilateral, you typically are going to see decreases in acuity and field and color, and you're going to see a relative afferent pupillary defect. And then it's really the context that that occurs in that helps us distinguish different disease entities. So, with optic neuritis, typically you're going to have pain. And that's oftentimes going to be in the younger populations compared to some of the other common optic neuropathies we see, like ischemic optic neuropathy, for instance. Dr Smith: Right. So maybe we can talk a little bit about, kind of, your overall diagnostic approach, right? A lot of this is, of course, based on age and context, but young people get ischemic lesions and older people can have inflammatory lesions. So, what's your overall approach to the patient you just described? Let's say it's a forty-eight-year-old woman who comes to the emergency department with subacute unilateral vision loss and there's dyschromatopsia, APD, reduced acuity. And, you know, let's just say a fairly, you know, benign-looking fundoscopic exam. What do you do to evaluate that patient? Dr Eggenberger: In that particular context, I think we're looking at other contextual clues. Is there other vascular risk factors or other things to point you in one direction or the other? One of the important parts you mentioned was the fundus exam. So, we know with ischemic optic neuropathy, 100% of the time with AIOM, you're going to see disc edema. And so, in the context of that story, we want to confirm on our exam an optic neuropathy, and then we can kind of focus on the retrobulbar courses or different types of optic neuropathies. From an exam perspective, in that particular patient we'd be looking to measure the acuity, quantify that. And in the ER, you're not going to be able to do a perfect field, but you'll get some sense of the field and how much field loss there is. And then as you mentioned, the afferent pupillary defect is critical. And we're going to get a little bit of the historical features in terms of pain. With typical retrobulbar optic neuritis, most of those patients are going to experience some pain, and usually it's pain on eye movements. And those would be the clinical things to focus on. Other exposures the patient may or may not have had, any other concomitant conditions, would all help point you in different directions, perhaps, and then we're probably on towards imaging. Dr Smith: Yeah, maybe you can talk a little bit about that? What's the appropriate use of imaging? I mean, presumably the patients, like the one I just threw out there, are pretty much all going to get neuroimaging. What's your approach to that? How do you protocol the study? What should we be looking for? Dr Eggenberger: In our clinic, we would typically be ordering an MRI orbit and brain, and each of those has a specific purpose. The orbit is going to show us the extent of the optic neuropathy. So, we're particularly looking for a longitudinally extensive optic nerve lesion or more than half of the optic nerve involved. And most patients acutely, if it isn't an “itis" situation, we'll see enhancement. And then the MR brain is going to be useful for looking for other evidence of demyelination within the central nervous system. We may at some point get down to doing an MR cord, but I think acutely it's going to be brain and orbit that most of our patients are getting. Dr Smith: Let's say that we did the scan and, sure enough, there's sort of a shorter segment, so less than half the length of the nerve region of enhancement. What's the rest of your diagnostic evaluation look like for that patient? Dr Eggenberger: So, in that particular case, we would look at the remainder of the brain. So, we're looking for other evidence of demyelination and any other contextual clues, systemically that would point you one direction or another. But with a shorter segment involved, one of the more common things we might encounter would be multiple sclerosis-related optic neuritis. Dr Smith: Would you look for aquaporin-4 and MOG in a patient with what appears to be an isolated, uncomplicated short segment optic neuritis? Dr Eggenberger: So, I think it really depends a bit on the context. I would never fault anybody for looking at MOG or an aquaporin-4 in that context because those are really treatment-altering diagnoses, but the yield in this particular case with a short segment involved and depending on the acuity and other features is probably going to be pretty low. Dr Smith: I really liked as an aside- I wasn't going to go there next, but you kind of got me thinking about it, you have a really nice section in your article. Which, all of it's great, but talking about how to manage low titer MOG antibodies. I wonder if you could talk about that because I think that's a lesson, maybe, that is transferable to a lot of other testing that we do. in terms of pre-prior probability and titer and so forth. Dr Eggenberger: Yeah, that's really an important point. So, we've seen this come up a number of times where the MOG antibody is a very good test, but in low titer it has a relatively low positive predictive value, perhaps 50%. In those cases, particularly without a classic clinical context, you have to be extremely alert for some other diagnosis that could mimic what you think is inflammatory demyelinating optic neuritis, but in fact is infectious or some other cause. Dr Smith: Yeah, super, super important and helpful. In terms of aquaporin-4, how does that compare in terms of predictive values, lower titer positive results? Dr Eggenberger: So aquaporin-4, the test has a very high specificity. So, it's quite useful if positive. You have to keep in mind there can be some false negatives, but the test otherwise is quite specific. And that is a diagnosis, you know, we never want to miss. It's a vicious disease. It tends to be a blinding disease, particularly without treatment. Bad things happen when we miss that, and we want to get on that diagnosis early and do pretty aggressive early and prophylactic treatment. Dr Smith: Your article covers not only the common causes of optic neuritis and, you know, MS, isolated optic neuritis, MOGAD NMO, you talk about a bunch of other things. I wonder, in this patient that we've been discussing, in the absence of any other historical information that seems relevant---or maybe you can define what would seem relevant---would you do other evaluation in that individual, other serologic evaluation and so forth, just in terms of diagnosis? Dr Eggenberger: In that particular case, without other red flags, I don't think I would initially. And follow-up is going to give you a lot of this context. So, you'd be on the lookout for other systemic conditions. So, if the patient had some arthropathy, if the patient had any pulmonary disease hints, if there was anything else that could lead you on a broader expedition. But I think in the context of this case, acutely in the ER, I probably wouldn't do a big lab plug for this. I probably would kind of go down the most likely road and start our treatments, and then follow that patient up. Dr Smith: Yeah, I know your article does a really great job, I think, of outlining when do you need to think about some of these less common causes. Well, can we talk about treatment, Eric? Because I want to move on to some other things. But- so, we've got a patient with isolated optic neuritis, nothing else, you know, in terms of the other antibodies we've talked about. What state-of-the-care- or, state-of-the-art treatment for that patient? Dr Eggenberger: So, the acute treatment for these inflammatory, optic neuritis-type cases is very similar Initially. High dose steroids remains kind of the standard. And then, in MS-related optic neuritis, we may or may not see a taper. So many times it's just an acute treatment of three to five days high dose. Whether that's oral or PO, we could institute either depending on the particular case. And then the taper would depend on the potential cause. So, for instance, with these antibody-driven diseases---so with MOG- or particularly with aquaporin-4---if it's a longitudinally extensive region of optic nerve involved, we tend to use a longitudinally extensive taper. And so, we use prednisone in those cases for several months while we're getting everything else set and deciding what the overall course is going to bring. Dr Smith: What about IV versus oral? There must be something about my practice. I was telling this to Lindsey. Every time on our hospital service, we seem to have at least two patients with optic neuropathies, which I always enjoy, but I find it's a little weird to admit someone who's doing just fine otherwise to the hospital with three days of IV SOLU-MEDROL. So, I'm always trying to figure out, like, how can I get this patient home? And your article had the best term I've heard in a long time, which is “SOLU smoothies.” I mean, are there other strategies that you sometimes use, other than just high-dose IV methylprednisolone? Dr Eggenberger: So, I agree with you. It's sometimes hard to admit somebody for just an IV therapy. And we'll do this as an outpatient, high-dose IV, but we'll also use high-dose orals. And in times in the past when there's been methylprednisolone shortage, we've used high-dose oral or IV dexamethasone as well. I think the IV form, although it's the gold standard, the high-dose oral forms have pretty equivalent bioavailability and are pretty tolerable in my experience. And certainly more convenient. Dr Smith: I wonder if we should switch and maybe talk a little bit about aquaporin-4, I mean, you emphasized that this is a vicious disease---I love the way you describe that---and often blinding. What updates do you have in terms of our therapeutic approach to NMO? That's been rapidly evolving of late. Dr Eggenberger: Right, so these are cases we're always going to share with neuroimmunology. And it requires kind of a multidisciplinary approach, in my opinion, for ideal or for best outcomes. And so, all of these patients are going to get put on prophylactic medications. So, this is a disease you just can't leave untreated. Bad stuff will happen for sure. And we now, fortunately, have some approved, FDA-approved medications that can positively impact the course of this disease. So, that's been a welcome addition. Dr Smith: What are the FDA-approved medications at this point for NMO? Dr Eggenberger: So, there are several at this point, and this is an area that's in growth, fortunately. And again, these are cases we're going to be sharing with our neuroimmunology colleagues. So, these are IV medications typically aimed at complement or CD19. And they all are relatively effective at quieting the course of the disease. Dr Smith: Maybe we can talk a little bit about MOG? I think that most of our listeners are probably pretty familiar with aquaporin-4 and NMO, what- maybe you could describe MOG a little bit and the therapeutic approach for patients with MOG-associated disease? Dr Eggenberger: So, MOG has been a real interesting kind of condition to learn more about. We certainly see a lot of MOG, and I'm sure we saw MOG before it was formally described, but I think we just thought it was kind of a benign, maybe monophasic MS type of presentation. But MOG tends to come in with a loss of acuity that kind of rivals aquaporin-4. So, the acuity tends to be pretty, pretty depressed, but it's very steroid-responsive. So, a lot of times these are the patients, you'll see that their vision will start to improve even when they're on the initial few days of the high-dose steroids. And many times we can get their vision back to 20/20 or very close to that. Dr Smith: And do these patients need chronic management? Dr Eggenberger: So, that's an area of controversy to some degree. About 50% of the optic neuritis MOG-related cases are going to have a relapsing course. And because the disease is steroid-responsive, many times we'll follow these patients after a first attack to see if this is the condition that's going to declare itself to be relapsing or if this is just going to be a monophasic kind of presentation of optic neuritis. We don't have great biomarkers to separate patients who are going to be in that 50% monophasic course versus the other half. It'll be relapsing. And so, it depends on the patient. If there's somebody that's, as many of these patients are, been very steroid responsive, they get back to 20/20, we can teach them about the disease so that if they do have a relapse, we can get them high-dose steroids in a relatively rapid fashion and they're otherwise healthy, we're probably going to watch that patient. And if it's somebody that doesn't recover 100%, there's other issues with treating them with high-dose steroids potentially in the future, then we may learn more towards an earlier prophylactic approach in that patient. Dr Smith: And what would that approach look like? Is it different from NMO or using more IVIG or B cell depletion as opposed to complement inhibition, for instance? Dr Eggenberger: In MOG, we know that the B cell depletion strategies don't work as well. And so most times we're turning to IVIG, and we found that pretty effective. That's kind of our go-to at this point. Dr Smith: Eric, it's a joy talking to you and I'd love to keep going about content, but I'll refer our listeners to your outstanding article. I mean, you're such a highly regarded neuro-ophthalmologist and educator. I wonder if you could talk to us about why you've done neuro-ophthalmology, and maybe this is an opportunity for you to convince all of our great residents that are listening or students what's great about being a neuro-ophthalmologist. Dr Eggenberger: I think neuro-ophthalmology is by far the most interesting part of neurology. So, it's an area that I think a lot of general neurologists, in my view, don't get enough of in their residency. But it's kind of the essence of neurology, where in neurology you're localizing down to the millimeter and in neuro-ophthalmology, we're localizing down to the micron level. We have several new emerging diseases like these varieties of optic neuritis we're focused on. We're learning lots about those. You get to be involved in lots of different areas of neurology. So, we'll see not just demyelinating conditions, we'll see trauma as it relates to the visual system. And we'll see tumor, and we see all different flavors, stroke, and in any piece of neurology, commonly we'll have some vision aspect that we that we get involved in. So, we see a wide variety of conditions. So, I think it's been a really exciting place to be within neurology. And it's rapidly changing at this point. We're getting new therapeutics. So, it's, I think it's a great time to be a neuro-ophthalmologist. Dr Smith: Yeah, listening to you talk and just reflecting on it, it's really true. Neuro-ophthalmology does cover the entire span of neurology, right? I'm a neuromuscular guy and we see a lot of ocular myasthenia, which is another super exciting area. But we've been talking about optic neuritis, and your article talks about infectious causes and the paraneoplastic and a whole host of things. So, you're a great advocate and salesperson for your field. You convinced me. Dr Eggenberger: Efferent neuro-ophthalmology we love, we could talk about ocular myasthenia and other aspects for another hour. And we get involved in all kinds of cases: third nerve palsies, ocular myasthenia, trauma that involves the efferent system, all different aspects. It's really a great subspecialty, and you get to see a bit of all of neurology. Dr Smith: I'm trying to remember who it was, Eric. It was an attending of mine at medical school. I went to medical school at the Mayo Clinic in Rochester, and I want to say it was Manny Gomez, who was a very famous tuberous sclerosis person, who told me that neuro-ophthalmology was the most elegant specialty within neurology. That stuck with me. Thank you so much for joining me today. I really appreciate it. Dr Eggenberger: Thank you. I appreciate it as well. Dr Smith: So again, today I've been interviewing Dr Eric Eggenberger about his really wonderful article on optic neuritis, which appears in the most recent issue of Continuum on neuro-ophthalmology. Be sure to check out Continuum audio episodes from the neuro-ophthalmology and other issues. And listeners, thank you very much for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at continpub.com/audioCME. Thank you for listening to Continuum Audio.

Approach to Vision Loss With Dr. Nancy Newman

Play Episode Listen Later Apr 9, 2025 29:00

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

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20250320-03 - В Дубае прошёл национальный этап конкурса «Живая классика» & В ОАЭ усиливают надзор за контентом в соцсетях

Radio Russian Emirates

Play Episode Listen Later Mar 20, 2025 2:32

Новости на радио «Русские Эмираты» в Дубае:- В Дубае прошёл национальный этап Международного конкурса юных чтецов «Живая классика». Это соревновательное мероприятие по чтению вслух отрывков из прозаических произведений российских и зарубежных писателей. Учредитель и организатор международного конкурса – Фонд «Живая классика».- Национальный медиаофис (NMO) Объединенных Арабских Эмиратов призвал пользователей социальных сетей уважать национальные ценности уважения, толерантности и сосуществования при публикации контента в интернете.

nmo

#178 - USATF Indoor Champs & Crashing a Quinceañera (Unhinged On Location)

NonMembers Only

Play Episode Listen Later Mar 3, 2025 73:09

We somehow got media credentials (shoutout to Natalie) and made our way to the USATF Indoor Championships—but not without a classic NMO logistical whoopsie.Once in, we witnessed elite track & field action, learned about the true athleticism of race walking (which we're officially rebranding as Thunder Strike), and got to chat with some legends, including Olympic gold medalist Dawn Harper-Nelson, shot put gold medalist Chase Jackson and pole vault champ Katie Moon—who may or may not have named her pole Paul.Back at our hotel we had an unexpected VIP hotel tour that quickly spiraled into a full-on quinceañera experience. Also in this episode: Erin's kids experience their first track meet, make some friends with other media, and ask hard hitting questions.Listen now and join the Thunder Strike movement.

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EP 561: Guns & Gear with NMO

Audacious with Chion Wolf

Play Episode Listen Later Feb 14, 2025 93:56

On this episode, Nolan Osborne, aka NMO, is back to cover his evolving thoughts on guns and gear. These subjects were meant to be covered in his previous episode but time ran short so, he's back to dig into these ever popular topics. NOTABLE GUEST QUOTES: “Your group size is too small.” @nmo HORNADY PODCAST REFERENCED BY NMO --------------------------- SUPPORT WILD SHEEP: Go to Wild Sheep Foundation to find a membership option that suits your budget and commitment to wild sheep. DEALS & OFFERS: OnX Maps is now available in Canada! Get your FREE trial today. And if you're already a member, check out the exclusive offers and perks available when you upgrade to an Elite Member. Tired of garbage instant coffee when you're in the backcountry? Check out This Is Coffee and get yourself some great instant coffee for whenever you're in the backcountry or on the road. --------------------------- SUPPORT MOUNTAIN GOATS: Go to Rocky Mountain Goat Alliance to find a membership option that suits your budget and commitment to conserving mountain goats and their habitat.

canada guns tired gear nmo wild sheep foundation rocky mountain goat alliance nolan osborne

MasterChef winner Christine Ha and poet Edward Hirsch on turning blindness into brilliance

Play Episode Listen Later Jan 31, 2025 49:15

What can you gain when you lose your vision? Christine Ha was in her early 20s when she began losing her sight. Instead of giving up on her dreams, she taught herself how to cook - so well, in fact, that she became the first and only person who is blind to win MasterChef. Now, she’s a celebrated chef and author who’s proving that great cooking is about taste, texture, and trust - not sight. And Edward Hirsch, a poet who began losing his sight later in life, discovered something unexpected - exhilaration. He says that blindness has made him more alive, more curious, and more connected to the world in ways he never expected. Resources: List of resources for people with low vision by the American Council of the Blind Lighthouse Guild (as mentioned by Edward Hirsch) Suggested episodes: Revealing Our Blind Spots About Blindness GUESTS: Christine Ha: Winner of MasterChef Season 3. She has neuromyelitis optica (NMO), in which a person's own immune system attacks the optic nerves and spinal cord Edward Hirsch: Poet and president of the John Simon Guggenheim Memorial Foundation. Wrote a guest essay in the NYT: “I am Going Blind, and I Now Find It Strangely Exhilarating.” He has retinitis pigmentosa, a rare genetic disease that causes progressive vision loss Support the show: https://www.wnpr.org/donateSee omnystudio.com/listener for privacy information.

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EP 557: Incredible Sheep Hunting Stories with NMO

Play Episode Listen Later Jan 17, 2025 92:13

On this episode, a key figure in the history of The Journal of Mountain Hunting and BTK podcast graces the mics again to share some incredible stories from the 2024 guiding season. NMO's experience, stories, perspectives and insights are always a pleasure to hear and share. @nmo --------------------------- SUPPORT WILD SHEEP: Go to Wild Sheep Foundation to find a membership option that suits your budget and commitment to wild sheep. DEALS & OFFERS: OnX Maps is now available in Canada! Get your FREE trial today. And if you're already a member, check out the exclusive offers and perks available when you upgrade to an Elite Member. Tired of garbage instant coffee when you're in the backcountry? Check out This Is Coffee and get yourself some great instant coffee for whenever you're in the backcountry or on the road. --------------------------- SUPPORT MOUNTAIN GOATS: Go to Rocky Mountain Goat Alliance to find a membership option that suits your budget and commitment to conserving mountain goats and their habitat.

