Podcasts about Movement disorders

Functional movement disorders are a common clinical concern for neurologists. The principle of “rule-in” diagnosis, which involves demonstrating the difference between voluntary and automatic movement, can be carried through to explanation, triage, and evidence-based multidisciplinary rehabilitation therapy. In this episode, Gordon Smith, MD, FAAN speaks Jon Stone, PhD, MB, ChB, FRCP, an author of the article “Multidisciplinary Treatment for Functional Movement Disorder” in the Continuum® August 2025 Movement Disorders issue. Dr. Smith is a Continuum® Audio interviewer and a professor and chair of neurology at Kenneth and Dianne Wright Distinguished Chair in Clinical and Translational Research at Virginia Commonwealth University in Richmond, Virginia. Dr. Stone is a consultant neurologist and honorary professor of neurology at the Centre for Clinical Brain Sciences at the University of Edinburgh in Edinburgh, United Kingdom. Additional Resources Read the article: Multidisciplinary Treatment for Functional Movement Disorder Subscribe to Continuum®: shop.lww.com/Continuum Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @gordonsmithMD Guest: @jonstoneneuro Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. This exclusive Continuum Audio interview is available only to you, our subscribers. We hope you enjoy it. Thank you for listening. Dr Smith: Hello, this is Dr Gordon Smith. Today I've got the great pleasure of interviewing Dr Johnstone about his article on the multidisciplinary treatment for functional neurologic disorder, which he wrote with Dr Alan Carson. This article will appear in the August 2025 Continuum issue on movement disorders. I will say, Jon, that as a Continuum Audio interviewer, I usually take the interviews that come my way, and I'm happy about it. I learn something every time. They're all a lot of fun. But there have been two instances where I go out and actively seek to interview someone, and you are one of them. So, I'm super excited that they allowed me to talk with you today. For those of our listeners who understand or are familiar with FND, Dr Stone is a true luminary and a leader in this, both in clinical care and research. He's also a true humanist. And I have a bit of a bias here, but he was the first awardee of the Ted Burns Humanism in Neurology award, which is a real honor and reflective of your great work. So welcome to the podcast, Jon. Maybe you can introduce yourself to our audience. Dr Stone: Well, thank you so much, Gordon. It was such a pleasure to get that award, the Ted Burns Award, because Ted was such a great character. I think the spirit of his podcasts is seen in the spirit of these podcasts as well. So, I'm a neurologist in Edinburgh in Scotland. I'm from England originally. I'm very much a general neurologist still. I still work full-time. I do general neurology, acute neurology, and I do two FND clinics a week. I have a research group with Alan Carson, who you mentioned; a very clinical research group, and we've been doing that for about 25 years. Dr Smith: I really want to hear more about your clinical approach and how you run the clinic, but I wonder if it would be helpful for you to maybe provide a definition. What's the definition of a functional movement disorder? I mean, I think all of us see these patients, but it's actually nice to have a definition. Dr Stone: You know, that's one of the hardest things to do in any paper on FND. And I'm involved with the FND society, and we're trying to get together a definition. It's very hard to get an overarching definition. But from a movement disorder point of view, I think you're looking at a disorder where there is an impairment of voluntary movement, where you can demonstrate that there is an automatic movement, which is normal in the same movement. I mean, that's a very clumsy way of saying it. Ultimately, it's a disorder that's defined by the clinical features it has; a bit like saying, what is migraine? You know? Or, what is MS? You know, it's very hard to actually say that in a sentence. I think these are disorders of brain function at a very broad level, and particularly with FND disorders, of a sort of higher control of voluntary movement, I would say. Dr Smith: There's so many pearls in this article and others that you've written. One that I really like is that this isn't a diagnosis of exclusion, that this is an affirmative diagnosis that have clear diagnostic signs. And I wonder if you can talk a little bit about the diagnostic process, arriving at an FND diagnosis for a patient. Dr Stone: I think this is probably the most important sort of “switch-around” in the last fifteen, twenty years since I've been involved. It's not new information. You know, all of these diagnostic signs were well known in the 19th century; and in fact, many of them were described then as well. But they were kind of lost knowledge, so that by the time we got to the late nineties, this area---which was called conversion disorder then---it was written down. This is a diagnosis of exclusion that you make when you've ruled everything out. But in fact, we have lots of rule in signs, which I hope most listeners are familiar with. So, if you've got someone with a functional tremor, you would do a tremor entrainment test where you do rhythmic movements of your thumb and forefinger, ask the patient to copy them. It's very important that they copy you rather than make their own movements. And see if their tremor stops briefly, or perhaps entrains to the same rhythm that you're making, or perhaps they just can't make the movement. That might be one example. There's many examples for limb weakness and dystonia. There's a whole lot of stuff to learn there, basically, clinical skills. Dr Smith: You make a really interesting point early on in your article about the importance of the neurological assessment as part of the