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Top 5 Episodes of 2024

MS-Perspektive - der Multiple Sklerose Podcast mit Nele Handwerker

Play Episode Listen Later Dec 27, 2024 93:40

Join Sarah as she counts down the top 5 Agent Survival Guide Podcast episodes of 2024! Find out if your favorite episode made the cut… and thanks for listening this year! Number Five: [02:22] Number Four: [21:29] Number Three: [31:18] Number Two: [39:18] Number One: [01:04:19] Contact the Agent Survival Guide Podcast! Email us ASGPodcast@Ritterim.com or call 1-717-562-7211 and leave a voicemail. Follow Us on Social! Ritter on Facebook, https://www.facebook.com/RitterIM Instagram, https://www.instagram.com/ritter.insurance.marketing/ LinkedIn, https://www.linkedin.com/company/ritter-insurance-marketing TikTok, https://www.tiktok.com/@ritterim X, https://twitter.com/RitterIM and Youtube, https://www.youtube.com/user/RitterInsurance Sarah on LinkedIn, https://www.linkedin.com/in/sjrueppel/ Instagram, https://www.instagram.com/thesarahjrueppel/ and Threads, https://www.threads.net/@thesarahjrueppel Tina on LinkedIn, https://www.linkedin.com/in/tina-lamoreux-6384b7199/ Links to Individual Episodes: 5 Perks of Being a Part-Time Insurance Agent: https://pod.fo/e/28ab20 Agent's Guide to Email Communication Resources: https://pod.fo/e/28ab27 Developing a Retention Mindset ft. Blake Amos: https://pod.fo/e/28ab52 Key Changes for ACA Open Enrollment 2025 ft. Ross Baker: https://pod.fo/e/28aaeb Using a SWOT Analysis to Review Your Insurance Business: https://pod.fo/e/28ab7f Additional Episodes You Might Like: 5 Things About Prepping for the Insurance License Exam: https://pod.fo/e/28ab2c 9 Essential Tools for Beginner Insurance Agents: https://pod.fo/e/28ab2e How Much Can Agents Make Selling Under-65 Insurance: https://pod.fo/e/28aaf7 Simplify Marketplace Enrollments with HealthSherpa: https://pod.fo/e/27a351 Steps to Get Ready for OEP: Federal & State Exchanges: https://pod.fo/e/28aaf6 What Today's Financial Environment Means for Medicare Beneficiaries & Agents: https://pod.fo/e/28aafb Resources for Insurance Agents: Developing an Agency — Your Guide to Getting Started: https://www.ritterim.com/agency-guide/ Email Template for Client Check-in: https://ritterim.com/documents/client-check-in-email-template.docx FMO vs. IMO vs. NMO vs. MGA vs. GA: What's the Difference? https://ritterim.com/blog/fmo-vs-imo-vs-nmo-vs-mga-vs-ga-whats-the-difference/ How Professional Organizations Make You a Better Agent: https://ritterim.com/blog/how-professional-organizations-make-you-a-better-agent/ Increase Sales and Productivity with the Busy Medicare Agent's Sales Planner: https://www.ritterim.com/blog/increase-sales-and-productivity-with-the-busy-medicare-agents-sales-planner/ Modern Medicare Marketing for Today's Agents: https://www.ritterim.com/modern-marketing-guide/ Request a Portfolio Review from Ritter Insurance Marketing: https://ritterim.com/portfolio/ Ritter Agent Handbook: https://docs.ritterim.com/documents/compliance/Ritter-Agent-Handbook-2024.pdf Ritter Insurance Marketing Official Site: https://ritterim.com/ Stay Organized with the Busy ACA Agent's Sales Calendar: https://www.ritterim.com/blog/stay-organized-with-the-busy-aca-agents-sales-calendar/ The Complete Guide to Client Loyalty and Retention: https://ritterim.com/client-retention-guide/ The Complete Guide to Selling Affordable Care Act Insurance Plans: https://ritterim.com/aca-ebook/ The Ultimate Agent Resource List Pt. 1: Market Yourself: https://www.ritterim.com/blog/the-ultimate-agent-resource-list-pt.-1-market-yourself/ Your Step-By-Step Guide to Getting Started in Insurance Sales: https://ritterim.com/free-guide/?utm_source=asg_podcast_link Not affiliated with or endorsed by Medicare or any government agency. The resources in Agent's Guide to Email Communication Reesources are the opinions of staff and agents who work with Ritter Insurance Marketing. We cannot guarantee that an agent's business will succeed if utilizing these recommendations. An agents is solely responsible for making all decisions and taking actions related to their business.

#281: Therapeutische Entscheidungen bei Schwangerschaft und Stillzeit mit MS mit Prof. Dr. Celia Oreja-Guevara

Play Episode Listen Later Dec 9, 2024 21:25

Bei Frauen mit MS fördern eine stabile Erkrankung und kluge Therapieentscheidungen eine sichere Schwangerschaft und Stillzeit. Alle Fragen und Antworten zum Nachlesen gibt es auf meinem Blog: https://ms-perspektive.de/281-celia-oreja-guevara Prof. Celia Oreja-Guevara berät einmal pro Woche Frauen mit Multipler Sklerose und Kinderwunsch in der Universitätsklinik San Carlos in Madrid. Sie findet es am besten wenn die MS seit zwei Jahren unter Kontrolle ist. Dann stehen die Chancen auf eine entspannte Schwangerschaft sehr gut. Da Frauen mit MS bei der Geburt im Durchschnitt etwas älter sind, spielt die künstliche Befruchtung eine Rolle. Empfehlenswert ist die etwas teurere In-vitro-Variante, da sie höhere Erfolgschancen hat und Paaren Zeit und Enttäuschungen erspart bleiben. Generell hat sich gezeigt, dass eine Mutterschaft den langfristigen Verlauf der Erkrankung kaum beeinflusst und diesem für viele Menschen wichtigen Teil des Lebensglücks nichts im Wege steht. Durch moderne, effektive Therapien sind selbst hochaktive Verläufe sehr gut zu kontrollieren. Diejenigen, die stillen möchten, können dies tun. Dennoch sollte die Gesundheit immer an erster Stelle stehen, und wenn es schwierig oder sehr zeitaufwendig wird, sei es aus therapeutischen oder anderen Gründen, kann man ohne schlechtes Gewissen auf Ersatzmilch zurückgreifen. Wichtiger ist es, Schüben und möglichen Spätfolgen vorzubeugen, als um jeden Preis zu stillen. Erfahre mehr über die verschiedenen Themen rund um Schwangerschaft, Stillzeit und Immuntherapie für Frauen mit MS. Das Interview wurde ursprünglich in englisch für den internationalen Podcast entführt und ist eine Übersetzung. Inhaltsübersicht Einleitung - Wer ist Prof. Celia Oreja-Guevara? Allgemeine Informationen über den Kinderwunsch bei MS Spezielle Informationen zu Schwangerschaft und Geburt bei MS Stillen bei Multipler Sklerose Verabschiedung Einleitung - Wer ist Prof. Celia Oreja-Guevara? Ich bin Celia Oreja-Guevara, stellvertretende Vorsitzende der Neurologie und Leiterin des Multiple-Sklerose-Zentrums am Universitätskrankenhaus San Carlos in Madrid, Spanien. Ich bin Professorin für Neurologie an der Universität Complutense in Madrid. Nach meinem Medizinstudium an der Universität Madrid habe ich meine Doktorarbeit in Neuroimmunologie am Max-Planck-Institut für Neurobiologie in München abgeschlossen. Anschließend absolvierte ich eine Facharztausbildung in der Neurologischen Abteilung der Universität Bochum, gefolgt von einem einjährigen Stipendium für Neurobildgebung am Universitätsklinikum San Raffaele in Mailand. Seitdem hatte ich verschiedene Positionen inne, darunter leitende Neurologin an der Universität Düsseldorf, Deutschland, Leiterin der Neurologie am Hospital de Fuenlabrada und Vorsitzender des Multiple-Sklerose-Zentrums am Universitätsklinikum La Paz, beide in Madrid, Spanien. Ich bin Co-Vorsitzender des Wissenschaftlichen Gremiums für Multiple Sklerose der Europäischen Akademie für Neurologie. Meine Forschungsschwerpunkte sind klinische und bildgebende Zusammenhänge bei MS, Familienplanung, der Einsatz der optischen Kohärenztomographie in der symptomatischen Therapie, Neuromyelitis optica (NMO) und die Bewertung neuer Medikamente zur Behandlung von MS und NMO. Meine Hobbys sind Technik, ich kaufe Gadgets, repariere Computer, besuche Technikausstellungen … Außerdem reise ich gerne überall hin und schaue mir gerne Comedy und Liebesfilme an. Gibt es noch etwas, das du den Zuhörern mitteilen möchtest? Ja, gern. Für Patientinnen mit Multipler Sklerose ist eine Schwangerschaft mit den richtigen Vorbereitungen absolut möglich. Daher ist eine gründliche Familienplanung unerlässlich, um sowohl die Krankheit als auch die Schwangerschaft effektiv zu bewältigen und die Gesundheit von Mutter und Kind zu schützen. Wie und wo können Interessierte deinen Forschungsaktivitäten folgen? Twitter LinkedIn PubMed Vielen Dank für die positiven Einblicke in das Thema Schwangerschaft und Stillzeit bei MS. Bis bald und mach das Beste aus Deinem Leben, Nele Mehr Informationen und positive Gedanken erhältst Du in meinem kostenlosen Newsletter. Hier findest Du eine Übersicht zu allen bisherigen Podcastfolgen.

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Episode 119 Part Two - Dr. Summer: A Journey Through MS and NMO

Move It or Lose it - The Podcast

Play Episode Listen Later Sep 19, 2024 29:42 Transcription Available

In part two of my conversation with Dr. Summer, we dive deep into her journey of becoming a physician after facing significant life challenges, including a divorce and becoming a single parent to her two boys. As we covered in the first part of this conversation, Dr. Summer was misdiagnosed with MS before receiving the correct diagnosis of neuromyelitis optica (NMO).After attending undergrad in Missouri and med school in Pennsylvania, Summer's path to becoming a physician was unconventional, marked by personal trials and triumphs. She shares her experience of transitioning to a power wheelchair and how it affected her work and interactions with patients.Summer emphasizes that being a physician is not just about treating physical ailments but also about understanding the emotional and spiritual aspects of health. This perspective is crucial, especially for patients dealing with chronic conditions like MS and NMO.Towards the end of our discussion, Dr. Summer shares her insights on the healthcare system and the challenges faced by both patients and providers. She addresses the frustrations of navigating insurance and the pressures that come with high patient loads. Despite these challenges, she remains committed to her patients and finds joy in her work.DISCLAIMERThe information in this podcast is for informational purposes only and is not intended as a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified healthcare providers with any questions you may have regarding a medical condition or treatment.Links and resources:Sign up for the 10 Weeks to Disrupt MS ProgramFollow Dr. Summer on TikTok Visit Summer Banzhaf, DO at Fairfield Medical Center If you're interested in having Kathy speak at your event, learn more hereFind out more about the DMAT Fitness Training programYou can find Kathy Chester at: msdisrupted@gmail.comdisruptfitnessgym@gmail.com moveitorloseit109@gmail.com Connect with @msdisrupted on Instagram, Facebook, TikTok Here are some additional products that help Kathy beat the Heat and Migraines. Take advantage of the coupon code.Koldtec - Cool Head WrapKOLD10To save $10 off every item in-store.2 items = $20 savings3 items = $30 savingshttps://www.koldtec.com/ Cold bean bag Releafpack15% discount use code Disrupt15https://www.releafpack.com

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Episode 119 Part One - Dr. Summer: A Journey Through MS and NMO

Move It or Lose it - The Podcast

Play Episode Listen Later Sep 18, 2024 21:51 Transcription Available

I recently enjoyed speaking with the incredible Dr. Summer about her remarkable story. I've been following her journey on TikTok, and I was eager to dive into her experiences with neuromyelitis optica (NMO), a condition that was initially misdiagnosed as multiple sclerosis (MS). Summer's resilience and determination to overcome her challenges are truly inspiring.In the first part of a two-part interview, Summer shared her journey from being misdiagnosed with MS to receiving the correct diagnosis of NMO. She explained that NMO is often confused with MS due to their similarities, but it has distinct characteristics that can lead to more severe symptoms. Summer described her initial experiences with various treatments, including Gilenya and Tysabri, and how they didn't work for her condition. It was only after multiple attacks that her doctors reconsidered her diagnosis and adjusted her treatment plan.During our conversation, we discussed Dr. Summer's journey through misdiagnosis and the impact of her condition on her medical career, the emotional challenges of living with a chronic illness and the fear of unpredictability, advances in treatment options for NMO and the hope they bring to patients, and the power of resilience and determination in overcoming health challenges.DISCLAIMERThe information in this podcast is for informational purposes only and is not intended as a substitute for professional medical advice, diagnosis, or treatment. Always seek the advice of your physician or other qualified healthcare providers with any questions you may have regarding a medical condition or treatment.Links and resources:Sign up for the 10 Weeks to Disrupt MS ProgramFollow Dr. Summer on TikTok Visit Summer Banzhaf, DO at Fairfield Medical Center If you're interested in having Kathy speak at your event, learn more hereFind out more about the DMAT Fitness Training programYou can find Kathy Chester at: msdisrupted@gmail.comdisruptfitnessgym@gmail.com moveitorloseit109@gmail.com Connect with @msdisrupted on Instagram, Facebook, TikTok Here are some additional products that help Kathy beat the Heat and Migraines. Take advantage of the coupon code.Koldtec - Cool Head WrapKOLD10To save $10 off every item in-store.2 items = $20 savings3 items = $30 savingshttps://www.koldtec.com/ Cold bean bag Releafpack15% discount use code Disrupt15https://www.releafpack.com

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NMOSD and MOGAD With Dr. Elia Sechi

Play Episode Listen Later Aug 21, 2024 16:47

Awareness of the specific clinical and MRI features associated with AQP4-NMOSD and MOGAD and the limitations of currently available antibody testing assays is crucial for a correct diagnosis and differentiation from MS. Growing availability of effective treatment options will lead to personalized therapies and improved outcomes. In this episode, Gordon Smith, MD, FAAN speaks with Elia Sechi, MD, author of the article “NMOSD and MOGAD,” in the Continuum August 2024 Autoimmune Neurology issue. Dr. Smith is a Continuum® Audio interviewer and professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Sechi is a neurology consultant in the neurology unit of the Department of Medical, Surgical and Experimental Sciences at the University Hospital of Sassari in Sassari, Italy. Additional Resources Read the article: NMOSD and MOGAD Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @gordonsmithMD Guest: @EliaSechi 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 Smith: Hello. This is Dr Gordon Smith. Today, I've got the great pleasure of interviewing Dr Elia Sechi about his article on aquaporin-4 antibody-positive NMOSD and MOGAD, which appears in the August 2024 Continuum issue on autoimmune neurology. Dr Sechi, before we dig into this really exciting topic about NMOSD and MOGAD, perhaps you can tell our listeners a little bit about yourself, where you practice, how you got interested in this topic. Dr Sechi: Hi, Dr Smith, and thank you for having me. So, my story begins here in Italy, actually - I did my med school and residency in neurology at the University Hospital of Sassari here in Sardinia. And after residency, I was lucky enough to be accepted at the Mayo Clinic in Rochester, Minnesota for a research fellowship - and that's where I spent the next three-and-a-half years, approximately. My fellowship was focused on autoimmune neurology, specifically demyelinating diseases of the CNS associated with antibodies – so, of course, NMOSD and MOGAD mostly, but also myelitis, MS, and autoimmune encephalitis – so, there's where I built most of my expertise in the field. And then, it was at the beginning of the pandemic (of the COVID pandemic) that I came back here to Italy to practice. And now, I work mostly as a neurohospitalist, and I also have my subspecialty outpatient service for patients with autoimmune neurological diseases. Dr Smith: I wonder if you might just give us a minute or two about what it was like training in Mayo? I went to medical school there, and, you know, at the time, I thought that was just normal healthcare and normal training, and, you know, it was only later that I realized how amazing that was. I mean, this is where aquaporin-4 was discovered - I mean, what was that like? It must have been really cool training there with that team. Dr Sechi: Yeah. You know, it's the temple of autoimmune neurology. It's fantastic. It's a great environment, very stimulating. You know, I think the great strength is that they see many patients with rare diseases, so, you get really confident with MRI features and clinical features with the history of the diseases, and this is important to recognize the typical features and differentiate from MS to do a good differential. And, of course, you know, the team is fantastic - superstars in the field. It's very, very stimulating. So, it's something that I definitely recommend. It was a fantastic experience. Dr Smith: Well, you know what's great is, I don't know if you follow sports, but, you know, like, in the United States and college football, people refer to Gator Nation – right, these are all people who are fans of the Florida Gators. Or, maybe it's AC Milan nation in Italy. I don't want to get there (Roma, whatever), but there are all these people who've trained at Mayo, and, uh, what's great is it's a small world, right? So, I'm super excited to meet you and talk about this, because - I'm going to add you to my Rolodex, because when I see these patients (I'm a neuromuscular guy, but I do a fair bit of inpatient time), I'm always calling a small number of people, so I'm really pleased to meet you so I can put you on speed dial and ask you questions about these patients. I wonder if, maybe, we can begin? You know, in our preparatory discussions, I shared that I just came off our hospital service, and we had several of these patients, you know, where we were thinking about NMO or MOGAD as a cause for their problem - and I wonder if you just have any pearls or pitfalls in when we should suspect this, right? Most of us recognize bilateral optic neuritis, longitudinally extensive myelitis - we need to be thinking about these. Any pearls or pitfalls for when we should or should not be looking for these disorders? Dr Sechi: Yeah, I think this is a great question. I think the first thing to pay attention is the phenotype. So, the clinical MRI phenotype that are typically associated with NMOSD and MOGAD, they are quite characteristic - and it's important to be aware of those phenotypes and how they differ from MS, because in my experience, one of the common misinterpretation (misconception) in clinical practice is just to test for AQP-4 and MOG antibodies in any patient with new-onset demyelinating disease of the CNS, even if it's typical MS. And, this is quite wrong, because MS is way more common in clinical practice - it's sixty, eighty times more common than NMO and MOGAD - and so, if you test all those patients without filter (indiscriminately) for antibodies, you increase the risk of false positivity exponentially, even if you have a highly specific test. So, first of all, I think it's good to select the right patients to test. As you said, patients with LTM, extensive involvement of the optic nerves on MRI, ADEM - there's also patients with cortical encephalitis phenotype (which is a rare phenotype of MOGAD), but not definitely good to test the typical MS patients. This is the first thing. Dr Smith: Yeah, I mean, that's an issue in all of neurology, isn't it, right? I mean, it's an issue in sort of just sending, you know, the Mayo panel, the autoimmune encephalitis panels - you need to select patients carefully, but I think this attention to prior probability is something that we need to really focus on in multiple areas. So, I wonder if you might expand a little bit on assays. I do a lot of work in myasthenia and I know which labs do a really good job with, you know, acetylcholine receptor antibody testing and those that maybe do not, and there are different methodologies for testing - do you have any wisdom in terms of how to select a lab, what to look for, and how to interpret the results you see based on the particular assay that's being used? Dr Sechi: Yeah, that's a critical point. I agree. And especially if you work in myasthenia, you're very well aware of the differences between different assays, and nowadays, most of the high-quality assays are cell-based assays (either fixed or live) - it's the same in myasthenia, and people need to pay attention to some of the less-specific assays. Let's say ELISA, for instance - testing AQP-4 and MOG antibodies with ELISA is quite dangerous, because the risk of false positivity is quite high. So, it's good to know what assays to trust most and also good to know what's the right specimen to send for antibody test. For instance, with AQP-4, we know that serum testing is recommended only, and the CSF doesn't add much, but with MOG, we know that approximately 10% of patients have an isolated positivity in the CSF, which is interesting, because it means that when you have a patient with a strong diagnostic suspicion as a phenotype that is highly suggestive for MOGAD and the serum testing is negative, you may consider testing the CSF to increase your sensitivity. So, this is very important. Dr Smith: So, I have a question for you that may seem a little naïve, but I bet other people are thinking it - can you tell us why it is that these disorders affect optic nerve and spinal cord preferentially? And I think, for NMO, the whole area postrema thing seems awfully specific to me. What's the deal? Why are these areas preferentially affected by these antibody-mediated disorders? Dr Sechi: This is a tough question. For NMO, we know, probably, there is higher expression of some of the isoforms. Let's say there is a higher density of AQP-4 molecules that target the most affected regions - so, of course, AQP-4 is preferentially expressed in the subependymal regions around the ventricles and in the spinal cord and optic nerves, but you may have, also, solutions along the cortical spinal tracts in case of the brain involvement. The area postrema is kind of a different explanation, because there is a sort of permeability - increased permeability - of the blood-brain barrier there. So, there are several factors in MOGAD - this is not very clear, so, this is a great topic to study in the future, I think. Dr Smith: This is a really interesting area, and one that's really benefited by significant therapeutic development. I wonder if you might look a little bit in the future and tell us, maybe, the agent, or perhaps the target, that you're most excited about therapeutically that's coming down the road these days? Dr Sechi: There are trials ongoing for MOGAD, which is the real need in terms of treatment, because for NMO, we already have three, four drugs that have been approved and which efficacy have been demonstrated by randomized clinical trials, and those are B-cell depleting agents, IL-6 inhibitors, and complement inhibitors. For MOGAD, this is still a gray zone, because the optimal treatment strategies remains to be defined. There are ongoing trials that are quite promising on IL-6 inhibitors and the inhibitors of the neonatal Fc receptor (which is also used in myasthenia gravis as you know). And something that seems to be quite effective - a good option for long-term treatment in these patients and relapse prevention - is also the periodic administration of IVIG (intravenous immunoglobulin), which is a nice option, for instance, in the children where you want to avoid immunosuppressants of other types. So, I think IL-6 is going to show to be very effective in the end. We'll see. We'll see. Dr Smith: So, I wonder if I might just give you a vignette and get your thoughts about, kind of, acute management, right? I just took care of a patient who had a longitudinally extensive myelitis and she was essentially paraplegic and actually came in progressing fairly rapidly, and we, of course, started her on IV methylprednisolone, sent off the proper diagnostic testing - the question I have is, how quickly do you advance therapy and go to IVIG or plasma exchange when you're encountering these, right? It takes, you know, I think the turnaround time is, you know, often about a week to get these tests back (at least several days) - I mean, should we be going very quickly to plasma exchange in someone who has a severe phenotype? Is it okay to do three to five days of IV methylprednisolone and wait for the results to come back? What's the right approach? Dr Sechi: I think this is a great question, actually. You know, management of the acute attacks probably is the most important thing, you know, to allow a good recovery, and I think timing of PLEX administration should be very short - so, the threshold for PLEX should be low, especially when the attack is severe, and this has to be done regardless of antibody testing results, which is typically not available before one or two weeks (at least a year in Italy), I think, in many hospitals. So, I think the risk-benefit ratio of administering PLEX is in favor of treatment in these patients, because the side effects (the potential side effects) are very rare and can be prevented. Some diseases, they can mimic NMO or MOGAD - they're very rare, and they can really worsen with PLEX. As an example, we can say spinal cord infarction can worsen, maybe, because of hypotension due to PLEX. Or some very rare infections, like one case, a bad case of intramedullary spinal cord abscess that looked really similar to an AQP-4 IgG-related LTM - and it was bad, because the patient had no fever, no signs of infection, the CSF culture was negative initially, so we ended up doing a biopsy after failure of PLEX and steroids. So, it is recommended to start within the first three to five days, preferentially, in severe cases, and this is great for the outcome of the patient, so, I do recommend PLEX as a second treatment option. And I'm not sure about IVIG acutely. There is some data on MOG, but it's still controversial - it works a lot when PLEX fails, but it can be considered after PLEX, of course. And there are some very rare patients that do not improve, even after IV methylprednisolone, PLEX, or IVIG, and so, you need to consider some rescue therapies. In those patients, it's kind of complicated, because there are some options, like IL-6 inhibitors seem to be quite effective and quite fast-acting for MOGAD attacks, and also eculizumab and complement inhibitors can be an option in patients with AQP-4 - but maybe less in patients with MOG. So, these are the possibilities (very quickly). Dr Smith: So, you mentioned FcRn inhibitors a moment ago, and I wonder, do you see a future where - and I think you were mentioning them as maybe more chronic therapy? Correct me if I'm wrong. Dr Sechi: Yeah, yeah. Dr Smith: Do you foresee a role for these agents in acute management? I mean, there are some that, you know, very quickly lower immunoglobulin levels, though just looking out in the future, you think that these sort of infusion therapies that we think about chronic therapy (you mentioned, you know, complement inhibitors) are going to be useful in acute management? Dr Sechi: Yeah, it depends. It's a good option to try. I'm not sure about the time to action. It's very dependent on that, because IL-6 inhibitors and complement inhibitors are very fast-acting (I think they can be effective already within twelve hours, 24 hours, which is good), but it's reasonable that, also, Fc inhibitors can be an alternative in the future. As far as I know, there is not much in the literature, but it's good to try in the future in case, acutely. Dr Smith: Well, exciting times indeed. Elia, thank you so much for a great discussion. I thoroughly enjoyed this. I look forward to visiting you soon, and I want to congratulate you on a really great article that's very interesting and very clinically useful. Dr Sechi: Well, thank you, Dr Smith. This is my pleasure, and thank you for great questions. I had a great time and hope the readers of Continuum will like the article and the nice figures we have put together. So, thank you, thank you very much. Dr Smith: Well, again, congratulations. And for our listeners today, I've been interviewing Dr Elia Sechi, whose article on aquaporin-4 antibody-positive NMOSD and MOGAD appears in the most recent issue of Continuum, which is on autoimmune neurology. It's a very exciting issue. Please check out Continuum Audio episodes from this and other issues of Continuum. And thanks to you all 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.

Overview and Diagnostic Approach in Autoimmune Neurology With Dr. Sean Pittock

Play Episode Listen Later Aug 7, 2024 26:40

Autoimmune neurology is a rapidly evolving subspecialty that focuses on neurologic disorders with atypical immune responses. In this episode, Aaron Berkowitz, MD, PhD FAAN, speaks with Sean J. Pittock, MD, an author of the article “Overview and Diagnostic Approach in Autoimmune Neurology,” in the Continuum August 2024 Autoimmune Neurology issue. Dr. Berkowitz is a Continuum® Audio interviewer and professor of neurology at the University of California San Francisco, Department of Neurology and a neurohospitalist, general neurologist, and a clinician educator at the San Francisco VA Medical Center and San Francisco General Hospital in San Francisco, California. Dr. Pittock is the director for the Center for Multiple Sclerosis and Autoimmune Neurology at Mayo Clinic in Rochester, Minnesota. Additional Resources Read the article: Overview and Diagnostic Approach in Autoimmune Neurology Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @AaronLBerkowitz Transcript Full transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum, the premier topic-based neurology clinical review and CME journal from the American Academy of Neurology. Thank you for joining us on Continuum Audio, which features conversations with Continuum's guest editors and authors who are the leading experts in their fields. Subscribers to the Continuum journal can read the full article or listen to verbatim recordings of the article and have access to exclusive interviews not featured on the podcast. Please visit the link in the episode notes for more information on the article, subscribing to the journal, and how to get CME. Dr Berkowitz: This is Dr Aaron Berkowitz, and today, I'm interviewing Dr Sean Pittock about his article, “Introduction to Autoimmune Neurology and Diagnostic Approach”, which he wrote with his colleague, Dr Andrew McKeon. This article is a part of the August 2024 Continuum issue on autoimmune neurology. Welcome to the podcast, Dr Pittock. Could you introduce yourself to our audience? Dr Pittock: Well, thank you very much, Dr Berkowitz. So, yeah, I'm a neurologist at the Mayo Clinic. I direct the neuroimmunology laboratory with Dr McKeon and Dr Mills here, and I have also been very much involved in the autoimmune neurology section at the American Academy of Neurology. Dr Berkowitz: So, many of you probably know Dr Pittock - or if you don't know, you've certainly diagnosed diseases that he has described and written about, and so it's a real honor to get to talk to you today and pick your brain a little bit about some of these complex diseases. So, autoimmune neurology is certainly one of the most exciting subspecialties of our field. I feel like when I talk to students and they ask me to make a case for why they should consider neurology as a career, I tell them, “Of course, I have many reasons I love neurology”, but one thing I mention is that, although many other fields of medicine may have made incredible advances as far as treatments, I can't think of too many other fields outside neurology where entirely new diseases have been described since I've been in training and come out of training - and many of those have been in your field of autoimmune neurology. I can think of cases where I've heard you or one of your colleagues on a neurology podcast describing a new antibody, new disease, and a few weeks later, we see that disease and give a patient a diagnosis that had been elusive from other physicians and hospitals. It's a very exciting, gratifying area. It's also daunting, like, every time I go to the AAN and hear one of your colleagues, there's a new disease, and we realize, “Oops! Was I missing that?” or, “Am I going to see this?” And so, hoping to pick your brain a bit today about some of the key concepts and how to keep them in mind so our listeners can recognize, diagnose, and treat these conditions, even if they can't remember every single antibody in your article and all the new ones you and your colleagues will probably discover between now and when this, um, podcast is released. So, before we get into some of the important clinical aspects of these conditions, could you just lay out sort of the broad breaststrokes, the lay of the land of cell-mediated versus antibody-mediated paraneoplastic versus nonparaneoplastic cell surface versus intracellular - how can we sort of organize this area in our minds? Dr Pittock: Yeah. It's complex, and it's really an evolving story. But the importance, really, from the perspective of the reader and the perspective of the clinician is that we're talking about disorders where we can actually do something - we can actually impact patients. And we think about the concept of stopping and restoring in neurology now. We're talking about disorders where we have the potential to stop these inflammatory immune-mediated disorders and, potentially, by stopping early, we may be able to restore function - so, a really important new and evolving field in neurology, because you don't want to miss these conditions. Trying to get your head around the complexity of these entities is difficult, but what we've done in this chapter is, really, to try and lay the groundwork for the following chapters, but provide somewhat of a simplistic approach, but a practical approach that really, I think, can help clinicians. So, the way I think of it, a lot of autoimmune neurology really has stemmed from the discovery of antibodies that cause neurological disease, and the examples of those would be going back to myasthenia gravis (with antibodies to the acetylcholine receptor), going back to Lambert-Eaton syndrome. And then, you know, even if you go back to the older traditional paraneoplastic disorders (the Hu, the Ri, the Yo), at the end of the day, you really have two essential entities, if you want to be very simple. The first is disorders that are caused by an antibody, and the second are disorders where the antibodies you detect are not causing the disorder, but they're telling you that there's predominantly a cellular or T-cell mediated attack of the nervous system. And I think thinking about the diseases in those kind of simple terms helps us when we think about what would be the best treatment to use in these types of cases. Dr Berkowitz: Fantastic. I think that's very helpful. And just to make sure it's clear in the minds of our listeners when we're dividing into these sort of causative antibodies versus antibodies that might be, uh (I don't know if I'm using the word properly), but, sort of epiphenomena (or they're present, but they're not causative) as you said, can you just give some examples of the ones on either side and how making this distinction helps us in practice? Dr Pittock: Yes. So, antibodies that are causative of disease - I think, you know, the one that I've done a lot of work on is in neuromyelitis optica, where you have antibodies that are targeting a water channel that sits on an astrocyte, and so it causes NMOSD, or what we consider an autoimmune astrocytopathy. And we know that when the antibody binds to the target, many things can happen. So, when aquaporin-4 antibodies bind to aquaporin-4, they can do a lot of things. They can cause internalization, they can activate complement that results in the killing of the cell - but there can be other situations. For example, when NMDA-receptor antibodies bind to the NMDA receptor, then a variety of different things can occur different to water channel autoimmunity - where, for example, the receptor (the NMDA receptor) is downregulated off the cell surface, and that results, to some extent, in the neuropsychiatric phenomenon that we see in NMDA-receptor autoimmunity. And, obviously, when you have a situation where the antibodies are causing the disease, removal of those antibodies, or the reduction in the production of those antibodies, is going to help patients. Now, on the other side, we have antibodies that we detect in the blood or in the spinal fluid, and those antibodies are targeting proteins that are inside the cell - so those antibodies we don't consider as being pathogenic. Now, remember, there are sometimes situations where proteins that are inside the cell occasionally can be available for antibodies to bind at certain situations. So, for example, in the synapse, amphiphysin or the septins, may at times become available. And so, sometimes, there are targets or antibodies that are somewhat in between those two simplistic concepts. But when we're talking about antibodies that are targeting proteins on the inside of the cell, remember that antibodies don't just suddenly occur. There's a whole process of presentation of target antigen at the lymph node, and then both a T- and a B-cell response. The B-cell response potentially produces the antibodies but also triggers and stimulates T-cells, and those T-cells then go on to cause the disease. And those T-cells are very problematic, because those classical paraneoplastic and the newer ones we've described (and many have described) - these are associated with quite severe neurological disability, and they're very, very difficult to treat. And if you ask me, “Where is the holy grail of autoimmune neurology therapeutic research?” It's in trying to actually figure out ways of treating the predominantly T-cell mediated paraneoplastic and autoimmune neurological disorders. We're making great headway in terms of the treatments of the antibody-mediated neurological disorders. Dr Berkowitz: That's a helpful overview. So, sticking with this framework, you mentioned as sort of the “causative antibody” category and the antibodies that are predominantly for intracellular antigens, but not believed to be causative - I want to make sure I'm understanding this correctly and we can convey it to our listeners - I believe you said in your paper, then, that the antibodies that are predominantly causative are more likely to be associated with conditions that are very treatable, as compared to the intracellular antibodies that are not thought to be causative, as you just said the disability can be irrecoverable or very hard to treat. And I believe another theme in your paper that you brought out is the antibodies that tend to be causative tend to be cell surface and tend to be less likely to be associated with underlying cancer (although not a perfect rule), and the intracellular antigens more commonly associated with cancer in those cases to look very hard for a cancer before giving up. Are those themes that I understand them from your paper properly, or anything else to add there? Dr Pittock: Yes, I think that that's exactly the message that we were trying to get across, so that's good news that you've picked up on the themes. I think, yeah, in simple terms, remember that when a cytotoxic T-cell identifies the peptide that its T-cell receptor will target, the ultimate outcome is poor, all right? T-cells are like the marines - they don't mess around. Once they find their target, they eliminate that target, and so, it's really difficult to treat those types of diseases if you get them late. And most patients with cytotoxic T-cell mediated paraneoplastic neurological disorders, oftentimes, by the time they get to a center of excellence, the boat has left the dock in many respects - in other words, it's too late. So, you know, I will often see patients, for example, with progressive cerebellar degeneration (say, in the context of Purkinje cell autoantibody type 1 antibodies and a breast cancer), and if those patients are in a wheelchair at the time that I see them, there's very, very little that we can do. So, you really want to try and get that patient into the office, you know, when they're using a cane (or not), and then, potentially, you have the opportunity - using very aggressive immunosuppressive medications - to make a difference. And that is quite different to other scenarios, where, for example, if you have NMDA-receptor encephalitis - as many of the readers will know, this is a condition that is very treatable, and most patients do very well, because the antibodies, they're disrupting function, but they're not killing the neuron, as we see in those more aggressive, paraneoplastic cytotoxic T-cell mediated diseases. Dr Berkowitz: Also, in terms of searching for an underlying cancer, another theme in your paper as I understood (but want to make sure I'm understanding and conveying to our listeners and hear your thoughts), that the cell surface and treatable antibody-mediated syndromes, as you mentioned (NMO, NMDA) tend to be less associated with underlying cancers (although can be), whereas the intracellular antigens, um, a much higher percentage of those patients are going to end up having underlying cancers. Is that correct, or any notable exceptions to be aware of in that framework? Dr Pittock: Yeah, I think the major exception to the rule for the antibodies that are targeting intracellular antigens is the GAD65 antibody story. We generally don't consider the stiff person syndrome, cerebellar ataxia, or other autoimmune neurological disorders associated with very high levels of GAD65 antibodies - those are generally not paraneoplastic. And then there are always exceptions on both sides. You know, one of the benefits of understanding the implications of certain antibodies is trying to understand, you know, what is the likelihood of identifying a malignancy, which antibodies are high-risk antibodies (in other words, high-risk paraneoplastological disorders), and which are low risk in terms of cancer? And, you know, age and the demographic of the individual is often important, because we know, for example, with NMDA-receptor antibodies, the frequency of ovarian teratoma varies with the age of the patient. Dr Berkowitz: Fantastic. And we encourage our listeners to read your articles – certainly, some very helpful tables and figures that help to elucidate some of these broad distinctions Dr Pittock is making - but just to summarize for the antibody-related part of autoimmune neurology, we have one category of cell-surface antibodies and another of intracellular antibodies. Both can cause very severe and varied neurologic presentations, but the cell surface tend to be more treatable, less likely to be associated with the underlying cancer, and the intracellular less treatable, more likely to be associated with the underlying cancer - but, as with everything in neurology and medicine, exceptions on both sides. Is that a fair aerial view of some of the details we've discussed so far, Dr Pittock? Dr Pittock: Yeah, I think so. I mean, I also think that, you know, not only, at least, for the antibody-mediated disorders (you know, as we discussed) we have drugs that will reduce the production of those antibodies, but we're also learning a lot more about the cytokine and chemokine signatures of these disorders. For example, NMO, water-channel antibody-mediated diseases are associated with elevated levels of IL-6. We know, for example, in LGI1 encephalitis and other encephalitides, that IL-6 also is elevated at the time of that encephalitic process. And so, the potential to target IL-6 with, you know, drugs that inhibit IL-6 and the IL-6 receptor, these potentially have, you know, a role to play in the management of these types of patients - whereas in the T-cell mediated disorders, you know, no advance has been made in the treatment of those conditions, I would say, in over 50 years. So, for example, the standard of treatment is steroids and then drugs that impact the bone marrow, and so we really haven't moved forward in that respect. And that, I think, is an area that really needs drive and enthusiastic out-of-the-box thinking so that we can try to get better treatments for those patients. Dr Berkowitz: This has been a helpful overview. I look to dive into some of the scenarios that frontline practitioners will be facing thinking about these diseases. An important point you make in your article is that autoimmune and antibody-mediated neurologic syndromes can affect any level of the neuraxis. Even just our discussion so far, you've talked about anti-NMDA receptor encephalitis, you've talked about myasthenia gravis (that's at the neuromuscular junction), you've talked about paraneoplastic cerebellar degeneration - there can be an “itis” of any of our neurologic structures and that “itis” can be antibody-mediated. So, one of the key messages you give us is, one, that these are sort of in the differential diagnosis for any presenting neurologic syndrome, and, two, sort of one of the key features of the history, really, to keep in mind (since we could be anywhere along the neuraxis) is the subacute presentation when this should really sort of be top of mind in our differential diagnosis - so, many of these patients are going to be mystery cases at the outset. And one striking element you bring out in the paper is that, sometimes, the MRI, CSF, electrophysiology studies may be normal or nonspecifically abnormal, and although it's very helpful when we can send these antibody panels out, in some cases, resources are limited or institutions have certain thresholds before you can send these out (because neurologists love to send them in). Sometimes, they are not necessarily appropriate. So, love to hear your thoughts on when we should be sending these panels. What are some clues? Um we have a subacute neurologic presentation at any level of the neuraxis, and when it's not anti-NMDA receptor encephalitis, that is sort of a clear phenotype in many cases. How you would approach a patient, maybe, where the MRI is either normal or borderline abnormal (or people are squinting at the medial temporal lobe and saying, “Maybe they're a little brighter than normal”), CSF is maybe normal or nonspecifically, um, and the protein is a little high, but no cells? What clues do you use to say, you know, “These are the patients where we should be digging deep into antibody panels and making sure these are sent and not miss this diagnosis?” Dr Pittock: Well, thank you. That's a good question. So, I think, you know, first of all, these are complex cases. So, the patient is sitting in front of you and you're trying to figure out, first of all, Is this a hardware or a software problem? Are we definitively dealing with an encephalitis or an organic neurological entity that's immune-mediated? And, you know, the way I think of it is, for me, you see a patient, it's a twenty-five-piece jigsaw puzzle and you've got two pieces, and you're trying to say, “Well, if I step back and look at those two pieces, do I have any sense of where we're going with this patient?” So, the first thing you need to do is to collect data, both the clinical story that the patient tells you (and I think you make the good point that that subacute onset is really a big clue), but subacute onset, also fluctuating course, sometimes, can be important. The history of the patient - you know, Is the patient somebody who has a known history of autoimmune disease? Because we know that patients that have thyroid autoimmunity are more likely to have diabetes, they're more likely to have gastrointestinal motility or dysmotility, they're more likely to have a variety of different immune-mediated conditions. So, is there a family history or a personal history of autoimmunity? Is the patient at high risk for malignancy? Are there clues that this potentially could be a tumor-initiated immune process affecting the nervous system? The neurological exam also is extremely important because, again, that helps you, first of all, kind of define and get some objectivity around what you're dealing with. So, does the patient have hyperreflexia? Are there signs that there is neurological involvement? And then, really, what I think we need to do is to try and frame the predominant neurological presentation. So, what is the major issue? Because a lot of these patients will have multiple complaints, multiple symptoms, and it's very important to try and identify the major presentation. And that's important, because the neural autoantibody tests are now presentation-defined - in other words, they're built around the neurological presentation, because the old approach of just doing, apparently, a plastic evaluation is gone, because we've got to a stage where we have now so many neural antibodies, you can't test every single neural antibody. So, if you're suspecting that there may be an autoimmune neurological component, then you really need to think about what would be the most appropriate comprehensive evaluation I need to do for this patient. So, for example, if a patient comes in with a subacute-onset encephalopathy, you're probably going to want the autoimmune encephalitis evaluation, and then you have to pick whether it's going to be serum or spinal fluid - and as we outlined in the paper, there are certain antibodies that are better detected in serum versus spinal fluid. So, for example, in adults over the age of 50, LGI1 is much more accurately detected in serum than spinal fluid, and the absolute opposite is true for NMDA-receptor antibody detection. One of the most important components of the neurological evaluation is the spinal fluid, but actually looking at the white cell count - and in fact, sometimes, it's quite interesting to me that I'll often see patients referred with a diagnosis of encephalitis and autoimmune encephalitis, and yet they haven't had a spinal fluid examination. So, the presence of a white cell count, you know, greater than five is hugely helpful - it's like two pieces of that twenty-five-piece jigsaw, because that really tells you that there is something inflammatory going on. And now, in terms of imaging, you're right - some patients will have normal MRI. And if you really do think that there's evidence of - you know, for example, you do an MRI, but you're getting a good sense that there's a temporal lobe seizure occurring, MRI looks normal, the EEG shows some abnormalities in the mesial temporal area - you know, considering additional imaging modalities (like PET scan of the brain), I think, is reasonable. We know that in NMDA-receptor encephalitis cases, 30% of patients will have normal MRI but they'll often have abnormalities on the PET scans. So, I think, what we do is we try to gather data and gather information that allows us to add in pieces of that jigsaw so that, eventually, after we've done this evaluation, we can see now we have ten pieces. If we step back, we say, “Yes, now we know what this condition is”, and then we essentially plan out the therapeutic approach dependent on what we've found. In terms of identification of underlying malignancy, you know, different people have different approaches. Our approach generally has been to try to get a PET-CT scan of the body as our first go-to test, because, actually, we found that CT chest abdomen and pelvis really actually delivers the same amount of radiation - and from a cost perspective, it's about the same - and we have found that PET-CTs really do provide a higher sensitivity for cancer detection. Dr Berkowitz: Perfect. A lot of very helpful clinical pearls there. So, in closing, Dr Pittock, I've learned a lot from you today. I'm sure our listeners will as well. What does the future hold in this field? What's coming down the pipeline? What are we going to be learning from you and your colleagues that are going to help us take care of patients with these diseases going forward? Dr Pittock: Well, thank you, Dr Berkowitz, for that question. I think the future is very bright and very exciting, and, hopefully, some of the more junior members will be enthused by this Continuum series, and, hopefully, we'll go into this area. So, let's talk about the future. The future, I think, is going to be of great interest. Firstly, there's going to be continued discovery of novel biomarkers, and the reasons for that is because of the technical and technological advances we've seen. So, for example, there have been many, many antibodies discovered by us and others that have been discovered on the basis of, for example, phage technology. In fact, the Kelch 11 biomarker discovery in collaboration with UCSF and our group was done on the basis of Joe DeRisi and Michael Wilson's phage approach. And we're actually using that now at Mayo Clinic, and we've discovered about three or four new antibodies just in the last couple of years using this technology (and that here is led by John Mills and Div Dubey). And then, we're also going to see, I think, the evolution of protoarrays much more in biomarker discovery, so, we'll have more antibodies, and again, I think, generally, those antibodies will fall into the two categories we kind of described - so, you know, in terms of the approach to those conditions, maybe not so much change. I do think, though, that the introduction and the utility of comprehensive cytokine and chemokine analysis in the future will assist us in making diagnoses of seronegative encephalitis, but also potentially will direct therapy. So, for example, cytokine A is elevated - maybe that would be a potential target for therapy that's available for these patients with rare and potentially very disabling disorders. Then, when we look at the cytotoxic T-cell mediated disorders, I think the major areas of advance are going to be in better understanding the immunophenotype of cytotoxic T-cell mediated diseases, and then the potential development of tolerization strategies using the specific targets, those specific epitope targets that are involved in paraneoplastic and nonparaneoplastic diseases, and seeing if we can vaccinate patients, but move that immune response into more of a tolerogenic immune response rather than a cytotoxic killing response. And then I think, lastly, we're going to see a dramatic revolution in CAR-T therapeutic approaches to these types of disorders moving forward - and not just, you know, CAR-T therapies that are targeting, you know, CD19 or CD20, but CAR-Ts that are actually personalized and developed so that they can target the specific B- and T-cells in an individual patient and actually do a very fine removal of that autoimmune pathologic process that I think would have significant benefit for patients not only in stopping progression, but also in significantly reducing the potential of side effects - so, a much more targeted approach. So, that's where I think the next ten years is going to be. I think it's very exciting. It's going to require the collaboration of neurologists with, you know, immunologists, hematologists, you know, across the board. So, a very exciting future, I think, for this field. Dr Berkowitz: Exciting, indeed. And we have learned so much from you and your colleagues at the Mayo Clinic about these conditions, and I definitely encourage our listeners to read your article on this phenomenal issue that really gives us a modern, up-to-date overview of this field and what's coming down the pipeline. So, a real honor to get to speak with you, pick your brain about some of the clinical elements, pitfalls and challenges, and also hear about some of the exciting signs. Thank you so much, Dr Pittock, for joining me today on Continuum Audio. Dr Pittock: Thank you very much. Dr Berkowitz: Again, today, I've been interviewing Dr Sean Pittock, whose article with Dr Andrew McKeon on an introduction to autoimmune neurology and diagnostic approach 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 so much to our listeners for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use this link in the episode notes to learn more and subscribe. AAN members, you can get CME for listening to this interview by completing the evaluation at Continpub.com/audioCME. Thank you for listening to Continuum Audio.