treatment of the patient. I wonder if you could talk to our listeners about that. Dr Stone: So, I think, you know, there's a perception that- certainly, there was a perception that that the neurologist is there to make a diagnosis. When I was training, the neurologist was there to tell the patient that they didn't have the kind of neurological problem and to go somewhere else. But in fact, that treatment process, when it goes well, I think begins from the moment you greet the patient in the waiting room, shake their hand, look at them. Things like asking the patient about all their symptoms, being the first doctor who's ever been interested in their, you know, horrendous exhaustion or their dizziness. You know, questions that many patients are aware that doctors often aren't very interested in. These are therapeutic opportunities, you know, as well as just taking the history that enable the patient to feel relaxed. They start thinking, oh, this person's actually interested in me. They're more likely to listen to what you've got to say if they get that feeling off you. So, I'd spend a lot of time going through physical symptoms. I go through time asking the patient what they do, and the patients will often tell you what they don't do. They say, I used to do this, I used to go running. Okay, you need to know that, but what do they actually do? Because that's such valuable information for their treatment plan. You know, they list a whole lot of TV shows that they really enjoy, they're probably not depressed. So that's kind of useful information. I also spend a lot of time talking to them about what they think is wrong. Be careful, that they can annoy patients, you know. Well, I've come to you because you're going to tell me what's wrong. But what sort of ideas had you had about what was wrong? I need to know so that I can deal with those ideas that you've had. Is there a particular reason that you're in my clinic today? Were you sent here? Was it your idea? Are there particular treatments that you think would really help you? These all set the scene for what's going to come later in terms of your explanation. And, more importantly, your triaging of the patient. Is this somebody where it's the right time to be embarking on treatment, which is a question we don't always ask yourself, I think. Dr Smith: That's a really great point and kind of segues to my next question, which is- you talked a little bit about this, right? Generally speaking, we have come up with this is a likely diagnosis earlier, midway through the encounter. And you talked a little bit about how to frame the encounter, knowing what's coming up. And then what's coming up is sharing with the patient our opinion. In your article, you point out this should be no different than telling someone they have Parkinson's disease, for instance. What pearls do you have and what pitfalls do you have in how to give the diagnosis? And, you know, a lot of us really weren't trained to do this. What's the right way, and what are the most common land mines that folks step on when they're trying to share this information with patients? Dr Stone: I've been thinking about this for a long time, and I've come to the conclusion that all we need to do with this disorder is stop being weird. What goes wrong? The main pitfall is that people think, oh God, this is FND, this is something a bit weird. It's in a different box to all of the other things and I have to do something weird. And people end up blurting out things like, well, your scan was normal or, you haven't got epilepsy or, you haven't got Parkinson's disease. That's not what you normally do. It's weird. What you normally do is you take a deep breath and you say, I'm sorry to tell you've got Parkinson's disease or, you have this type of dystonia. That's what you normally say. If you follow the normal- what goes wrong is that people don't follow the normal rules. The patient picks up on this. What's going on here? This doctor's telling me what I don't have and then they're starting to talk about some reason why I've got this, like stress, even though I don't- haven't been told what it is yet. You do the normal rules, give it a name, a name that you're comfortable with, preferably as specific as possible: functional tremor, functional dystonia. And then do what you normally do, which is explain to the patient why you think it's this. So, if someone's got Parkinson's, you say, I think you've got Parkinson's because I noticed that you're walking very slowly and you've got a tremor. And these are typical features of Parkinson. And so, you're talking about the features. This is where I think it's the most useful thing that you can do. And the thing that I do when it goes really well and it's gone badly somewhere else, the thing I probably do best, what was most useful, is showing the patient their signs. I don't know if you do that, Gordon, but it's maybe not something that we're used to doing. Dr Smith: Wait, maybe you can talk more about that, and maybe, perhaps, give an example? Talk about how that impacts treatment. I was really impressed about the approach to physical therapy, and treatment of patients really leverages the physical examination findings that we're all well-trained to look for. So maybe explore that a little bit. Dr Stone: Yeah, I think absolutely it does. And I think we've been evolving these thoughts over the last ten or fifteen years. But I started, you know, maybe about twenty years ago, started to show people their tremor entrainment tests. Or their Hoover sign, for example; if you don't know Hoover sign, weakness of hip extension, that comes back to normal when the person's flexing their normal leg, their normal hip. These are sort of diagnostic tricks that we had. Ahen I started writing articles about FND, various senior neurologists said to me, are you sure you should write this stuff down? Patients will find out. I wrote an article with Marc Edwards called “Trick or Treat in Neurology” about fifteen years ago to say that actually, although they're they might seem like tricks, there really are treats for patients because you're bringing the diagnosis into the clinic room. It's not about the normal scan. You can have FND and MS. It's not about the normal scan. It's about what you're seeing in front of you. If you show that patient, yes, you can't move your leg. The more you try, the worse it gets. I can see that. But look, lift up your other leg. Let me show you. Can you see now how strong your leg is? It's such a powerful way of communicating to the patient what's wrong with them diagnostically, giving them that confidence. What it's also doing is showing them the potential for improvement. It's giving them some hope, which they badly need. And, as we'll perhaps talk about, the physio treatment uses that as well because we have to use a different kind of physio for many forms of functional movement disorder, which relies on just glimpsing these little moments of normal function and promoting them, promoting the automatic movement, squashing down that abnormal pattern of voluntary movement that people have got with FND. Dr Smith: So, maybe we can talk about that now. You know, I've got a bunch of other questions to ask you about mechanism and stuff, but let's talk about the approach to physical therapy because it's such a good lead-in and I always worry that our physical therapists aren't knowledgeable about this. So, maybe some examples, you have some really great ones in the article. And then words of wisdom for us as we're engaging physical therapists who may not be familiar with FND, how to kind of build that competency and relationship with the therapist with whom you work. Dr Stone: Some of the stuff is the same. Some of the rehabilitation ideas are similar, thinking about boom and bust activity, which is very common in these patients, or grading activity. That's similar, but some of them are really different. So, if you have a patient with a stroke, the physiotherapist might be very used to getting that person to think and look at their leg to try and help them move, which is part of their rehabilitation. In FND, that makes things worse. That's what's happening in Hoover sign and tremor entrainment sign. Attention towards the limb is making it worse. But if the patient's on board with the diagnosis and understands it, they'll also see what you need to do, then, in the physio is actively use distraction in a very transparent way and say to the patient, look, I think if I get you to do that movement, and I'll film you, I think your movement's going to look better. Wouldn't that be great if we could demonstrate that? And the patient says, yeah, that would be great. We're kind of actively using distraction. We're doing things that would seem a bit strange for someone with other forms of movement disorder. So, the patients, for example, with functional gait disorders who you discover can jog quite well on a treadmill. In fact, that's another diagnostic test. Or they can walk backwards, or they can dance or pretend that they're ice skating, and they have much more fluid movements because their ice skating program in their brain is not corrupted, but their normal walking program is. So, can you then turn ice skating or jogging into normal walking? It's not that complicated, I think. The basic ideas are pretty simple, but it does require some creativity from whoever's doing the therapy because you have to use what the patient's into. So, if the patient used to be a dancer- we had a patient who was a, she was really into ballet dancing. Her ballet was great, but her walking was terrible. So, they used ballet to help her walk again. And that's incredibly satisfying for the therapist as well. So, if you have a therapist who's not sure, there are consensus recommendations. There are videos. One really good success often makes a therapist want to do that again and think, oh, that's interesting. I really helped that patient get better. Dr Smith: For a long time, this has been framed as a mental health issue, conversion disorder, and maybe we can talk a little bit about early life of trauma as a risk factor. But, you know, listening to you talk, it sounds like a brain network problem. Even the word “functional”, to me, it seems a little judgmental. I don't know if this is the best term, but is this really a network problem? Dr Stone: The word “functional”, for most neurologists, sounds judgmental because of what you associate it with. If you think about what the word actually is, it's- it does what it says on the tin. There's a disordered brain function. I mean, it's not a great word. It's the least worst term, in my view. And yes, of course it's a brain network problem, because what other organ is it going to be? You know, that's gone wrong? When software brains go wrong, they go wrong in networks. But I think we have to be careful not to swing that pendulum too far to the other side because the problem here, when we say asking the question, is this a mental health problem or a neurological one, we're just asking the wrong question. We're asking a question that makes no sense. However you try and answer that, you're going to get a stupid answer because the question doesn't make sense. We shouldn't have those categories. It's one organ. And what's so fascinating about FND---and I hope what can incite your sort of curiosity about it---is this disorder which defies this categorization. You see some patients with it, they say, oh, they've got a brain network disorder. Then you meet another patient who was sexually abused for five years by their uncle when they were nine, between nine and fourteen; they developed an incredibly strong dissociative threat response into that experience. They have crippling anxiety, PTSD, interpersonal problems, and