university california social media san francisco minnesota md rochester mills american academy cart mri mayo clinic neurology ri multiple sclerosis diagnostic autoimmune aan continuum hu associate editor ucsf cme eeg berkowitz california san francisco csf michael wilson mckeon john mills nmda kelch pet ct san francisco general hospital cd20 cd19 nmo nmosd purkinje pittock aaron berkowitz san francisco va medical center joe derisi gad65 lgi1 teshamae monteith

August 2024 Autoimmune Neurology Issue With Dr. Eoin Flanagan

Play Episode Listen Later Jul 31, 2024 21:18

In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Eoin P. Flanagan, MBBCh, FAAN who served as the guest editor of the Continuum® August 2024 Autoimmune Neurology issue. They provide a preview of the issue, which publishes on August 1, 2024. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Flanagan is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Additional Resources Continuum website: ContinuumJournal.com Subscribe to Continuum: shop.lww.com/Continuum More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Guest: @EoinFlanagan14 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, 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 have access to exclusive audio content not featured on the podcast. If you're not already a subscriber, we encourage you to become one. For more information, please visit the link in the show notes. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today, I'm interviewing Dr Eoin Flanagan, who recently served as Continuum's guest editor for our latest issue on autoimmune neurology. Dr Flanagan is a neurologist at Mayo Clinic in Rochester, Minnesota, where he's a professor of neurology. Eoin, why don't you introduce yourself to our listeners? Dr Flanagan: Yeah, it's a great pleasure to be here today. I'm a neurologist. I'm originally from Ireland – I did my medical school training over there, and then came over to the Mayo Clinic to train in neurology and in neuroimmunology. And delighted to be able to edit this exciting issue of autoimmune neurology of Continuum. I think, um, it's a really fascinating area that's moving very quickly, and I'm hoping that we can educate listeners to be able to feel comfortable when they come to see these patients and to realize how much of a growing specialty it is and how we're getting treatments, and we can really help these patients. Dr Jones: Yeah, it's a pretty exciting area. And, so, not only are you the Guest Editor for our latest issue of Continuum, this is the first-ever Continuum issue dedicated to autoimmune neurology, so I want to thank you for taking it on. This is something that our readers have been asking for for many years. I hope the topic wasn't too daunting. Dr Flanagan: No, absolutely, it's a pleasure to be able to do it, and it's just great when you read all the articles to kind of feel where the field is going and how much of a benefit we can now make for our patients. So, that's been a real joy to do. Dr Jones: Well, congratulations, and it's a magnificent issue. You have a lot to be proud of putting this group of authors together. So, for a few of our issues now, we've had the opportunity on the Continuum Audio podcast to interview the Guest Editor, which is really fun for me. I have to confess it's really a joy to talk to someone who is up to the minute not only in their narrow area of expertise at the article level, but, really, across the entire breadth of the subspecialty. And so, you've had an opportunity to delve into all relevant topics in autoimmune neurology. When you look at the issue as a whole, or the field as a whole, what do you think the biggest debate or controversy in the world of autoimmune neurology is right now? Dr Flanagan: Yeah, I think there's some changes happening. You know, initially, people used to recognize a disease called Hashimoto's encephalitis, where patients would have a presentation of encephalitis in the setting of thyroid antibodies. And what we're now realizing is that many of these patients actually have antibodies to neural-specific targets, because we know that the antibodies that target the thyroid don't really impact the brain. And what we're now realizing is that there's many antibodies out there that bind to different receptors in the brain (the NMDA receptor, for example, AMPA receptor), so we're really trying to refine the field towards these different antibody-associated disorders - and each different disorder may behave very differently. A patient with NMDA receptor encephalitis, for example, may be in the ICU, in hospital, may take them six, nine months to recover. On the other hand, a patient with LGI1-antibody encephalitis may get five days of steroids and be almost back to normal within a few weeks. So, it's a really broad spectrum. And, I think, what we're now learning is that each antibody has a role in helping define the disease, guide your treatment, guide your search for cancer - but, also, they behave differently - so these neural-specific antibodies are really important, while the older antibodies (like the thyroid antibodies) may just be a bystander and something that's happening in the background in a patient who's more prone to autoimmune disease. Dr Jones: Very helpful, and I think that resonates with our listeners who have taken care of patients with autoimmune neurologic disorders, and it really is, I think, a great prototype in our specialty, maybe (for lack of a better word) of how observations start at the bedside, and then discoveries are made at the bench, and those benefits are brought back to patients. You know, there's been a recognition of autoimmunity in neurology for a long time, right - responsiveness to immunosuppression, even before the biomarkers were discovered - tell us a little story about how that works for our listeners. Dr Flanagan: Yeah, so, I think one of the first steps is defining a clinical syndrome. So what you'll find is that some of these syndromes (for example, neuromyelitis optica spectrum disorder, where they have longitudinally extensive lesions within a spinal cord) provoked people to be interested that these looked different to MS, and then that went to the lab, and the aquaporin-4 antibodies were discovered - or, more recently, MOG antibodies were discovered. The aquaporin-4 antibody-associated neuromyelitis optica spectrum disorder is a good prototype, because that went to the laboratory. Initially, they saw complement deposition on the pathology of these patients, they saw antibody deposition - the antibody was then discovered to aquaporin-4. And then, many labs around the world went to their own labs and they tried to delve in to determine what the pathogenesis was, and they found that complement was important in cell killing, that interleukin-6 elevation was important, and that complement appeared to be important. So, then, what they did was they tried to find treatments that would target those pathways. So, and now, we have treatments that are successful for this disease that can target complement, target interleukin-6, and target B cells (be it CD19 or CD20). So, we now have many different treatments, and this disease used to be very severe (so, had a 33% mortality at five years), and now these patients can live a long life with these treatments. So, I think that gives you an example of how you can follow the immunology of the disease and use targeted treatments to help our patients, and I think we can use that as a good prototype for many of the other antibodies, because every year we discover two to three new antibodies, and each disease is a bit different in its mechanism. So, there are now clinical trials in NMDA receptor encephalitis starting up. There's clinical trials in MOG antibody-associated disease. And I think we're going to see that as we move forward, that these treatment trials will come and we'll be able to help our patients better with proven treatments that we know work, rather than a history of we would just use five days of steroids and then we didn't know exactly what to do in the long term - and we could manage some of the relapse as well, but we couldn't really take care of the disease in the background - so, I think the NMO is a good model for moving forward, and the pharmaceutical companies are supporting moving forward with different trials for the disease. Dr Jones: So, a key message there is understanding the biology so we can be a little more targeted and less indiscriminate in the immunomodulation we're going to use. And we have parallels to that in the neuromuscular world, right, like using B-cell depletion for MuSK-associated neuromuscular junction disorders, as opposed to the trial-and-error approach, right? That's got to be a little more patient-centric and you get to a therapeutic response faster, right? Dr Flanagan: I think so. Yeah, and I think, in the future, that might be something where, you know, a different patient, if they had elevated cytokines that pointed more to an IL-6 elevation, then maybe, in that patient, you would target IL-6, while the next patient with the same disease has more prominent complement activation, maybe you would target complement, or another patient has more prominent B-cell markers elevated, that you would target B cells. So, I think, we're really moving towards a more individualized treatment in some of these disorders. So, it's a very exciting time, but we've only really made that breakthrough in one of the antibodies, and we have probably sixty, seventy antibody-mediated disorders now. So, it's going to get complicated, but it's also going to be, really, an exciting time for our patients, and I think an exciting time for neurology trainees and people who see patients in practice that we can now make diagnoses and guide their treatment that, previously, you know, these patients were told they might have presumed infectious encephalitis or we didn't know the exact cause. Dr Jones: So targeted not only to the diagnosis, but to the individual. Dr Flanagan: Yeah. Dr Jones: So, that's a level of complexity that I think is going to blow a lot of our minds, right? And it's exciting, but I think it also is a little daunting, right? Dr Flanagan: Absolutely. Yeah. Yeah, it's going to be complicated, and these are rare diseases, so they're difficult to do clinical trials in. But I think we can be guided, and our experience tells us that if you follow the mechanisms, that you can find targeted treatments. Now, you can also find targeted treatments in MS - you know, it took us a longer time to find successful high-efficacy treatments, but now we're doing much better with many high-efficacy treatments available. But, I think in these autoantibody-mediated diseases, really looking at the mechanisms and trying to figure out that and then targeting the treatment in that direction makes the most sense and is the most likely to be successful. Dr Jones: So, one of the purposes of Continuum is to educate our readers and our listeners, and because neurology is so broad, because it is evolving so quickly, it's really hard to stay current. And so, again, that's part of the purpose of the journal. I think one of the challenging areas is autoimmune neurology, because it changes fast, and it's complicated, and the treatments are high stakes and complicated to administer - so, I think this is an important topic. I know from my own experience in clinical practice, one of the challenging scenarios is you see a patient who may have an autoimmune neurological disorder, you obtain some serum or CSF markers of neurologic autoimmunity, right? And of the ten antibodies you check, one of them comes back, and it's a low titer-positive antibody. I know that's something that you get a lot of questions about. How do you approach that? Dr Flanagan: Yeah, I think, you know, we're all neurologists, and, you know, it's immediately back to the history, the examination, and the investigations, and what do they support - so, are you really dealing with an antibody-mediated disorder? And I think, from a neuroimmunology laboratory standpoint, we're always trying to get better tests, remove those less-specific tests (so, move away from the thyroid peroxidase antibodies) and really hone in on the exact targets and their mechanisms. So, I suppose, when you find a low-positive result, it's really important to go back to that clinical. And, I think, you know, that is job security for neurologists, right? Because you really have to interpret these in context. And, I think when you're seeing autoimmune cases, you need to have a good, broad understanding of differential diagnosis, because there are many different disorders that can present in a similar way, and you don't want to get distracted by that low-positive antibody and then put a patient on long-term immunosuppression that has many different risks. So, there is a potential for misdiagnosis, and I think that's an emerging area that we're recognizing that we always have to put the antibodies into clinical context. And, you know, there are more and more studies coming out that will help guide you, and I think the issue in Continuum will help guide you in terms of your understanding of, you know, what does a positive antibody mean? And it'll give a little bit on the methodology of how the antibodies are tested and how that can help you – or, sometimes, be it the titer may be very high that can help you. So, different aspects of the antibody test results can also help guide you in the likelihood of that being kind of a true positive versus a false positive. But I think always back to the history, exam, and the investigations, too. Dr Jones: You're being very gracious there, and I'm glad you bring it up that it's really not just about the laboratory performance of the test, right? It's about the pretest probability of the clinical syndrome if it doesn't clinically resemble an autoimmune neurological disorder. So, I'm not going to pretend to be an expert in Bayesian statistics, but I think we should recognize that if we obtain any test when there's a low likelihood of the syndrome or the diagnosis being present, we're more likely to have false positives than in other scenarios or other settings. So, I think that is a charge to the clinician, where if we are obtaining these tests, we do really need to think about the likelihood of there being a clinical autoimmune neurology syndrome, right? Dr Flanagan: That's exactly right. You know, one of the teachings that I sometimes give to the trainees is that, you know, if you have a ninety-year-old patient with mild cognitive impairment who comes into the emergency department with some worsened altered mental status, you know, you want to check for a urinary tract infection, you want to check a chest x-ray - you don't want to test neural antibodies upfront. So, you always have to consider the setting and avoid overtesting, because like any test, they're not perfect, and you can run into trouble if you order it too frequently - so, that's another thing that we try to educate people. And then if you do order the test, we like to educate people on, you know, what the positive test results mean, and is there any potential for false positives like we talked about? Dr Jones: And I think, keeping in mind - obviously, there are exceptions - but the subacute onset of multifocal neurological disorder is really suggestive of autoimmunity. It doesn't mean that it can't happen in other contexts. And it has been exciting not only on the diagnostic side, but on the therapeutic side. There are so many exciting new treatments. What do you think is on the horizon beyond what we've seen in the last few years with small- and large-molecule therapies for these disorders? Dr Flanagan: Yeah, I think there's new things. You know, people are always looking at different approaches. So, for example, there's a lot of interest in tolerance, and is there a way you could tolerize yourself out of some of these autoimmune conditions? There's a lot of work on CAR-T treatments, looking particularly in the field of lupus and other systemic autoimmune diseases, and I suspect that they will also be applied to autoimmune neurologic conditions. And then the other thing to mention is that we're seeing the more frequent use of immune checkpoint inhibitors in patients with lots of different types of cancers, including neuroendocrine tumor. So I think, in the future, everybody's going to have to learn about autoimmune neurology, because we're going to be seeing these patients more often, because there's going to be more neurologic immune-related adverse effects related to those immune checkpoint inhibitor treatments – so, I think we're going to continue to see autoimmune neurologic disorders pop up. And, you know, the immune checkpoint inhibitors are almost real-world laboratory experiments, because you're ramping up the immune system, and you can trigger many different types of autoimmune conditions. We're actually learning a lot from these patients that can help us in the way we diagnose and the way we treat these patients in the future, but I will say that, sometimes, they can cause a challenge, because some of these patients have difficult-to-control cancer - you need to up their immune system, but then they get autoimmune complications. We try and dampen down the immune system, and then we need to kind of ramp it back up to treat the cancer. And we've had some challenges where managing such cases can be difficult with that balance of cancer-directed immunotherapy versus immune-related adverse events, and, sometimes, that can pose a challenge for autoimmune neurologists when we see these patients. Dr Jones: So, those are challenges, and I imagine it's a challenging and often rewarding field. What is the most rewarding thing about caring for patients with autoimmune neurological disorders? Dr Flanagan: I think it's a few things. You know, one is that it's a multidisciplinary area, so many of these patients will have different subspecialties of neurology involved. So, we'll get to work with our colleagues, and we may work with our oncology colleagues, we work with our ophthalmologist, and we work with our physical medicine and rehab team – so, it's a real team approach to help the patient. So, that's one aspect that's very enjoyable, because everybody needs to work together. And then, you know, these are treatable conditions. So we can have patients who are in the intensive care unit - you know, quadriplegic, in a coma - and then we treat them, we see them back, and they can be back close to normal. So, particularly, with some of these antibodies that target the cell-surface receptors (like NMDA receptor encephalitis, MOG antibodies), these patients can really go from being really, really sick in the ICU to coming back to normal – so, that's very satisfying, and much of that is related to the improvements we have in treatments, and then we can manage them in the long term with some of these newer treatments that are coming along for these diseases. So, I think it's a very exciting area and exciting time for our patients with these disorders, and we're getting more and more clinical trials, so we're hoping that we'll have more and more treatments available into the future. Dr Jones: I think that has to be part of why the interest in autoimmune neurology has grown so much. I know as an educator - I hear this a lot from trainees - you know, the level of interest in MS and autoimmune neurology has really only grown over time. It must be because of better understanding of the pathobiology of disease, better treatment options, and something that our listeners may not know. Not only is Dr Flanagan an expert in autoimmune neurology - he's very well trained, he did fellowship in MS and autoimmune neurology, and behavioral neurology, right? Dr Flanagan: That's correct. Yeah. Yeah. Dr Jones: And, you know, it's going to sound like I'm trying to flatter Eoin here, but I'm really not (this is going to lead to a question). Eoin is, you know, very well recognized for his work in autoimmune neurology and discovery in this area. Uh, he happens to be one of the best doctors I know. And Eoin, you've won the Teacher of the Year Award several times. So, for our listeners who are looking into their careers and trying to manage multiple areas of interest, how do you do it? You do so many different things so well. Dr Flanagan: Well, you know, I'm lucky to have had the opportunity to work here at the Mayo Clinic and in the neuroimmunology lab. So, we have a lot of resources, and it's an exciting area, you know? We need to bring up the next generation of leaders, so we need to be enthusiastic about these conditions, and we really can do a lot for these patients. So I think when I cover on the hospital service - you work with the residents or work with the fellows and clinic - you know, these cases (when they come around) are really enjoyable to see you can get an answer, we can figure out what type of treatment to do, and we can really help these patients. So, I think that makes it a very exciting area and an easy area to teach residents and to convey some of the excitement that's happening in the field. So, it's just a great honor to be able to work with trainees to kind of let them know the field. And, you know, there's more and more fellowship opportunities in different centers in neuroimmunology, and I think more residents are becoming interested in the field of autoimmune neurology because of so much happening. But, in saying that, with these challenges, it's very hard to keep up with all these antibodies - I find it hard. There's 70 different antibodies - it's hard to know every single thing about every single one. So, we need to continue to educate, to try and simplify, to try and help our younger people be able to manage these patients, because no matter who it is in neurology, you're going to encounter these patients - if you cover the hospital, if you see regular patients in clinic, if you do consult service, you'll come across these patients - and we're going to see them more and more with immune checkpoint inhibitors and other treatments coming along. So, I think it's an exciting area, and it's an important area for everyone to be aware of. So, it's just a great pleasure to be able to be involved in the field and see such enthusiasm in junior people. Dr Jones: So, in addition to doing all those things well, you're also very humble. So, that's a great answer, and I think it is important - even though these are collectively rare - the opportunity to treat these patients and have wonderful outcomes is great, and I think the ability to recognize and feel comfortable. And, hopefully, Continuum has a place in that. I think your issue, Dr Flanagan, is a stellar issue and, uh, will be a benchmark for a generation of neurologists and how to approach these disorders. So, I want to thank you for being our Guest Editor for that topic and joining us today for such a thorough and fascinating discussion on autoimmune neurology. Dr Flanagan: Thanks so much. And thank you to the Continuum team for highlighting autoimmune neurology. It's an exciting field, and I think, really, there is a great group of authors that cover neuroimmunology comprehensively, and I think, hopefully, people will enjoy the edition. Dr Jones: Again, we've been speaking with Dr Eoin Flanagan, Guest Editor for Continuum's most recent issue on autoimmune neurology. Please check it out. And thank you to our listeners for joining today. Dr Monteith: This is doctor 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. Thank you for listening to Continuum Audio.