their FND is sort of somehow a part of that; part of that experience that they've had. So, to ignore that or to deny or dismiss psychological, psychiatric aspects, is just as bad and just as much a mistake as to dismiss the kind of neurological aspects as well. Dr Smith: I wonder if this would be a good time to go back and talk a little bit about a concept that I found really interesting, and that is FND as a prodromal syndrome before a different neurological problem. So, for instance, FND prodromal to Parkinson's disease. Can you talk to us a little bit about that? I mean, obviously I was familiar with the fact that patients who have nonepileptic seizurelike events often have epileptic seizures, but the idea of FND ahead of Parkinson's was new to me. Dr Stone: So, this is definitely a thing that happens. It's interesting because previously, perhaps, if you saw someone who was referred with a functional tremor---this has happened to me and my colleagues. They send me some with a functional tremor. By the time I see them, it's obvious they've got Parkinson's because it's been a little gap. But it turns out that the diagnosis of functional tremor was wrong. It was just that they've developed that in the prodrome of Parkinson's disease. And if you think about it, it's what you'd expect, really, especially with Parkinson's disease. We know people develop anxiety in the prodrome of Parkinson's for ten, fifteen years before it's part of the prodrome. Anxiety is a very strong risk factor for FND, and they're already developing abnormalities in their brain predisposing them to tremor. So, you put those two things together, why wouldn't people get FND? It is interesting to think about how that's the opposite of seizures, because most people with comorbidity of functional seizures and epilepsy, 99% of the time the epilepsy came first. They had the experience of an epileptic seizure, which is frightening, which evokes strong threat response and has somehow then led to a recapitulation of that experience in a functional seizure. So yeah, it's really interesting how these disorders overlap. We're seeing something similar in early MS where, I think, there's a slight excess of functional symptoms; but as the disease progresses, they often become less, actually. Dr Smith: What is the prognosis with the types of physical therapy? And we haven't really talked about psychological therapy, but what's the success rate? And then what's the relapse rate or risk? Dr Stone: Well, it does depend who they're seeing, because I think---as you said---you're finding difficult to get people in your institution who you feel are comfortable with this. Well, that's a real problem. You know, you want your therapists to know about this condition, so that matters. But I think with a team with a multidisciplinary approach, which might include psychological therapy, physio, OT, I think the message is you can get really good outcomes. You don't want to oversell this to patients, because these treatments are not that good yet. You can get spectacular outcomes. And of course, people always show the videos of those. But in published studies, what you're seeing is that most studies of- case series of rehabilitation, people generally improve. And I think it's reasonable to say to a patient, that we have these treatments, there's a good chance it's going to help you. I can't guarantee it's going to help you. It's going to take a lot of work and this is something we have to do together. So, this is not something you're going to do to the patient, they're going to do it with you. Which is why it's so important to find out, hey, do they agree with you with the diagnosis? And check they do. And is it the right time? It's like when someone needs to lose weight or change any sort of behavior that they've just become ingrained. It's not easy to do. So, I don't know if that helps answer the question. Dr Smith: No, that's great. And you actually got right where I was wanting to go next, which is the idea of timing and acceptance. You brought this up earlier on, right? So, sometimes patients are excited and accepting of having an affirmative diagnosis, but sometimes there's some resistance. How do you manage the situation where you're making this diagnosis, but a patient's resistant to it? Maybe they're fixating on a different disease they think they have, or for whatever reason. How do you handle that in terms of initiating therapy of the overall diagnostic process? Dr Stone: We should, you know, respect people's rights to have whatever views they want about what's wrong with them. And I don't see my job as- I'm not there to change everyone's mind, but I think my job is to present the information to them in a kind of neutral way and say, look, here it is. This is what I think. My experience is, if you do that, most people are willing to listen. There are a few who are not, but most people are. And most of the time when it goes wrong, I have to say it's us and not the patients. But I think you do need to find out if they can have some hope. You can't do rehabilitation without hope, really. That's what you're looking for. I sometimes say to patients, where are you at with this? You know, I know this is a really hard thing to get your head around, you've never heard of it before. It's your own brain going wrong. I know that's weird. How much do you agree with it on a scale of naught to ten? Are you ten like completely agreeing, zero definitely don't? I might say, are you about a three? You know, just to make it easy for them to say, no, I really don't agree with you. Patients are often reluctant to tell you exactly what they're thinking. So, make it easy for them to disagree and then see where they're at. If they're about seven, say, that's good. But you know, it'd be great if you were nine or ten because this is going to be hard. It's painful and difficult, and you need to know that you're not damaging your body. Those sort of conversations are helpful. And even more importantly, is it the right time? Because again, if you explore that with people, if a single mother with four kids and, you know, huge debts and- you know, it's going to be very difficult for them to engage with rehab. So, you have to be realistic about whether it's the right time, too; but keep that hope going regardless. Dr Smith: So, Jon, there's so many things I want to talk to you about, but maybe rather than let me drive it, let me ask you, what's the most important thing that our listeners need to know that I haven't asked you about? Dr Stone: Oh God. I think when people come and visit me, they sometimes, let's go and see this guy who does a lot of FND, and surely, it'll be so easy for him, you know? And I think some of the feedback I've had from visitors is, it's been helpful to watch, to see that it's difficult for me too. You know, this is quite hard work. Patients have lots of things to talk about. Often you don't have enough time to do it in. It's a complicated scenario that you're unravelling. So, it's okay if you find it difficult work. Personally, I think it's very rewarding work, and it's worth doing. It's worth spending the time. I think you only need to have a few patients where they've improved. And sometimes that encounter with the neurologist made a huge difference. Think about whether that is worth it. You know, if you do that with five patients and one or two of them have that amazing, really good response, well, that's probably worth it. It's worth getting out of bed in the morning. I think reflecting on, is this something you want to do and put time and effort into, is worthwhile because I recognize it is challenging at times, and that's okay. Dr Smith: That's a great number needed to treat, five or six. Dr Stone: Exactly. I think it's probably less than that, but… Dr Smith: You're being conservative. Dr Stone: I think deliberately pessimistic; but I think it's more like two or three, yeah. Dr Smith: Let me ask one other question. There's so much more for our listeners in the article. This should be required reading, in my opinion. I think that of most Continuum, but this, I really truly mean it. But I think you've probably inspired a lot of listeners, right? What's the next step? We have a general or comprehensive neurologist working in a community practice who's inspired and wants to engage in the proactive care of the FND patients they see. What's the next step or advice you have for them as they embark on this? It strikes me, like- and I think you said this in the article, it's hard work and it's hard to do by yourself. So, what's the advice for someone to kind of get started? Dr Stone: Yeah, find some friends pretty quick. Though, yeah, your own enthusiasm can take you a long way, you know, especially with we've got much better resources than we have. But it can only take you so far. It's really particularly important, I think, to find somebody, a psychiatrist or psychologist, you can share patients with and have help with. In Edinburgh, that's been very important. I've done all this work with the neuropsychiatrist, Alan Carson. It might be difficult to do that, but just find someone, send them an easy patient, talk to them, teach them some of this stuff about how to manage FND. It turns out it's not that different to what they're already doing. You know, the management of functional seizures, for example, is- or episodic functional movement disorders is very close to managing panic disorder in terms of the principles. If you know a bit about that, you can encourage people around you. And then therapists just love seeing these patients. So, yeah, you can build up slowly, but don't- try not to do it all on your own, I would say. There's a risk of burnout there. Dr Smith: Well, Dr Stone, thank you. You don't disappoint. This has really been a fantastic conversation. I really very much appreciate it. Dr Stone: That's great, Gordon. Thanks so much for your time, yeah. Dr Smith: Well, listeners, again, today I've had the great pleasure of interviewing Dr Jon Stone about his article on the multidisciplinary treatment for functional neurologic disorder, which he wrote with Dr Alan Carson. This article appears in the August 2025 Continuum issue on movement disorders. Please be sure to check out Continuum Audio episodes from this and other issues. And listeners, thank you once again for joining us today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. We hope you've enjoyed this subscriber-exclusive interview. Thank you for listening.

Paroxysmal movement disorders refer to a group of highly heterogeneous disorders that present with attacks of involuntary movements without loss of consciousness. These disorders demonstrate considerable and ever-expanding genetic and clinical heterogeneity, so an accurate clinical diagnosis has key therapeutic implications. In this episode, Kait Nevel, MD, speaks with Abhimanyu Mahajan, MD, MHS, FAAN, author of the article “Paroxysmal Movement Disorders” in the Continuum® August 2025 Movement 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. Mahajan is an assistant professor of neurology and rehabilitation medicine at the James J. and Joan A. Gardner Family Center for Parkinson's Disease and Movement Disorders at the University of Cincinnati in Cincinnati, Ohio. Additional Resources Read the article: Paroxysmal Movement Disorders Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @IUneurodocmom Guest: @MahajanMD Full episode transcript available here Dr Jones: This is Doctor Lyell Jones, editor in chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Nevel: Hello, this is Dr Kait Nevel. Today I'm interviewing doctor Abhi Mahajan about his article on diagnosis and management of paroxysmal movement disorders, which appears in the August 2025 Continuum issue on movement