social media ms elon musk minnesota teacher md rochester american academy icu cart mayo clinic neurology hashimoto autoimmune continuum associate editor flanagan cme eoin bayesian mog faan csf nmda ampa cd20 cd19 nmo mbbch lgi1 teshamae monteith

Episode #36 | When Disaster Strikes: Emergency Planning for People with Disabilities

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Play Episode Listen Later Jul 3, 2024 36:41

In this episode, we discuss emergency preparedness and inclusivity with our guest, Brian Kosczuk, a second-generation paramedic and Pennsylvania EMS Educator of the Year.Brian shares how living with a rare disease, myositis, and being a cardiac arrest survivor have allowed him to see different perspectives and how that shapes his role as a first responder, educator, and advocate.Brian also discusses the challenges and solutions for ensuring emergency alerts and responses are accessible to people with disabilities. From adaptive technologies to the role of local emergency managers in accommodating specific needs, he provides valuable insights into making emergency services more inclusive.Tune in as he gets us thinking about how to prepare for the worst.ABOUT US:The Demystifying NMO and MOG podcast is a Sumaira Foundation (TSF) project andwas made possible with the generous support of Genentech.SOCIAL & WEBSITE:Brian KosczukLinkedIn - https://tinyurl.com/2he45j6nDemystifying NMO podcastInstagram - www.instagram.com/demystifying_nmomogTwitter - twitter.com/DemystifyingNMOThe Sumaira FoundationWebsite - www.sumairafoundation.orgFacebook - www.facebook.com/TheSumairaFoundationVoices of NMO & MOG - www.sumairafoundation.org/awareness/voices-of-nmo/ADDITIONAL LINKSPreparing for Disaster for People with Disabilities and Other Special Needs(FEMA and the American Red Cross)https://tinyurl.com/ycjpxga2People with Disabilities (U.S. Dept. of Homeland Security) https://www.ready.gov/disabilityDisability and Health Emergency Preparedness (CDC)https://tinyurl.com/yg73h3uuSUPPORT THE PODCASTDonate to Illuminatehttps://www.sumairafoundation.org/advocacy/donate/CREDITS:Producer & Host - Brian DawsonMusic - Denys Kyshchuk from Pixabay

BrainWaves Quanta: PREVENTing relapses of Aqp4-Ab NMO

MedLink Neurology Podcast

Play Episode Listen Later Jun 27, 2024 19:46

music sound prevent preventing brainwaves pmid quanta new england journal of medicine relapses mike koenig nmo unheard music concepts trg banks lancet neurol aqp4 aitua

185. Clinical Trials for Multiple Sclerosis w/ Dr. Joshua Katz, MD

The MSing Link

Play Episode Listen Later Jun 19, 2024 28:40

We have a repeat guest today, one of my favorites, Dr. Joshua Katz. He is the director of the Elliot Lewis Center and a nationally recognized expert in MS, NMO, MOG associated disease and transverse myelitis. I've worked alongside Dr. Katz for many years and have many mutual patients. On today's episode, Dr. Katz and I talk all about clinical trials. He shares how to know what clinical trials are happening, how to participate in one, and what the process is like. Dr. Katz is the Director of the Elliot Lewis Center, and a nationally recognized expert in multiple sclerosis, neuromyelitis optica, MOG associated disease, and transverse myelitis. I've worked alongside Dr. Katz for many years and shared many patients. He's one of the few neurologists who truly listens to you and your symptoms and will spend the time to brainstorm solutions for living your best life with MS. Not only that, the Elliot Lewis Center provides cutting-edge care and access to all of the available therapeutic options and strategies. Website: https://elliotlewisms.com/about-us/ Facebook: https://www.facebook.com/ElliotLewisMS Additional Resources: https://www.doctorgretchenhawley.com/insider Reach out to Me: hello@doctorgretchenhawley.com Website: www.MSingLink.com Social: ★ Facebook: https://www.facebook.com/groups/mswellness ★ Instagram: https://www.instagram.com/doctor.gretchen ★ YouTube: https://www.youtube.com/c/doctorgretchenhawley?sub_confirmation=1 → Game Changers Course: https://www.doctorgretchenhawley.com/GameChangersCourse → Total Core Program: https://www.doctorgretchenhawley.com/TotalCoreProgram → The MSing Link: https://www.doctorgretchenhawley.com/TheMSingLink

director ms katz multiple sclerosis clinical trials mog nmo

Episode #35 | Movement as Medicine w/ Dr. Gretchen

social doctors ms rehab physical therapy pixabay genentech mog website dr better quality movement as medicine success00 nmo life00 credits producer

Play Episode Listen Later Jun 19, 2024 49:07

In this episode, we talk about how physical therapy can help people with demyelinating diseases, disabilities, and chronic illnesses.Some of you may recognize her from social media as Dr. Gretchen, who shares excellent videos about PT and exercise as part of her MSing Link wellness program.Gretchen Hawley is a Doctor of Physical Therapy and a Multiple Sclerosis Certified Specialist. She has been a keynote speaker at several MS conferences and a popular guest lecturer at educational events and MS support groups.She shares her thoughts on how a holistic approach to physical therapy that emphasizes the importance of adaptive strategies tailored to each individual's needs can make a difference by improving mobility, independence, and overall quality of life.ABOUT US:The Demystifying NMO and MOG podcast is a Sumaira Foundation (TSF) project andwas made possible with the generous support of Genentech.SOCIAL & WEBSITE:Dr. Gretchen HawleyWebsite - www.drgretchenhawley.comFacebook - www.facebook.com/DrGretchenPTInstagram - www.instagram.com/doctor.gretchenTwitter - x.com/DrGretchenPTYoutube - www.youtube.com/c/DoctorGretchenHawleyDemystifying NMO podcastInstagram - www.instagram.com/demystifying_nmomogTwitter - twitter.com/DemystifyingNMOThe Sumaira FoundationWebsite - www.sumairafoundation.orgFacebook - www.facebook.com/TheSumairaFoundationVoices of NMO & MOG - www.sumairafoundation.org/awareness/voices-of-nmo/TIMESTAMPS/TOPICS:00:01:02 Dr. Gretchen00:08:39 Neurplasticity00:16:07 Rehab vs. Maintenance00:20:05 Getting Started00:23:27 PT for Better Quality of Life00:25:59 Functional Exercise00:29:33 Modifications Can Lead to Success00:33:13 Heat Intolerance 00:35:28 Rest is Crucial00:42:30Finding a PTADDITIONAL LINKS:The MSing Link book - www.drgretchenhawley.com/the-msing-link-bookSUPPORT THE PODCASTDonate to Illuminatehttps://www.sumairafoundation.org/advocacy/donate/CREDITS:Producer & Host - Brian DawsonMusic - Denys Kyshchuk from Pixabay

Episode #34 | From Brain Fog to Clarity: Finding Voice and Purpose w/ Alanna Yee

social science clarity advancement american association pixabay brain fog humanizing genentech mog science magazine more than words nmo finding voice credits producer

Play Episode Listen Later May 29, 2024 33:19

In this episode, we are featuring Alanna Yee.The onset of autoimmune encephalitis and the frustrations leading to her diagnosis would change her life in ways she never could have imagined. These experiences inspired Alanna to begin sharing her own story to help others navigate similar challenges.Alanna generously shares her insights on how to effectively tell personal health stories. She guides us on where to begin, how to strike a balance, and how to respect our own privacy when sharing such personal narratives. Her perspective on the therapeutic value of sharing patient experiences and its potential to drive progress for rare diseases is truly enlightening.ABOUT US:The Demystifying NMO and MOG podcast is a Sumaira Foundation (TSF) project and was made possible with the generous support of Genentech.SOCIAL & WEBSITE:Alanna YeeFacebook - https://www.facebook.com/wherearemypillowsInstagram - www.instagram.com/wherearemypillowsTwitter - twitter.com/wampillowsDemystifying NMO podcastInstagram - www.instagram.com/demystifying_nmomogTwitter - twitter.com/DemystifyingNMOThe Sumaira FoundationWebsite - www.sumairafoundation.orgFacebook - www.facebook.com/TheSumairaFoundationVoices of NMO & MOG - www.sumairafoundation.org/awareness/voices-of-nmo/TIMESTAMPS/TOPICS:00:01:27 Alanna Yee00:08:08 How To Start Sharing Our Experiences00:11:45 More Than Words, Other Ways To Tell Our Stories00:16:11 Facts & Emotions00:23:53 Authenticity And Privacy00:29:41 Advice For People Considering Sharing Their Health StoriesADDITIONAL LINKSThe profoundly personal side of rare disease: Humanizing the therapeutic journey of patients from Science Magazine, a peer-reviewed academic journal by the American Association for the Advancement of Science. t.ly/Llg1USUPPORT THE PODCASTDonate to Illuminatehttps://www.sumairafoundation.org/advocacy/donate/CREDITS:Producer & Host - Brian DawsonMusic - Denys Kyshchuk from Pixabay

9 Essential Tools for Beginner Insurance Agents

MedLink Neurology Podcast

Play Episode Listen Later May 29, 2024 16:56

If you're just starting out in the insurance industry, this episode is a must listen! Discover key tools and resources for establishing your business, gaining leads, marketing, compliance, and more! Read text version Contact the Agent Survival Guide Podcast! Email us ASGPodcast@Ritterim.com or call 1-717-562-7211 and leave a voicemail. Resources: A Review of the Top Medicare Quote Engines for Insurance Agents: https://ritterim.com/blog/a-review-of-the-top-medicare-quote-engines-for-insurance-agents/ CallVault: https://ritterim.com/the-ritter-platform/#callvault CMS' New Definition of Marketing & How it Affects Agents Selling Medicare Plans: https://ritterim.com/blog/cms-new-definition-of-marketing-how-it-affects-agents-selling-medicare-plans/ FMO vs. IMO vs. NMO vs. MGA vs. GA: What's the Difference? https://link.chtbl.com/ASG508 Free eBooks & Guides: https://ritterim.com/guides/ How Insurance FMOs Work FREE eBook download: https://ritterim.com/how-insurance-fmos-work/ Knight School Training: https://ritterim.com/knight-school/ Lead Center: https://leads.integrity.com/login Meet Your Sales Team at Ritter: https://ritterim.com/meet-your-sales-team/ Medicare Center: https://integrity.com/MedicareCENTER/ Medicare Quote Engine Prospectus PDF: https://ritterim.com/documents/prospectus/medicare-quote-engine-prospectus.pdf Round Table Facebook Group: https://www.facebook.com/groups/RittersRoundTable/ Ritter Events Calendar: https://ritterim.com/events/ Ritter Insurance Marketing Joins Integrity Marketing Group: https://ritterim.com/blog/ritter-insurance-marketing-joins-integrity-marketing-group/ Shop & Enroll: https://ritterim.com/shop-and-enroll/ The Best Software for Tracking Your Medicare Commissions: https://ritterim.com/blog/the-ultimate-agent-resource-list-pt-3-staying-organized/ The Ritter Blog: https://ritterim.com/blog/ The Ritter Platform: https://ritterim.com/the-ritter-platform/ The Ritter Platform – Elevate Your Sales Process PDF: https://ritterim.com/documents/prospectus/the-ritter-platform-prospectus.pdf The Ultimate Agent Resource List Pt 1: Market Yourself: https://ritterim.com/blog/the-ultimate-agent-resource-list-pt-1-market-yourself/ The Ultimate Agent Resource List Pt. 3: Staying Organized: https://ritterim.com/blog/the-ultimate-agent-resource-list-pt-3-staying-organized/ Your Guide to Compliant Medicare Call Recording with CallVault PDF: https://ritterim.com/documents/prospectus/your-guide-to-compliant-medicare-call-recording-with-callvault.pdf Your Step-By-Step Guide to Getting Started in Insurance Sales eBook: https://ritterim.com/free-guide/ References: Acuity Scheduling: https://acuityscheduling.com/ AgentMethods: https://www.agentmethods.com/ Appointment scheduling with Google Calendar: https://workspace.google.com/resources/appointment-scheduling/ Calendly: https://calendly.com/ HubSpot Free Meeting Schedular: https://www.hubspot.com/products/sales/schedule-meeting Market Advisor: https://csg-actuarial-wordpress.appspot.com/software/market-advisor/ Medicare Program; Contract Year 2023 Policy and Technical Changes to the Medicare Advantage and Medicare Prescription Drug Benefit Programs; Policy and Regulatory Revisions in Response to the COVID-19 Public Health Emergency; Additional Policy and Regulatory Revisions in Response to the COVID-19 Public Health Emergency: https://www.federalregister.gov/documents/2022/05/09/2022-09375/medicare-program-contract-year-2023-policy-and-technical-changes-to-the-medicare-advantage-and Microsoft Bookings: https://www.microsoft.com/en-us/microsoft-365/business/scheduling-and-booking-app The Best 24 Appointment Scheduling Apps and Booking Software: https://blog.hubspot.com/sales/best-scheduling-app TrustedForm: https://activeprospect.com/trustedform/ Verisk Marketing Solutions: https://marketing.verisk.com/compliance/ Follow Us on Social! Ritter on Facebook, https://www.facebook.com/RitterIM Instagram, https://www.instagram.com/ritter.insurance.marketing/ LinkedIn, https://www.linkedin.com/company/ritter-insurance-marketing TikTok, https://www.tiktok.com/@ritterim X (fka) Twitter, https://twitter.com/RitterIM and Youtube, https://www.youtube.com/user/RitterInsurance Sarah on LinkedIn, https://www.linkedin.com/in/sjrueppel/ Instagram, https://www.instagram.com/thesarahjrueppel/ and Threads, https://www.threads.net/@thesarahjrueppel Tina on LinkedIn, https://www.linkedin.com/in/tina-lamoreux-6384b7199/

BrainWaves Best of BrainWaves 2019

Play Episode Listen Later May 28, 2024 83:53

MedLink Neurology Podcast is delighted to feature selected episodes from BrainWaves, courtesy of James E Siegler MD, its originator and host. BrainWaves is an academic audio podcast whose mission is to educate medical providers through clinical cases and topical reviews in neurology, medicine, and the humanities, and episodes originally aired from 2016 to 2021.Originally released: December 26, 20192019 was a big year. The year of the Mueller report. The American college admissions scandals. Brexit. But it was also the year the US Women's team won the World Cup and lobbied for the equal pay of women and men in sports. It was the year of NMO, in which several pivotal trials showed the benefit of disease-modulating therapy in this condition. The year Will Smith played Genie in Aladdin.2019 was a great year. And as we wrap up 2019, this week's episode includes some of the highlights. Enjoy!Produced by James E Siegler with support from Erika Mejia, Rajat Dhar, and the entire Siegler family. Music courtesy of Axletree, Chris Zabriskie, John Paston, Kevin Mcleod, Josh Woodward, Steve Combs, Lee Rosevere, Scott Holmes, Advent Chamber Orchestra, Coldnoise, and Pachyderm. Sound effects by Mike Koenig and Daniel Simion. BrainWaves' podcasts and online content are intended for medical education only and should not be used for clinical decision-making. Be sure to follow us on Twitter @brainwavesaudio for the latest updates to the podcast.REFERENCES[BRAIN FOOD]Devore EE, Kang JH, Breteler MM, Grodstein F. Dietary intakes of berries and flavonoids in relation to cognitive decline. Ann Neurol 2012;72(1):135-43. PMID 22535616Kennedy DO, Wightman EL, Reay JL, et al. Effects of resveratrol on cerebral blood flow variables and cognitive performance in humans: a double-blind, placebo-controlled, crossover investigation. Am J Clin Nutr 2010;91(6):1590-7. PMID 20357044Lefèvre-Arbogast S, Gaudout D, Bensalem J, et al. Pattern of polyphenol intake and the long-term risk of dementia in older persons. Neurology 2018;90(22):e1979-e1988. PMID 29703769Liu QP, Wu YF, Cheng HY, et al. Habitual coffee consumption and risk of cognitive decline/dementia: A systematic review and meta-analysis of prospective cohort studies. Nutrition 2016;32(6):628-36. PMID 26944757Miller MG, Hamilton DA, Joseph JA, Shukitt-Hale B. Dietary blueberry improves cognition among older adults in a randomized, double-blind, placebo-controlled trial. Eur J Nutr 2018;57(3):1169-80. PMID 28283823Morris MC, Tangney CC, Wang Y, et al. MIND diet slows cognitive decline with aging. Alzheimers Dement 2015;11(9):1015-22. PMID 26086182Newman JC, Covarrubias AJ, Zhao M, et al. Ketogenic diet reduces midlife mortality and improves memory in aging mice. Cell Metab 2017;26(3):547-57.e8. PMID 28877458Norton S, Matthews FE, Barnes DE, Yaffe K, Brayne C. Potential for primary prevention of Alzheimer's disease: an analysis of population-based data. Lancet Neurol 2014;13(8):788-94. Erratum in: Lancet Neurol 2014;13(11):1070. PMID 25030513Okkersen K, Jimenez-Moreno C, Wenninger S, et al. Cognitive behavioural therapy with optional graded exercise therapy in patients with severe fatigue with myotonic dystrophy type 1: a multicentre, single-blind, randomised trial. Lancet Neurol 2018;17(8):671-80. PMID 29934199Radd-Vagenas S, Duffy SL, Naismith SL,