disorders. Abhi, welcome to the podcast and please introduce yourself to the audience. Dr Mahajan: Thank you, Kait. Thank you for inviting me. My name is Abhi Mahajan. I'm an assistant professor of neurology and rehabilitation medicine at the University of Cincinnati in Cincinnati, Ohio. I'm happy to be here. Dr Nevel: Wonderful. Well, I'm really excited to talk to you about your article today on this very interesting and unique set of movement disorders. So, before we get into your article a little bit more, I think just kind of the set the stage for the discussion so that we're all on the same page. Could you start us off with some definitions? What are paroxysmal movement disorders? And generally, how do we start to kind of categorize these in our minds? Dr Mahajan: So, the term paroxysmal movement disorders refers to a group of highly heterogeneous disorders. These may present with attacks of involuntary movements, commonly a combination of dystonia and chorea, or ataxia, or both. These movements are typically without loss of consciousness and may follow, may follow, so with or without known triggers. In terms of the classification, these have been classified in a number of ways. Classically, these have been classified based on the trigger. So, if the paroxysmal movement disorder follows activity, these are called kinesigenic, paroxysmal, kinesigenic dyskinesia. If they are not followed by activity, they're called non kinesigenic dyskinesia and then if they've followed prolonged activity or exercise they're called paroxysmal exercise induced dyskinesia. There's a separate but related group of protogynous movement disorders called episodic attacks here that can have their own triggers. Initially this was the classification that was said. Subsequent classifications have placed their focus on the ideology of these attacks that could be familiar or acquired and of course understanding of familiar or genetic causes of paroxysmal movement disorders keeps on expanding and so on and so forth. And more recently, response to pharmacotherapy and specific clinical features have also been introduced into the classification. Dr Nevel: Great, thank you for that. Can you share with us what you think is the most important takeaway from your article for the practicing neurologist? Dr Mahajan: Absolutely. I think it's important to recognize that everything that looks and sounds bizarre should not be dismissed as malingering. Such hyperkinetic and again in quotations, “bizarre movements”. They may appear functional to the untrained eye or the lazy eye. These movements can be diagnosed. Paroxysmal movement disorders can be diagnosed with a good clinical history and exam and may be treated with a lot of success with medications that are readily available and cheap. So, you can actually make a huge amount of difference to your patients' lives by practicing old-school neurology. Dr Nevel: That's great, thank you so much for that. I can imagine that scenario does come up where somebody is thought to have a functional neurological disorder but really has a proximal movement disorder. You mentioned that in your article, how it's important to distinguish between these two, how there can be similarities at times. Do you mind giving us a little bit more in terms of how do we differentiate between functional neurologic disorder and paroxysmal movement disorder? Dr Mahajan: So clinical differentiation of functional neurological disorder from paroxysmal movement disorders, of course it's really important as a management is completely different, but it can be quite challenging. There's certainly an overlap. So, there can be an overlap with presentation, with phenomenology. Paroxysmal nature is common to both of them. In addition, FND and PMD's may commonly share triggers, whether they are movement, physical exercise. Other triggers include emotional stimuli, even touch or auditory stimuli. What makes it even more challenging is that FND's may coexist with other neurological disorders, including paroxysmal movement disorders. However, there are certain specific phenom phenotypic differences that have been reported. So specific presentations, for example the paroxysms may look different. Each paroxysm may look different in functional neurological disorders, specific phenotypes like paroxysmal akinesia. So, these are long duration episodes with eyes closed. Certain kinds of paroxysmal hyperkinesia with ataxia and dystonia have been reported. Of course. More commonly we see PNES of paroxysmal nonepileptic spells or seizures that may be considered paroxysmal movement disorders but represent completely different etiology which is FND. Within the world of movement disorders, functional jerks may resemble propiospinal myoclonus which is a completely different entity. Overall, there are certain things that help separate functional movement disorders from paroxysmal movement disorders, such as an acute onset variable and inconsistent phenomenology. They can be suggestibility, distractibility, entrainment, the use of an EMG may show a B-potential (Bereitschaftspotential) preceding the movement in patients with FND. So, all of these cues are really helpful. Dr Nevel: Great, thanks. When you're seeing a patient who's reporting to these paroxysmal uncontrollable movements, what kind of features of their story really tips you off that this might be a proximal movement disorder? Dr Mahajan: Often these patients have been diagnosed with functional neurological disorders and they come to us. But for me, whenever the patient and or the family talk about episodic movements, I think about these. Honestly, we must be aware that there is a possibility that the movements that the patients are reporting that you may not see in clinic. Maybe there are obvious movement disorders. Specifically, there's certain clues that you should always ask for in the history, for example, ask for the age of onset, a description of movements. Patients typically have videos or families have videos. You may not be able to see them in clinic. The regularity of frequency of these movements, how long the attacks are, is there any family history of or not? On the basis of triggers, whether, as I mentioned before, do these follow exercise? Prolonged exercise? Or neither of the above? What is the presentation in between attacks, which I think is a very important clinical clue. Your examination may be limited to videos, but it's important not just to examine the video which represents the patient during an attack, but in between attacks. That is important. And of course, I suspect we'll get to the treatment, but the treatment can follow just this part, the history and physical exam. It may be refined with further testing, including genetic testing. Dr Nevel: Great. On the note of genetic testing, when you do suspect a diagnosis of paroxysmal movement disorder, what are some key points for the provider to be aware of about genetic testing? How do we go about that? I know that there are lots of different options for genetic testing and it gets complicated. What do you suggest? Dr Mahajan: Traditionally, things were a little bit easier, right, because we had a couple of genes that have been associated with the robust movement disorders. So, genetic testing included single gene testing, testing for PRRT2 followed by SLC2A. And if these were negative, you said, well, this is not a genetic ideology for paroxysmal movement disorders. Of course, with time that has changed. There's an increase in known genes and variants. There is increased genetic entropy. So, the same genetic mutation may present with many phenotypes and different genetic mutations may present with the similar phenotype. Single gene testing is not a high yield approach. Overall genetic investigations for paroxysmal movement disorders use next generation sequencing or whole exome sequence panels which allow for sequencing of multiple genes simultaneously. The reported diagnostic yield with let's say next generation sequencing is around 35 to 50 percent. Specific labs at centers have developed their own panels which may improve the yield of course. In children, microarray may be considered, especially the presentation includes epilepsy or intellectual disability because copy number variations may not be detected by a whole exome sequencing or next generation sequencing. Overall, I will tell you that I'm certainly not an expert in genetics, so whenever you're considering genetic testing, if possible, please utilize the expertise of a genetic counsellor. Families want to know, especially as an understanding of the molecular underpinnings and knowledge about associated mutations or variations keeps on expanding. We need to incorporate their expertise. A variant of unknown significance, which is quite a common result with genetic testing, may not be a variant of unknown significance next year may be reclassified as pathogenic. So, this is extremely important. Dr Nevel: Yeah. That's such a good point. Thank you. And you just mentioned that there are some genetic mutations that can lead to multiple different phenotypes. Seemingly similar phenotypes can be associated with various genetic mutations. What's our understanding of that? Do we have an understanding of that? Why there is this seeming disconnect at times between the specific genetic mutation and the phenotype? Dr Mahajan: That is a tough question to answer for all paroxysmal movement disorders because the answer may be specific to a specific mutation. I think a great example is the CACNA1A mutation. It is a common cause of episodic ataxia type 2. Depending on when the patient presents, you can have a whole gamut of clinical presentations. So, if the patient is 1 year old, the patient can present with epileptic encephalopathy. Two to 5 years, it can be benign paroxysmal torticollis of infancy. Five to 10 years, can present with learning difficulties with absence epilepsy and then of course later, greater than 10 years, with episodic ataxia (type) 2 hemiplegic migraine and then a presentation with progressive ataxia and hemiplegic migraines has also been reported. So not just episodic progressive form of ataxia has also been reported. I think overall these disorders are very rare. They are even more infrequently diagnosed than their prevalence. As such, the point that different genetic mutations present with different phenotypes, or the same genetic mutation I may present with different phenotypes could also represent this part. Understanding of the clinical presentation is really incomplete and forever growing. There's a new case report or case series every other month, which makes this a little bit challenging, but that's all the more reason for learning about them and for constant vigilance for patients who show up to our clinic. Dr Nevel: Yeah, absolutely. What is our current understanding of the associated pathophysiology of these conditions and the pathophysiology relating to the genetics? And then how does that relate to the treatment of these conditions? Dr Mahajan: So, a number of different disease mechanisms have been proposed. Traditionally, these were all thought to be ion channelopathies, but a number of different processes have been proposed now. So, depending on the genetic mutation that you talk about. So certain mutations can involve ion channels such as CACMA1A, ATP1A3. It can involve solute carriers, synaptic vesicle fusion, energy metabolism such as ECHS1, synthesis of neurotransmitters such as GCH1. So, there are multiple processes that may be involved. I think overall for the practicing clinician such as me, I think there is a greater need for us to understand the underlying genetics and associated phenotypes and the molecular mechanisms specifically because these can actually influence treatment