Ready to Join an FMO? 10 Things to Consider

Play Episode Listen Later May 15, 2024 13:12

Field Marketing Organizations can take your business to the next level. In this episode, learn ten things to consider when doing your research, and all the benefits and resources Ritter Insurance Marketing has to offer! Read the text version Register with Ritter Insurance Marketing Contact the Agent Survival Guide Podcast! Email us ASGPodcast@Ritterim.com or call 1-717-562-7211 and leave a voicemail. Resources: 4 Perks of Partnering with an FMO: https://link.chtbl.com/ASG575 Do's and Don'ts of Medicare Compliance: https://ritterim.com/blog/dos-and-donts-of-medicare-compliance/ FMO vs. IMO vs. NMO vs. MGA vs. GA: What's the Difference? https://link.chtbl.com/ASG508 How Insurance FMOs Work FREE eBook: https://ritterim.com/how-insurance-fmos-work/ Shop & Enroll: https://ritterim.com/shop-and-enroll/ The Benefits of Joining a Top Insurance FMO: https://ritterim.com/blog/the-benefits-of-joining-a-top-insurance-fmo/ The Ritter Platform: https://ritterim.com/the-ritter-platform/ What Are Agents Responsible for Under HIPAA? https://ritterim.com/blog/what-are-agents-responsible-for-under-hipaa/ Follow Us on Social! Ritter on Facebook, https://www.facebook.com/RitterIM Instagram, https://www.instagram.com/ritter.insurance.marketing/ LinkedIn, https://www.linkedin.com/company/ritter-insurance-marketing TikTok, https://www.tiktok.com/@ritterim X (fka) Twitter, https://twitter.com/RitterIM and Youtube, https://www.youtube.com/user/RitterInsurance Sarah on LinkedIn, https://www.linkedin.com/in/sjrueppel/ Instagram, https://www.instagram.com/thesarahjrueppel/ and Threads, https://www.threads.net/@thesarahjrueppel Tina on LinkedIn, https://www.linkedin.com/in/tina-lamoreux-6384b7199/

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Episode #32 | Beyond Words: The Silent Support of Animal Companions

starting social illinois new mexico silent pixabay genentech mog beyond words animal companions nmo credits producer

Play Episode Listen Later Apr 11, 2024 47:20

In this emotional episode, we delve into the profound relationship between pets and mental health. Starting with the TSF AMbassador for New Mexico, Marie Abrego talks about the recent loss of her dachshund Bambi while traveling to raise awareness about NMO.Then, we are joined by TSF Ambassador for Illinois, AnneMarie Nawrocki, a licensed social worker and TSFs ambassador for Illinois; they explore the multifaceted benefits of pet ownership for individuals with disabilities and chronic illnesses. From reducing stress and providing emotional support to promoting opportunities to enhance physical health and promoting social connection, pets play a crucial role in improving overall well-being. The discussion also touches on coping with the loss of a beloved pet, highlighting the unique grieving process and the importance of support from friends and family. Through personal anecdotes and expert insights, this episode celebrates the transformative power of the human-animal bond in navigating life's challenges.ABOUT US:The Demystifying NMO and MOG podcast is a Sumaira Foundation (TSF) project andwas made possible with the generous support of Genentech.SOCIAL & WEBSITE:Marie AbregoWebsite - t.ly/ndARITwitter - https://twitter.com/nmo_marieAnneMarie NawrockiWebsite - t.ly/RN2TDLinkedIn - www.linkedin.com/in/annemarie-nawrocki-5426b7120/Demystifying NMO podcastInstagram - https://www.instagram.com/demystifying_nmomogTwitter - https://twitter.com/DemystifyingNMOThe Sumaira FoundationWebsite - https://www.sumairafoundation.orgFacebook - https://www.facebook.com/TheSumairaFoundationSUPPORT the PodcastDonate to Illuminatehttps://www.sumairafoundation.org/advocacy/donate/CREDITS:Producer & Host - Brian DawsonMusic - Denys Kyshchuk from Pixabay

1205. Voices of SRNA Volunteers | Part 1

Ask the Expert

Play Episode Listen Later Apr 8, 2024 37:00

The “Community Spotlight” edition of the “Ask the Expert” podcast series shares the stories of our community members. In this episode, Alexandra Goulimi and Angela Jackson joined Lydia Dubose of SRNA share their backgrounds and how they got involved with volunteering for SRNA [00:01:43]. Alexandra and Angela discussed their experiences with rare neuroimmune disorders and the support they found through SRNA's programs [00:13:41]. They also shared what they hope to see in the future related to rare neuroimmune disorders and SRNA [00:22:53] and offered advice for anyone who might be interested in getting involved [00:30:51]. Alexandra Goulimi was born in 1969 and lived in Germany until she moved to Greece in 2011. She has a background in Human Resources Development and holds a master's degree in Sociology and a PhD in Communications. In 2009 Alexandra met the Human Design System and has been experimenting since then with making decisions guided by her body's intelligence. In 2017 Alexandra was diagnosed with NMOSD. It was challenging to meet the initial shock and deal with the symptoms. She has navigated her NMO-journey guided in her decisions by her intuitive response. Alexandra's experience of NMO has led her to a profound understanding and a deeper love of herself and life. Angela Jackson has been a member of a book club for 20 years. She is also a published author. Angela was a VP of Account Management working for a software company responsible for Customer Success. On February 27, 2019, she woke up with a numb left thigh. 12 hours later she was paralyzed from the waist down, diagnosed with idiopathic transverse myelitis, and hospitalized. Her lifestyle changed: acceptance of the diagnosis, therapy, limitations, working from home, depending on others... Moving forward with a positive outlook on life, Angela joined SRNA, serving as a Peer Connect Leader and hosting the first Houston, Texas Walk-Run-N-Roll. Angela has an awesome family. She is thankful for loving and supportive family and friends.

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The Caregiver's Journal with Lance A. Slatton & Denise M. Brown: Chapter 2 "The Path to Diagnosis"

All Home Care Matters

Play Episode Listen Later Mar 13, 2024 72:57

The Caregiver's Journal hosted by Lance A. Slatton and Denise M. Brown. The Caregiver's Journal is the show where we are sharing the caregiving experiences, stories, and wisdom of family caregivers. Chapter 2 - "The Path to Diagnosis": In this journal entry, we welcomed Jesus Loreto, Sharon Hall, and Effie Parks who shared their stories and experiences on "The Path to Diagnosis". Jesus Loreto: Jesus is a Certified Caregiving Facilitator and member of the Patient Advocacy Council Guthy Jackson Charitable Foundation Caregiver for his beautiful wife Maria Elena who was diagnosed with Neuromyelitis Optica NMOSD (NMO) for 16 years. Jesus had been running a caregiver's support group for almost a decade and found it very rewarding to help others to navigate their diagnosis and manage their disease day to day. Jesus believes that by telling your story you can save lives, you make people realize they are not alone. They have readjusted to their new normal, and love life. They live with NMO but NMO is not their life. Sharon Hall: During Sharon's 18 years of caregiving, she has navigated the medical community, the social service community, and the support community. Her husband was diagnosed with frontotemporal degeneration, so she has added experience in young onset dementia.She was a care partner speaker at the Research Summit on Dementia Care and Services at the NIH in 2017. She has also presented at the 2017, 2018 and 2019 National Caregiver Conferences. Sharon has been a speaker in many webinars on dementia. She facilitates a local support group and an online chat for care partners. She also has a podcast with a dementia expert to give families much needed information. Sharon also contributed to the “Fighting Alzheimer's” insert in USA Today. Sharon is active in social media within the dementia community. Effie Parks: Effie Parks, originally from beautiful Montana, has become a guiding light in the rare disease community following her son Ford's diagnosis with CTNNB1 syndrome. Settling in Washington, she transformed her family's journey into a crusade for advocacy, support, and empowerment for families navigating similar challenges. As the host of the "Once Upon a Gene" podcast, Effie has been recognized for several awards including WEGO Health and Podcast Magazine for her impactful storytelling and resource-sharing in the realm of rare genetic disorders. Effie extends her advocacy through speaking engagements at medical and patient advocacy conferences, sharing her experiences and insights from her work to bridge the gap between all rare disease stakeholders. Her skill in community engagement, developed through her advocacy, empowers her efforts in building a supportive network and raising awareness. With a mission to leave the world better than she found it, Effie is dedicated to fostering a more informed and empathetic environment for those impacted by rare diseases. Her work embodies resilience and compassion, inspiring and uniting the rare disease community. Effie's journey is not just about sharing stories, it's about driving change and creating a lasting impact in the world of rare genetic conditions. Visit The Caregiver's Journal Official Website: https://thecaregiversjournalpodcast.com/ Connect with Lance A. Slatton: Official Website: https://www.lanceaslatton.com Official Website: https://www.allhomecarematters.com Connect with Denise M. Brown: Official Website: https://join.caringourway.com/

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Episode #31 | EUPATI Education in Action: Leda's Path to Patient Advocacy

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Play Episode Listen Later Mar 13, 2024 39:50

Episode #31 | EUPATI Education in Action: Leda's Path to Patient AdvocacyIn this episode, we delve into the world of patient advocacy with Leda Bresnov. Leda shares her transformative journey following her NMO diagnosis and the pivotal role patient advocacy and education played in reshaping her life. From her initial involvement as the Denmark Ambassador with the Sumaira Foundation to her experiences in EUPATI's Patient Academy, Leda's dedication to raising awareness and empowering fellow patients is making a significant impact in healthcare. Join us as Leda offers her insights into the power of patient involvement in healthcare decision-making, highlighting the importance of education and advocacy in shaping the future of healthcare.ABOUT US:The Demystifying NMO and MOG podcast is a Sumaira Foundation (TSF) project andwas made possible with the generous support of Genentech.SOCIAL & WEBSITE:Leda BresnovWebsite - https://www.sumairafoundation.org/ledas-nmo-story-i-want-to-live-while-i-live/Instagram - https://www.instagram.com/bresnov/Twitter -https://twitter.com/BresnovDemystifying NMO podcastInstagram - https://www.instagram.com/demystifying_nmomogTwitter - https://twitter.com/DemystifyingNMOThe Sumaira FoundationWebsite - https://www.sumairafoundation.orgFacebook - https://www.facebook.com/TheSumairaFoundationTIMESTAMPS/TOPICS:00:01:14 Leda Bresnov00:04:36 EUPATI Patient Expert Training Programme00:07:21 Patient Expert Training Programme00:11:02 Patient Input and Drug Development00:23:39 Self-Advocacy & Involvement in Healthcare Decision-MakingLINKS:EUPATI - https://eupati.eu/European NMOSD Toolkit - https://www.nmosd-in-focus.com/-/media/Themes/Horizon/nmosd-in-focus-com/nmosd-in-focus-com/Documents/European-NMOSD-Patient-Toolkit.pdfSUPPORT the PodcastDonate to Illuminatehttps://www.sumairafoundation.org/advocacy/donate/CREDITS:Producer & Host - Brian DawsonMusic - Denys Kyshchuk from Pixabay

Immune-Mediated Myelopathies with Dr. Michael Levy

Play Episode Listen Later Mar 13, 2024 18:42

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.

Episode #30 | Navigating NMO in Challenging Circumstances: Global Inequities in Care

Play Episode Listen Later Feb 21, 2024 54:41

In recent years, we have seen healthcare systems collapse under the strain of natural disasters and armed conflict and hundreds of millions of people being forcibly displaced. So, how do we meet the healthcare needs of people in humanitarian disasters, let alone those living through these nightmares with a rare disease such as NMO?To talk about the unique challenges of diagnosing and treating rare conditions like NMO in these low-resource settings, we are joined by Dr. Farrah Matten.She highlights common barriers such as lack of disease awareness, limited diagnostic testing availability, and restricted treatment access. Dr. Mateen also proposes concrete goals to better support patients facing the most challenging circumstances.ABOUT US:The Demystifying NMO and MOG podcast is a Sumaira Foundation (TSF) project andwas made possible with the generous support of Genentech.SOCIAL & WEBSITE:Farrah Mateen, MD, PhDWebsite - https://doctors.massgeneralbrigham.org/provider/Farrah+J+Mateen/255866Global Neurology Research Group - www.massgeneral.org/neurology/research/global-neurology-research-groupTwitter - https://twitter.com/FarrahMateenThe Sumaira FoundationWebsite - www.sumairafoundation.orgFacebook - www.facebook.com/TheSumairaFoundationLINKS:Mateen FJ. Neurological disorders in complex humanitarian emergencies and natural disasters. Ann Neurol. 2010 Sep;68(3):282-94. doi: 10.1002/ana.22135. PMID: 20818788.Mateen FJ. Neurocritical care in developing countries. Neurocrit Care. 2011 Dec;15(3):593-8. doi: 10.1007/s12028-011-9623-7. PMID: 21863357.Mateen FJ, Hanafi I, Birbeck GL, Saadi A, Schmutzhard E, Wilmshurst JM, Silsbee H, Jones LK Jr; AAN Quality Committee. Neurologic Care of Forcibly Displaced Persons: Emerging Issues in Neurology. Neurology. 2023 May 16;100(20):962-969. doi: 10.1212/WNL.0000000000206857. Epub 2023 Mar 1. PMID: 36859408; PMCID: PMC10186241.Mateen FJ. Rectifying global inequities in neuromyelitis optica diagnosis and treatment. Mult Scler. 2023 Jul;29(8):932-935. doi: 10.1177/13524585231179108. Epub 2023 Jun 10. PMID: 37300419.SUPPORT the PodcastDonate to Illuminatehttps://www.sumairafoundation.org/advocacy/donate/CREDITS:Producer & Host - Brian DawsonMusic - Denys Kyshchuk from Pixabay

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Structural Myelopathies with Dr. Ligia Onofrei

Play Episode Listen Later Feb 21, 2024 20:36

Compressive myelopathy caused by degenerative spine disease is common, but the pathophysiology is surprisingly complex and there are potential surprises in the evaluation of these patients. In this episode, Katie Grouse, MD, FAAN, speaks with Ligia Onofrei, MD, author of the article “Structural Myelopathies,” in the Continuum February 2024 Spinal Cord Disorders issue. Dr. Grouse is a Continuum® Audio interviewer and a clinical assistant professor at the University of California San Francisco in San Francisco, California. Dr. Onofrei is an associate professor of neurology and neuromuscular medicine at the University of Utah in Salt Lake City, Utah. Additional Resources Read the article: Structural 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 American Academy of Neurology website: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Guest: @Ligia_OnofreiMD 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 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 Grouse: This is Dr. Katie Grouse. Today, I'm interviewing Dr. Ligia Onofrei about our article on structural myelopathies in the February 2024 Continuum issue on spinal cord disorders. Dr Onofrei is an Associate Professor of Neurology in neuromuscular medicine at the University of Utah, in Salt Lake City, Utah. Welcome to the podcast. Just to kind of get started, I wanted to ask you, the topic of your Continuum article is cervical and thoracic structural myelopathies - what are these and how common are they? Dr Onofrei: So actually, structural myelopathies are the most common myelopathies that we encounter clinically. I know in neurology we tend to focus on things like MS or NMO or transverse myelitis as the myelopathies that we talk about most commonly, but we actually see them a fair bit. As you will see in my article, it's really hard to actually give you a precise number as to how common they are. We know they're common because we encounter them a lot, but there are also a lot of patients out there who have them who are undiagnosed. Structural myelopathies really refer to both the symptoms of myelopathy but also having compression of the spinal cord. That's what you have to have in order to have a structural myelopathy. Dr Grouse: How did you become interested in this area of neurology? Dr. Onofrei: It's a bit of a different kind of story in neurology than the usual career trajectory. Actually, when I was a resident, there was a patient at the VA who had Parkinson's disease and myelopathy, and he went undiagnosed for months because people kept blaming his dexterity issues and day changes on his Parkinson's. But, in fact, he really had a cervical myopathy that was actually quite severe. When we got him diagnosed. I remember thinking to myself, “I really want to learn more about it.” And I was asking around and what I saw, even though my attendance at the time were super smart and very well versed in neurological issues, they just weren't comfortable with degenerative disorders of the spine. I wanted to learn more. I read what was available and I actually went to the AAN Spine Course, which at the time was a full day. I met Dr JD Bartleson, who was my mentor - who became my mentor, I should say. He gave me some really terrific advice about how to learn more. When I finished my residency at the University of Utah, I went on to do a neuromuscular fellowship, also at the University of Utah. But during that fellowship, I actually had two months to spend as additional training time outside of neurology, and I chose to spend it with the spine and musculoskeletal physical medicine and rehabilitation specialists at the University of Utah. They taught me a lot about degenerative spine issues, musculoskeletal issues, and I felt I really, for the first time, had a really good grasp of the diagnosis, and also the interplay between degenerative spine issues and neurological disorders. And then after that, I did something even less typical for neurologists. After I graduated fellowship, I actually went on to have a clinic embedded within the neurosurgery department at our institution. I evaluated patients – like, a day a week - patients who had spine issues and were referred for surgical evaluation. I would evaluate the patients in conjunction with one of the neurosurgeons, and then we would decide together if they needed surgery. It was a really great education to understand the interplay between degenerative spine issues and neurological disorders. Dr Grouse: That sounds like a circuitous but very interesting path, and very fruitful in the end. You mentioned that even very adept clinicians can miss this important and actually common diagnosis. What are some early signs that are easily missed? Dr. Onofrei: I think, with myelopathy, the most important part is actually just thinking about it as a diagnostic possibility. If you think about it, then you will essentially ask the questions that are really important diagnosis. I think it can be especially difficult if it's a patient who has a preexisting neurological disorder because we get stuck in asking the kind of things we usually ask our patients with MS or Parkinson's, or whatever else they may have. But it's really important to understand the trajectory of symptoms always. If they're having dexterity changes, “Did that happen all of a sudden? Was there something else happening?” Asking about dexterity changes to start with is a super helpful, important part of the diagnosis. And then also asking about gait changes. Again, if they have a preexisting neurological diagnosis, asking them if they've had a big change, a rapid progression, if something else happened in their disease - that's the beginning step. It's actually very, very basic information, but asking about these changes is super important. Then, once people have identified those changes, then you can delve into the more specific questions that are really unique to myelopathy, like manipulating small objects, manipulating utensils - for example, zippers or buttons. That's a really sensitive way to ask for dexterity changes for myelopathy. For gait abnormalities, it's a little bit less unique to myelopathy. A lot of the symptoms overlap phenotypically with, like, peripheral neuropathies. For example, having difficulty on uneven ground or getting your toes caught on something. But identifying a shift in your gait is usually that key initial diagnostic clue. Dr Grouse: Really, really helpful. And, I think, always a great reminder with almost anything - you don't think of it, you won't diagnose it. Sounds like for myelopathies - structural myopathies – this could be especially true. Thinking about this article, what do you think would come as the biggest surprise to our listeners who read the article? Dr. Onofrei: It's a really great question. I think there can be a lot of different surprises in each little section. But, to me, the thing that stands out is how complex the pathophysiology of myelopathy actually really is. There's so much more than just direct compression of the spinal cord. When you have compression of the spinal cord, you are stretching the spinal cord; you are inducing changes to the gray matter, the white matter. But you're also changing the actual biology of the cells. When you're causing compression of the spinal cord, you're inducing hypoxic or ischemic injury, and that triggers a neuroinflammatory cascade and it causes apoptosis of the neurons and the oligodendroglia. I think what was really interesting to learn is that, when you're decompressing the spinal cord with surgery, that reduces that cascade of neuroinflammation but it doesn't eliminate it. You will still have some residual apoptosis of the cells even after decompression. This actually is probably one of the pieces of information that supports the idea that we really should be intervening at an earlier stage for these patients. Dr Grouse: Does this mean that, even after decompression, patients can continue to deteriorate or do worse as a result of that apoptosis and those changes? Dr Onofrei: I think that the way I would interpret that, more in practice, is that those patients might not improve. They might not have any improvement post surgery. In fact, any surgeon who is an ethical surgeon will tell you that they cannot promise improvement with decompressive surgery, but we do notice improvement in a significant proportion of patients. While you can never promise that there's actual hope for these patients, it's just that some patients may not improve and we don't have a great way to predict who will improve and who will not improve. Dr Grouse: I was also curious, when you mentioned about what chronic compression looks like, why does chronic compression look so different from acute compression of the cord, both how it presents and how the patients can look? Dr Onofrei: That's a really fantastic question. I think part of it is that, just like with other degenerative disorders of the spine – like, for example, lumbar stenosis with neurogenic claudication and cauda equina, there's an element of time and adaptation. When you have acute compression, you do not have those adaptive mechanisms in place, and you will have to deal with just acute loss of function. That's how I would think about it. The time component allows for some adaptive changes, and also for specifically degenerative myelopathies. When you have chronic compression, you usually have less compression than with an acute traumatic myelopathy. Dr Grouse: I want to ask, as well, what do you think is the biggest debate or controversy in this particular area - whether it comes to the underlying pathophysiology of what's going on, or else the management or treatment of it? Dr Onofrei: I would say, without a doubt, the biggest controversy is when to intervene. Obviously, that is a hugely important question for patients and physicians alike. There's a lot of debate because there are patients who remain stable with mild myelopathy for many years, and then there are people who decline. There is a yearly rate of decline for these patients. But right now, we don't have good ways to predict who will decline and who will remain stable. I think there's a huge potential for more research, especially in the field of imaging - and especially with diffusion tensor imaging - to see if that can be used as a way to predict who will be declining or who might respond better to treatment. Dr Grouse: That makes a lot of sense, and certainly, I think, something that a lot of our listeners grapple with as they try to counsel patients with these types of conditions. I was struck by another point you made in your article - which I thought was really interesting - which was that a common misconception is that pain is a significant manifestation of spinal cord dysfunction. And this made me think that this could definitely fall in the category of an easy mistake that you could make in this diagnosis. Tell us more about that. Dr Onofrei: Yeah, so we are very used to using pain as an alarm signal. I think it's important, again, at a provider level, to remind ourselves that, actually, function is a better proxy for dysfunction than pain for a lot of patients. But pain, again, continues to be a really important reason why patients come to us. From one perspective, even though pain is something that we worry about and patients think potentially has really bad consequences, pain can actually be reassuring in some ways. But for myelopathy, pain is usually an incidental finding, in the sense that, usually, pain with myelopathy will happen because you have axial pain – you know, pain because your posture is poor, or you might have a superimposed radiculopathy. Pain will be sometimes the symptom that will bring the patient to attention, but it's very unlikely to be a symptom of how bad the problem is or to actually tell you if there is underlying myelopathy. Dr Grouse: Thank you - that's a really important review, I think for all of us. Often we'll ask that as almost one of the first questions, when we're thinking about it. Tell us a little bit more. I was reviewing some of the common signs of cervical myelopathy and - it's funny - a lot of them, especially the early signs, may not even be the ones you first think of. I think you've mentioned it before - the gait dysfunction and slight loss of dexterity. I also was interested in (and this maybe may not be quite as an early one) myelopathic hand - if you wouldn't mind telling us a little bit more about that as well. Dr. Onofrei: Of course. Assessing function is very important, just by asking the patient what they do that requires dexterity. So, starting there and then moving on to trying to understand if there's any particular issues that would confound the patient's ability to perform these activities. Like, if they have arthritis of their hands or a painful finger (like a trigger finger, or something like that), that will change the way they can handle the types of activities that require them to be dexterous. That's the initial phase. Once they have had progression of their myelopathy, they will usually have more frank weakness. I think a lot of people will say they drop more objects, but that's probably the least helpful, from a clinical perspective, just because it happens with so many different pathologies. But really paying attention to loss of actual strength and then visually examining the hand – so, looking for loss of muscle for the hand and looking for loss of strength on exam. So, finger abduction is your most sensitive exam maneuver that you can do to assess for that. And even very subtle weakness can be a really good indication of myelopathy. And then, in patients who have more advanced pathologies, you'll see more significant atrophy of the hand - actual frank, like, muscle wasting and potentially fasciculations in the hand. I talk about the myelopathic hand from a pathophysiology perspective. I thought it was really interesting that you can see this myelopathic hand with compression at any level in the spinal cord. So, even if it's high cervical compression, you can still see the hand atrophy and weakness. So, it is important to visually inspect the hand, do the strength examination, and like I said, really ask the patient about their function. Dr Grouse: Thank you. That was really helpful. Being a neurologist, of course, I think, like many of our listeners, I'm a big fan of checking reflexes, and in your article, you mention some really interesting, different ones that we don't check every day. Do you have favorite or a few favorites that you'd like to call out for us to pay attention to? Dr. Onofrei: As I mentioned my article, hyperreflexia is a really common manifestation of myelopathy. While it's not always present, if you can elicit hyperreflexia, it's really helpful. I think you can do whatever reflexes are your favorites, as long as they're a measure of hyperreflexia. I do like the finger flexor reflex, and I included that in the paper. It's just one that people use less often, but it's super easy to do. And if it's asymmetric, in particular, it's a really helpful tool. But, again, I don't think it matters which ones you do as long as you do a complete exam and then you look at the presence of hyperreflexia. Dr Grouse: That's great, and I encourage everyone to check out the article and take a look at some of those reflexes that she referenced are very interesting. What role does DTI play for imaging of degenerative myelopathies, and what promise do they hold going forward? Dr Onofrei: Diffusion tensor imaging is a really interesting imaging modality for the spine. It's not as commonly used for the spine as it is for things like stroke, right? We all are super familiar with its amazing role in stroke and early diagnosis of stroke. In the spine, it's much more complicated. The spine is a much more difficult structure to image, in general. So, while it's not being used right now on a clinical basis routinely, there's a lot of active research in that arena to try to understand what the best protocol might be, and how to use it to either predict which patients might deteriorate or which patients might need to have earlier surgical intervention. I think the promise of it is really tremendous, but to date, there hasn't been a unified protocol. But I think that, as we have more sensitive imaging modalities, better software algorithms to analyze the images, we might actually be really able to have excellent sensitivity. Dr Grouse: Well, very interested to see how that develops over time. Just to finish up, is there any last sort of important key points you hope that our listeners will take away as they go forward into the world and look for patients with structural myelopathies? Dr. Onofrei: I think the most important things that I want people to remember from this article, number one, is that diagnosing myelopathy starts by thinking about myelopathy, first of all. If you're thinking about myelopathy, you're more likely to ask the questions to elicit myelopathies. And then, I do want people to think about the phenotypic overlap between myelopathies and other neurological disorders. Third, I think people just need to remember that they are already doing the work of discovering myelopathy, which is asking the questions, doing a really good history and a really good exam. Really, the key for the diagnosis is having a really good history, is understanding the function of the patient, and is doing a really good neurologic exam, especially in patients who have a preexisting neurological diagnosis. Having those serial neurologic exams is really, really important to understand if the patient has a new myelopathy or to give the patient a better understanding of how they might respond to surgery, or what proportion of their symptoms is really attributed to a neurological disorder versus a myelopathy. Dr Grouse: Thank you so much for coming to talk with us about this really important topic. Again, I can't encourage everyone enough to read this article. I think it was so helpful, so interesting, and just gets back to all the things I think we all love about neurology. Dr. Onofrei: Thank you for having me. Dr. Grouse: Again, today I've been interviewing Dr. Ligia Onofrei, whose article on structural myelopathies appears in the most recent issue of Continuum, on spinal cord disorders. 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, 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.

4 Perks of Partnering with an FMO

Play Episode Listen Later Feb 12, 2024 11:13

Discover how joining a field marketing organization can boost your insurance business growth in 2024. Whether you're just starting out, or you've recently become independent, we've got resources to help! Join Our FMO! Register with Ritter Insurance Marketing Ask the Agent Survival Guide Podcast! Email us ASGPodcast@Ritterim.com or call 1-717-562-7211 and leave a voicemail. Follow Us on Social! Ritter on Facebook, https://www.facebook.com/RitterIM Instagram, https://www.instagram.com/ritter.insurance.marketing/ LinkedIn, https://www.linkedin.com/company/ritter-insurance-marketing TikTok, https://www.tiktok.com/@ritterim Twitter, https://twitter.com/RitterIM and Youtube, https://www.youtube.com/user/RitterInsurance Sarah on LinkedIn, https://www.linkedin.com/in/sjrueppel/ Instagram, https://www.instagram.com/thesarahjrueppel/ and Threads, https://www.threads.net/@thesarahjrueppel Tina on LinkedIn, https://www.linkedin.com/in/tina-lamoreux-6384b7199/ Resources: 5 Things About Working with Ritter Insurance Marketing: https://link.chtbl.com/ASGF20230512 FMO vs. IMO vs. NMO vs. MGA vs. GA: What's the Difference? https://link.chtbl.com/ASG508 How Insurance FMOs Work: https://link.chtbl.com/ASGT20240208 Meet the sales team here at Ritter: https://www.ritterim.com/meet-your-sales-team/ The Benefits of Joining a Top Insurance FMO: https://link.chtbl.com/ASG425 Why Should Agents Work with Ritter Insurance Marketing? https://link.chtbl.com/ASGWhyRitter

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How Insurance FMOs Work

Play Episode Listen Later Feb 8, 2024 2:07

FMO, what does it stand for? Field Marketing Organization, that's what we are at Ritter Insurance Marketing! Download our eBook to learn about the types of marketing organizations, how they work, and how agents can benefit. How Insurance FMOs Work Free eBook Download Ask the Agent Survival Guide Podcast! Fill out the form: https://bit.ly/askasg email us ASGPodcast@Ritterim.com or call 1-717-562-7211 and leave a voicemail. Follow Us on Social! Ritter on Facebook, https://www.facebook.com/RitterIM Instagram, https://www.instagram.com/ritter.insurance.marketing/ LinkedIn, https://www.linkedin.com/company/ritter-insurance-marketing TikTok, https://www.tiktok.com/@ritterim Twitter, https://twitter.com/RitterIM and Youtube, https://www.youtube.com/user/RitterInsurance Sarah on LinkedIn, https://www.linkedin.com/in/sjrueppel/ Instagram, https://www.instagram.com/thesarahjrueppel/ and Threads, https://www.threads.net/@thesarahjrueppel Tina on LinkedIn, https://www.linkedin.com/in/tina-lamoreux-6384b7199/ Resources: 4 Reasons Why Ritter Should Be Your FMO Agency: https://link.chtbl.com/ASG391 5 Things About Working with Ritter Insurance Marketing: https://link.chtbl.com/ASGF20230512 FAQs About Working with Ritter Insurance Marketing: https://link.chtbl.com/ASG492 FMO vs IMO vs NMO vs MGA vs GA: What's the Difference? https://link.chtbl.com/ASG508 How to Get Started in Medicare Sales: https://link.chtbl.com/ASG569 The Benefits of Joining a Top FMO: https://link.chtbl.com/ASG425 Why Should Agents Register with Ritter Insurance Marketing? https://link.chtbl.com/ASGWhyRitter

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Episode #29 | Caregivers: Nobody Fights Alone

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Play Episode Listen Later Jan 29, 2024 38:26

We kick off Season 4 of the Demystifying NMO & MOG Podcast with a very special guest, Candice Galvan.Candice became an Ambassador for The Sumaira Foundation after her daughter was diagnosed with NMO. She joins us today to talk about her path to becoming an advocate and how she is helping care for others through her work as program manager for TSF's Human Collective Project.ABOUT US:The Demystifying NMO and MOG podcast is a Sumaira Foundation (TSF) project andwas made possible with the generous support of Genentech.SOCIAL & WEBSITE:Candice's Storyhttps://www.sumairafoundation.org/bellas-nmo-story-in-this-family-we-fight-together/Demystifying NMO podcastInstagram - https://www.instagram.com/demystifying_nmomogTwitter - https://twitter.com/DemystifyingNMOThe Sumaira FoundationWebsite - https://www.sumairafoundation.orgFacebook - https://www.facebook.com/TheSumairaFoundationTIMESTAMPS/TOPICS:00:01:34 Candice's Story00:11:28 Becoming an Advocate00:14:42 Explaining NMO to a 9-year-old00:17:57 Medical Marijuana00:22:10 TSF's Human Collective ProjectLINKS:Human Collective Project (HCP) Support Group Meetingshttps://www.sumairafoundation.org/community/human-collective-project-2/SUPPORT the PodcastDonate to Illuminatehttps://www.sumairafoundation.org/advocacy/donate/CREDITS:Producer & Host - Brian DawsonMusic - Denys Kyshchuk from Pixabay

MS Care at RUSH: Whole Brain Health, Patient Education and Reaching Underserved Populations with Augusto Miravalle, MD

Rounding at Rush

Play Episode Listen Later Jan 25, 2024 24:32

The RUSH Multiple Sclerosis Center features a team of world-class clinicians and researchers, dedicated to offering the most advanced, comprehensive and individualized treatment protocols to patients affected by multiple sclerosis (MS), neuromyelitis optica (NMO), spectrum disorders (NMOSD) and other autoimmune disorders affecting the central nervous system. In this episode, Augusto Miravalle, MD, the Chief of the Section of Multiple Sclerosis at RUSH, discusses the importance of whole brain health for MS patients, his work to reach and treat underserved populations, and the vital role patient education plays for beneficial short and long-term outcomes. “One of my priorities is to improve healthcare literacy [about MS]. It's been demonstrated that patients who have a high level of literacy do better [in their care]. They have better clinical outcomes and they have a better understanding of the importance of certain types of lifestyle interventions.”

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Ep. 88: How a rare disease diagnosis birthed a non-profit with The Sumaira Foundation's Sumaira Ahmed

The Indian Edit

Play Episode Listen Later Jan 8, 2024 60:38

Sumaira Ahmed is a force! Upon being diagnosed with a rare neuroimmune condition (Neuromyelitis optica spectrum disorder/ NMOSD, whose symptoms can include vision loss, paralysis, and weakness), Sumaira couldn't find the community she needed, so she went right ahead and launched a foundation (two months later!) to create that support for herself and patients around the world. The Sumaira Foundation has since advocated for patients, funded disease research, increased NMO awareness globally and truly been a game changer in the field. Hear how this young dancer and Bollywood aspirant (who was crowned the first Miss Bangladesh-USA) turned into a fearless non-profit leader and champion for patients suffering from this rare disease.Join me with the wonderful Sumaira - now on your favorite podcast app, Spotify or iTunes and please please take a second to rate us wherever you're listening so the voices of these inspiring women can be heard all over the world!SHOWNOTES FOR EPISODE 88:Read more about Sumaira's work at The Sumaira Foundation and connect with her and The Sumaira Foundation on InstagramInfinite Vision: How Aravind Became the World's Greatest Business Case for CompassionQuestions? Comments? Get in touch @theindianeditpodcast on Instagram ! Want to talk gardens? Follow me @readyourgardenSpecial thanks to Sudipta Biswas and the team @ Boon Castle / Flying Carpet Productions for audio post-production engineering!

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Top 5 Episodes of 2023

MS Living Well: Key Info from Multiple Sclerosis Experts

Play Episode Listen Later Dec 29, 2023 68:19

We're counting down the top 5 Agent Survival Guide Podcast episodes of 2023! Did your favorite episode make the cut? Join Sarah as she highlights the year's most popular episodes. Episode Number Five: [01:31] Episode Number Four: [15:38] Episode Number Three: [40:09] Episode Number Two: [50:02] Episode Number One: [56:29] Ask the Agent Survival Guide Podcast! Fill out the form: https://bit.ly/askasg email us ASGPodcast@Ritterim.com or call 1-717-562-7211 and leave a voicemail. Follow Us on Social! Ritter on Facebook, https://www.facebook.com/RitterIM Instagram, https://www.instagram.com/ritter.insurance.marketing/ LinkedIn, https://www.linkedin.com/company/ritter-insurance-marketing TikTok, https://www.tiktok.com/@ritterim Twitter, https://twitter.com/RitterIM and Youtube, https://www.youtube.com/user/RitterInsurance Sarah on LinkedIn, https://www.linkedin.com/in/sjrueppel/ Instagram, https://www.instagram.com/thesarahjrueppel/ and Threads, https://www.threads.net/@thesarahjrueppel Tina on LinkedIn, https://www.linkedin.com/in/tina-lamoreux-6384b7199/ Links to Individual Episodes: How to Overcome Common Insurance Sales Objections ft. Dan Ford: https://link.chtbl.com/2023DanFord Effective Marketing Strategies for Insurance Agents: https://link.chtbl.com/ASG523 Annuities vs. 401(k)s: Examining Differences That Can Matter to Clients: https://link.chtbl.com/ASG506 4 Perks of Being a Part-Time Insurance Agent: https://link.chtbl.com/ASG521 FMO vs. IMO vs. NMO vs MGA vs GA: What's the Difference? https://link.chtbl.com/ASG508 Resources: 3 Email Marketing Campaigns Insurance Agents Should Be Sending: https://link.chtbl.com/ASGAgentMethods2 5 Things About Working with Ritter Insurance Marketing: https://link.chtbl.com/ASGF20230512 7 Ways to Get Involved in Your Community: https://link.chtbl.com/ASG453 8 Relationship Marketing Strategies for Insurance Agents featuring ReminderMedia's Luke Acree and Andrew Saksa: https://link.chtbl.com/ASG448 Agent Survival Guide Podcast Official Site: https://www.ritterim.com/podcast Apps to Make Your Small Business More Efficient: https://link.chtbl.com/ASGA034 Best Practices for Training Downline Agents: https://link.chtbl.com/ASG522 College Majors That Work Well In the Insurance Industry: https://link.chtbl.com/ASG516 Community-Based Marketing for Insurance Agents: https://link.chtbl.com/ASG533 Developing an Agency – Your Guide to Getting Started: https://www.ritterim.com/agency-guide/ Different Types of Annuities Explained: https://www.ritterim.com/blog/understanding-the-details-of-annuities/#different-types-of-annuities Empowering Agents Through Technology featuring Aaron Kassover from AgentMethods: https://link.chtbl.com/ASG458 Find your Sales Specialist at Ritter Insurance Marketing: https://www.ritterim.com/meet-your-sales-team/ Fixed Annuities vs. Indexed Annuities: What's the Difference? https://link.chtbl.com/ASG495 How Insurance FMOs Work: https://www.ritterim.com/how-insurance-fmos-work/ Register with Ritter Insurance Marketing: https://app.ritterim.com/public/registration Understanding Single-Premium Immediate Annuities: https://www.ritterim.com/blog/understanding-single-premium-immediate-annuities/ Understanding the Details of Annuities: https://link.chtbl.com/ASG343 Using a SWOT Analysis to Review Your Insurance Business: https://link.chtbl.com/ASG559 What Are Insurance Hierarchies & How Do They Work? https://link.chtbl.com/ASG517 Your Step-by-Step Guide to Getting Started in Insurance Sales eBook: https://www.ritterim.com/free-guide/ References: Agent Methods Official Site: https://www.agentmethods.com/ CMS Medicare Communications and Marketing Guidelines: https://www.cms.gov/Medicare/Health-Plans/ManagedCareMarketing/FinalPartCMarketingGuidelines CMS Memo [May 10, 2023] Definition of Marketing: https://www.ritterim.com/documents/cms-memos/cms-definition-of-marketing-5-10-23.pdf Medicare Advantage Requirements: https://www.ecfr.gov/current/title-42/chapter-IV/subchapter-B/part-422/subpart-V Part D Communication Requirements: https://www.ecfr.gov/current/title-42/chapter-IV/subchapter-B/part-423/subpart-V ReminderMedia Official Site: https://remindermedia.com/

Recipe for Resilience: The Blind Cook and NMOSD

Play Episode Listen Later Dec 19, 2023 38:12

Christine Ha, an award-winning blind chef and restauranteur, shares her experience grappling with neuromyelitis optica spectrum disorder (NMOSD). Facing relapses with the inability to walk and feed herself that challenged her independence, she leaned on the support from family and friends. As she lost her sight due to optic neuritis in both eyes, Ms. Ha had to embark on a journey of rediscovery in the kitchen, starting with the fundamentals. Winning MasterChef Season 3 marked a turning point, propelling her culinary career forward despite the obstacles posed by her disability. NMOSD is an autoimmune disease in which an antibody attacks water channels on astrocyte cells in the optic nerves, spinal cord and sometimes the brain. Attacks or relapses can be devastating and incomplete recovery from attacks is typical. Like Ms. Ha, some people living with the condition can be misdiagnosed with multiple sclerosis. A blood test for the aquaporin-4 antibody is key to getting diagnosed correctly early. Since 2019, highly effective treatment options have been FDA-approved that reduce relapses by 77-94%. Barry Singer MD, Director of The MS Center for Innovations in Care, interviews: Christine Ha, "The Blind Cook". Her first cookbook, Recipes from My Home Kitchen, was a New York Times best-seller. Ms. Ha's first restaurant in Houston, The Blind Goat, was named a semi-finalist for 2020 Best New Restaurant in America by the James Beard Foundation. She was also named a James Beard finalist for Best Chef in Texas in 2022. Michael Levy MD PhD, Associate Professor at Harvard Medical School and Director of the Neuroimmunology Clinic and Research Laboratory

Using a SWOT Analysis to Review Your Insurance Business

Play Episode Listen Later Dec 12, 2023 11:10

What does your business strategy look like for 2024? Now is the time to review and plan with a SWOT analysis! We'll help you get organized so you can evaluate your insurance business and plan what comes next. Ask the Agent Survival Guide Podcast! Fill out the form: https://bit.ly/askasg email us ASGPodcast@Ritterim.com or call 1-717-562-7211 and leave a voicemail. Follow Us on Social! Ritter on Facebook, https://www.facebook.com/RitterIM Instagram, https://www.instagram.com/ritter.insurance.marketing/ LinkedIn, https://www.linkedin.com/company/ritter-insurance-marketing TikTok, https://www.tiktok.com/@ritterim Twitter, https://twitter.com/RitterIM and Youtube, https://www.youtube.com/user/RitterInsurance Sarah on LinkedIn, https://www.linkedin.com/in/sjrueppel/ Instagram, https://www.instagram.com/thesarahjrueppel/ and Threads, https://www.threads.net/@thesarahjrueppel Tina on LinkedIn, https://www.linkedin.com/in/tina-lamoreux-6384b7199/ Resources: 3 Ways to Boost Morale in the Workplace: https://link.chtbl.com/ASG556 365 Days of Motivation: https://link.chtbl.com/ASGF20231110 Apps to Make Your Small Business More Efficient: https://link.chtbl.com/ASGA034 Building a Business Plan Knight School Module: https://www.ritterim.com/knight-school/solid-foundation/building-a-business-plan/ Community-Based Marketing for Insurance Agents: https://link.chtbl.com/ASG533 Developing an Agency — Your Guide to Getting Started: https://www.ritterim.com/agency-guide/ Effective Marketing Strategies for Insurance Agents: https://link.chtbl.com/ASG523 Empowering Agents Through Technology: https://www.ritterim.com/blog/interview-empowering-agents-through-technology/ FMO vs. IMO vs. NMO vs. MGA vs. GA: What's the Difference? https://link.chtbl.com/ASG508 Increase Sales and Productivity with the Busy Medicare Agent's Sales Planner: https://www.ritterim.com/blog/increase-sales-and-productivity-with-the-busy-medicare-agents-sales-planner/ Modern Medicare Marketing for Today's Agents: https://www.ritterim.com/modern-marketing-guide/ Stay Organized with the Busy ACA Agent's Sales Calendar: https://www.ritterim.com/blog/stay-organized-with-the-busy-aca-agents-sales-calendar/ Things to Think About Post-AEP: https://link.chtbl.com/ASG558 The Ultimate Agent Resource List Pt. 1: Market Yourself: https://www.ritterim.com/blog/the-ultimate-agent-resource-list-pt.-1-market-yourself/ References: 20+ SWOT Analysis Templates, Examples & Best Practices: https://venngage.com/blog/swot-analysis-templates/ SWOT Analysis: https://www.mindtools.com/amtbj63/swot-analysis SWOT analysis: Examples and templates: https://asana.com/resources/swot-analysis SWOT Analysis: How To Do One: https://blog.hubspot.com/marketing/swot-analysis SWOT Analysis: How To With Table and Example: https://www.investopedia.com/terms/s/swot.asp

EP512: Mountain Meditations with Nolan Osborne

Play Episode Listen Later Nov 17, 2023 67:03

Adam sits down with his good friend and longstanding member of the JMH/BTK team Nolan Osborne to talk about guide life, gear, media/marketing, and the new gig that has NMO moving on to a new role in the industry. @nmo --------------------------- DEALS & OFFERS: OnX Maps is now available in Canada! Get your FREE trial today. And if you're already a member, check out the exclusive offers and perks available when you upgrade to an Elite Member. Keep your eyes and ears open for an incredible offer from MYSTERY RANCH coming soon! Trust us, you won't want to miss this deal. --------------------------- SUPPORT WILD SHEEP: Go to Wild Sheep Foundation to find a membership option that suits your budget and commitment to wild sheep. --------------------------- SUPPORT MOUNTAIN GOATS: Go to Rocky Mountain Goat Alliance to find a membership option that suits your budget and commitment to conserving mountain goats and their habitat.

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EP494: Sheep Hunting Q&A with NMO (Repost)

Play Episode Listen Later Jul 28, 2023 55:55

With the BC sheep season opening just a few days after this goes live, we've got another repost for you this week, this time with NMO tackling sheep hunting questions from the audience. Nolan covers gear, optics, glassing tips, mindset, and a whole host of other subjects in this Q&A from last year. If you missed it when we first released it, you'll want to check this episode out if you're heading into the sheep mountains this season. If you listened to it, there are some good tips worth hearing again. --------------------------- DEALS & OFFERS: Get free shipping on SPARTAN Precision products like the Javelin Bipod with the code BTK23. OnX Maps is now available in Canada! Get your FREE trial today. And if you're already a member, check out the exclusive offers and perks available when you upgrade to an Elite Member. Wanna be ready for any hunt this season? Try the BTK Mountain Hunter training program, no risk, with a 14-day FREE trial. Need boots? Check out the full CRISPI line-up at www.crispius.com to find a model that suits your hunting style and terrain. Looking for a pack that will stand up to the rigors of backcountry hunting, heavy loads, and keep performing season after season? Check out the full MYSTERY RANCH line-up and find a pack that suits your needs. --------------------------- SUPPORT WILD SHEEP: Go to Wild Sheep Foundation to find a membership option that suits your budget and commitment to wild sheep. --------------------------- SUPPORT MOUNTAIN GOATS: Go to Rocky Mountain Goat Alliance to find a membership option that suits your budget and commitment to conserving mountain goats and their habitat.

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Episode 26 | The Employment Impact of NMO & MOG w/ Dr. Farrah Mateen

Play Episode Listen Later Jun 27, 2023 54:38

In the second part of our series on working with NMO and MOG, we are joined by Dr. Farrah Mateen. This year she published work that focuses on the socioeconomic impact of NMOSD on patients and caregivers. The work of Dr. Mateen and her team provides us with one of the most in-depth looks at the psychosocial toll, risks, unmet needs, and opportunity loss due to NMOSD.ABOUT US:The Demystifying NMO and MOG podcast is a Sumaira Foundation (TSF) project and was made possible with the generous support of Genentech.SOCIAL & WEBSITE:Farrah Mateen, MD, PhDWebsite - https://doctors.massgeneralbrigham.org/provider/Farrah+J+Mateen/255866Global Neurology Research Group - www.massgeneral.org/neurology/research/global-neurology-research-groupTwitter - https://twitter.com/FarrahMateenConnect With UsWebsite - https://www.sumairafoundation.orgFacebook - https://www.facebook.com/TheSumairaFoundationInstagram - https://www.instagram.com/demystifying_nmomogTwitter - https://twitter.com/DemystifyingNMOTIMESTAMPS/TOPICS:00:01:15 Dr. Farrah Mateen00:03:29 Impact of NMOSD on Employment00:05:53 What We Can Learn From This Research00:07:48 Barriers to Employment00:10:45 Burden of Treatment00:15:38 Time to Diagnosis00:21:17 Age of Onset and Future Opportunities00:24:48 The Role of Mental Health on Returning to Work00:29:32 Unmet Needs00:38:36 Disclosing Illness00:41:11 Comparing NMOSD's Impact00:44:49 Impact on Caregivers02:34:00 Future of this ResearchLINKS:Mateen FJ, Trápaga Hacker CM. Understanding the employment impact of neuromyelitis optica spectrum disorder in the USA: Mixed methods. Front Neurol. 2023 Mar 9;14:1142640. doi: 10.3389/fneur.2023.1142640. PMID: 36970509; PMCID: PMC10033531. https://www.frontiersin.org/articles/10.3389/fneur.2023.1142640/fullTrapaga Hacker CM, Hjerthen IG, Shirkoohi A, et al. Impact of NMOSD on employment: a global survey. Presented at: 2023 ACTRIMS Forum; February 23-25; San Diego, CA. Abstract P320. https://www.frontiersin.org/articles/10.3389/fneur.2023.1142640/fullCREDITS:Producer & Host - Brian DawsonGuest Photo - Mass General HospitalMusic - Denys Kyshchuk from Pixabay

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Living a Full Life with an Autoimmune Disease | Taylor Ann Macey

The LivGreater Podcast

Play Episode Listen Later Jun 27, 2023 35:16

Taylor Ann Macey lives Greater by living her life to the fullest with a devastating disease. She pursues what she is passionate about and lives as though tomorrow is never promised. She loves to learn new things, find new adventures, work hard, and play harder. Since much of what happens with her body is out her control, she takes exquisite care of her mental health to manage the ups and downs of chronic illness. As a Life Coach and Nutrition Coach who specializes in mindset work and body recomposition, Taylor Ann helps women with autoimmune conditions simplify their autoimmune wellness and create the weight and health they've always wanted. Enjoy the conversation with Taylor Ann and be inspired!Connect with Taylor Ann:Website: TaylorAnnMacey.comInstagram: TaylorAnnMaceyFacebook: Autoimmune Warrior Thank you so much for listening!Subscribe on Apple Podcasts, follow us on Instagram, and like us on Facebook! THANK YOU so much for listening!Subscribe on Apple Podcasts, follow us on Instagram, and like us on Facebook!Shop LivGreater Tees, Hoodies, Crew Sweatshirts, and More!

Episode 25 | Responding To Life's Challenges Featuring Dr. Maggie Kang

Neurology Today - Neurology Today Editor’s Picks

Play Episode Listen Later Jun 13, 2023 41:32

Many people will recognize this episode's guest as “Nell's mom.” But today, we are focusing on the journey of Dr. Maggie Kang, whose world was shaken to its core when her daughter was diagnosed with NMOSD. Bogged down by the stress and the uncertainty of the future, she consulted a coach. Maggie soon realized she was the barrier to moving forward. The results were so profound she became a certified life coach focused on supporting the rare disease community, especially moms.Last year she shared her experiences at TEDxCherryCreekWomen, and she is here today to continue that conversation about how those early days impacted her family and, ultimately, what she learned that could help us all work through pain and suffering.ABOUT US:The Demystifying NMO and MOG podcast is a Sumaira Foundation (TSF) project andwas made possible with the generous support of Genentech.SOCIAL & WEBSITE:Maggie KangWebsite - https://maggiekangmd.comVoices of NMO - www.sumairafoundation.org/maggies_nmo_story_finding_miraclesTEDxCherryCreekWomen - https://youtu.be/Dgr_Ng9Dt6cConnect With UsWebsite - https://www.sumairafoundation.orgFacebook - https://www.facebook.com/TheSumairaFoundationInstagram - https://www.instagram.com/demystifying_nmomogTwitter - https://twitter.com/DemystifyingNMOTIMESTAMPS/TOPICS:00:00:59 Dr. Maggie Kang00:02:16 Nell's Story00:07:35 Changes in Family Dynamics00:10:11 Balancing Mom vs. Doctor00:11:58 Realizing You Need Help00:17:19 Not Everyday Will Be Rosy00:18:35 How Life Coaching Can Help00:20:48 Working Through Pain00:21:55 Writing Your Narrative00:26:04 The Ripple Effect of Finding Joy00:28:57 Responding With Pain and Suffering00:31:10 Mom GuiltLINKS:My Hospital Story by Nell Choi - https://www.amazon.com/My-Hospital-Story-Nell-Choi/dp/1982262842CREDITS:Producer & Host - Brian DawsonGuest Photo - Maggie KangMusic - Denys Kyshchuk from Pixabay

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410: Choosing Pain WTF with Dr. Maggie Kang

Doctor Me First

Play Episode Listen Later Jun 12, 2023 31:42

Dr. Maggie is a Radiologist and a mom whose daughter was diagnosed with neuromyelitis optica (NMO) at age nine. The moment of terror of seeing the brain MRI of her daughter displaying an inflammatory episode of NMO put her in the downward spiral of grief that so many experience when faced with such a diagnosis. While watching her child struggle with the most innate parts of her brain functions, Dr. Maggie found herself on the other side of the table, making difficult medical decisions of intubation or facility transfer for better care. The pain she experienced in seeing her child go from perfectly normal and healthy to critically ill while she feared the uncertainty of the future shaped how she now helps other people understand the difference between pain and suffering. It can be difficult to feel intense emotions and sit with those feelings, especially as a doctor. But if we can acknowledge our pain and begin to navigate it, it doesn't hold the power over us that we think it does, and it won't last as long as it normally would otherwise. When she was finally able to work through her pain, Dr. Maggie was able to gain perspective and realize that she could be present in the new normal and take joy in the small moments and little victories. And while suffering can be indefinite, something that you will have to face in small moments every day, acknowledging the pain of those moments can help you move through them and appreciate the progress of the journey out of your suffering. After her experience, she became certified in coaching and now helps other moms navigate the devastation that comes with having a child that suffers from rare chronic diseases. By helping them acknowledge their own grief, she helps them understand the difference between pain and suffering and how to be present and support their child through their diagnosis. Tune in today to learn more about the magic that Dr. Maggie is bringing into the world and how she is helping parents and children everywhere navigate their grief by understanding the differences between pain and suffering. “When you actually accept and move through your pain, it doesn't last nearly as long as you think.” Dr. Maggie Kang Connect with Dr. Kang: Maggie Kang MD Freebie Instagram | Facebook | LinkedIn 2 WAYS TO GET INCREDIBLE HELP AT A LOW-COST!!! Buy my Kindle Book,Doctor Me First, on Amazon Come sit with me in the Badass Collective Slack Group.

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Overcoming Suffering: Dr. Maggie Kang's Journey Through Pain

This Daring Adventure

Play Episode Listen Later May 18, 2023 30:14

Introducing Dr. Maggie Kang, a physician, mother, coach, and rare disease advocate who turned a personal challenge into an opportunity for growth and inspiration. When her daughter was diagnosed with a rare autoimmune disease, Dr. Kang found coaching as a way to cope with her stress and support her family. Through this journey, she learned the importance of embracing pain and shifting perspectives to overcome adversity. With her powerful message of hope and resilience, Dr. Kang has become an inspiration to others facing similar challenges and has made a lasting impact on the lives of those she has touched.Dr. Kang is a board-certified radiologist trained at Yale, mom of two kids, one with a rare disease. She was the radiologist who was the first to see her nine-year-old daughter's horrifying brain MRI in the ER. Her daughter was diagnosed with a rare disease, neuromyelitis optica.The ordeal motivated Maggie to shift her focus from radiology to mental well-being. Now a certified Life Coach, Maggie dedicates her time to supporting parents of kids in the rare and chronic disease communities. She also works with physician moms of kids with chronic needs one-on-one in her private coaching practice, MaggieKangMD LLC. Maggie told her story on the TEDx stage, sharing her powerful message that you can choose to accept pain or create suffering. Link to TEDx talk: The Truth About Pain and Suffering Will Change Your Life | Maggie Kang | TEDxCherryCreekWomenDr. Kang has transformed her family's life by embracing pain and shifting perspectives. After her daughter was diagnosed with a rare autoimmune disease, Dr. Kang sought coaching to help manage her stress and support her family. This journey led her to the realization that pain is an inevitable part of life, but suffering is a choice. By processing her pain and moving through it, Dr. Kang has become a source of strength and inspiration to her daughter and countless others facing similar challenges.This is Dr. Maggie Kang's story:Dr. Maggie Kang's life took a dramatic turn when her once-healthy daughter was diagnosed with a rare disease called neuromyelitis optica at just nine years old. Facing the darkest moments of their lives, they spent five weeks in the ICU, grappling with fear, grief, and uncertainty. As the pandemic unfolded, Maggie sought solace in coaching, which helped her understand that pain and suffering are distinct, and that the latter is a choice. Embracing this wisdom, she began processing her grief and discovered the transformative power of accepting pain.In this episode, you will be able to:Uncover the challenges of rare autoimmune diseases and discover valuable support from foundations.Master the art of embracing pain for transformative shifting of perspectives.Implement crucial self-care techniques for primary caregivers to avoid burnout and manage stress.Harness the power of positivity to reframe negative narratives and elevate your life.Conquer fear and uncover the secret to experiencing joy in all areas of life.Community SupportThe support of a community of people who understand and empathize with the challenges faced by those living with a rare or chronic disease cannot be underestimated. Building connections, sharing experiences, and providing emotional support can help individuals and families tremendously in managing their circumstances. Dr. Maggie Kang's family found solace and camaraderie within the rare disease community they connected with through the NMO foundation. This sense of belonging and support significantly contributed to their ability to navigate their struggles and find comfort in knowing that they were not alone. Dr. Kang ultimately emphasizes the...

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Fertility treatments for women with MS, stroke systems of care, ravalizumab for NMOSD

Play Episode Listen Later Apr 20, 2023 5:59

In this week's podcast, Neurology Today's editor-in-chief discusses a new study finding fertility treatments did not lead to MS relapses for women, a AHA consensus statement that finds stroke systems need improvement, and ravalizumab at less frequent doses was effective for neuromyelitis optica spectrum disorder.

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Optic Neuritis with Dr. John Chen

Mayo Clinic Ophthalmology Podcast

Play Episode Listen Later Apr 19, 2023 13:22

Dr. John Chen, renown Neuro-ophthalmologist takes us through the history of optic neuritis, starting with the optic Neuritis Treatment Trial. Lots has changed since that time, and Dr. Chen teaches us about new, atypical causes of optic neuritis like MOGAD and NMO. Subscribe to the podcast: https://MayoClinicOphthalmology.podbean.com Follow and reach out to us on Twitter: @mayocliniceye

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EP448: Guiding in the Mackenzie Mountains with Peter Gutsche

Play Episode Listen Later Feb 17, 2023 58:01

On this episode, NMO sits down with Peter Gutsche to talk about wild sheep conservation and guiding at Arctic Red River Outfitters. They discuss the Wild Sheep Society of BC's recent Northern Fundraiser, membership, and Peter's journey to becoming a guide. www.wildsheepsociety.com @petergutsche @wildsheepsocietybc --------------------------- DEALS & OFFERS: Need boots? Check out the full CRISPI line-up at www.crispius.com to find a model that suits your hunting style and terrain. Get 15% OFF at Black Rifle Coffee Company or Black Rifle Coffee Company Canada when you use code JOURNAL. --------------------------- SUPPORT WILD SHEEP: Go to Wild Sheep Foundation to find a membership option that suits your budget and commitment to wild sheep. --------------------------- SUPPORT MOUNTAIN GOATS: Go to Rocky Mountain Goat Alliance to find a membership option that suits your budget and commitment to conserving mountain goats and their habitat.

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EP446: BTK Q&A