decisions, right? So, you mentioned that specific genetic testing understanding of the underlying molecular mechanism can influence specific treatments. As an example, a patient presenting with proximal nocturnal dyskinesia with mutation in the ADCY5 gene may respond beautifully to caffeine. Other examples if you have SLC2A1, so gluc-1 (glucose transporter type 1) mutation, a ketogenic diet may work really well. If you have PDHA1 mutation that may respond to thiamine and so on and so forth. There are certain patients where paroxysmal movement disorders are highly disabling and you may consider deep brain stimulation. That's another reason why it may be important to understand genetic mutations because there is literature on response to DBS with certain mutations versus others. Helps like counselling for patients and families, and of course introduces time, effort, and money spent in additional testing. Dr Nevel: Other than genetic testing, what other diagnostic work up do you consider when you're evaluating patients with a suspected paroxysmal movement disorder? Are there specific things in the history or on exam that would prompt you to do certain testing to look for perhaps other things in your differential when you're first evaluating a patient? Dr Mahajan: In this article, I provide a flow chart that helps me assess these patients as well. I think overall the history taking and neurological exam outside of these paroxysms is really important. So, the clinical exam in between these episodic events, for example, for history, specific examples include, well, when do these paroxysms happen? Do they happen or are they precipitated with meals that might indicate that there's something to do with glucose metabolism? Do they follow exercise? So, a specific example is in Moyamoya disease, they can be limb shaking that follows exercise. So, which gives you a clue to what the etiology could be. Of course, family history is important, but again, talking about the exam in between episodes, you know, this is actually a great point because out– we've talked about genetics, we've talked about idiopathic paroxysmal movement disorders, –but a number of these disorders are because of acquired causes. Well, of course it's important because acquired causes such as autoimmune causes, so multiple sclerosis, ADEM, lupus, LGI1, all of these NMDAR, I mentioned Moyamoya disease and metabolic causes. Of course, you can consider FND as under-acquired as well. But all of these causes have very different treatments and they have very different prognosis. So, I think it's extremely important for us to look into the history with a fine comb and then examine these patients in between these episodes and keep our mind open about acquired causes as well. Dr Nevel: When you evaluate these patients, are you routinely ordering vascular imaging and autoimmune kind of serologies and things like that to evaluate for these other acquired causes or it does it really just depend on the clinical presentation of the patient? Dr Mahajan: It mostly depends on the clinical presentation. I mean, if the exam is let's say completely normal, there are no other risk factors in a thirty year old, then you know, with a normal exam, normal history, no other risk factors. I may not order an MRI of the brain. But if the patient is 55 or 60 (years) with vascular risk factors, then you have to be mindful that this could be a TIA. If the patient has let's say in the 30s and in between these episodes too has basically has a sequel of these paroxysms, then you may want to consider autoimmune. I think the understanding of paraneoplastic, even autoimmune disorders, is expanding as well. So, you know the pattern matters. So, if all of this is subacute started a few months ago, then I have a low threshold for ordering testing for autoimmune and paraneoplastic ideology is simply because it makes such a huge difference in terms of how you approach the treatment and the long-term prognosis. Dr Nevel: Yeah, absolutely. What do you find most challenging about the management of patients with paroxysmal movement disorders? And then also what is most rewarding? Dr Mahajan: I think the answer to both those questions is, is the same. The first thing is there's so much advancement in what we know and how we understand these disorders so regularly that it's really hard to keep on track. Even for this article, it took me a few months to write this article, and between the time and I started and when I ended, there were new papers to include new case reports, case series, right? So, these are rare disorders. So most of our understanding for these disorders comes from case reports and case series, and it's in a constant state of advancement. I think that is the most challenging part, but it's also the most interesting part as well. I think the challenging and interesting part is the heterogeneity of presentation as well. These can involve just one part of your body, your entire body can present with paroxysmal events, with multiple different phenomenologies and they might change over time. So overall, it's highly rewarding to diagnose such patients in clinic. As I said before, you can make a sizeable difference with the medication which is usually inexpensive, which is obviously a great point to mention these days in our health system. But with anti-seizure drugs, you can put the right diagnosis, you can make a huge difference. I just wanted to make a point that this is not minimizing in any way the validity or the importance of diagnosing patients with functional neurological disorders correctly. Both of them are as organic. The importance is the treatment is completely different. So, if you're diagnosing somebody with FND and they do have FND and they get cognitive behavioral therapy and they get better, that's fantastic. But if somebody has paroxysmal movement disorders and they undergo cognitive behavioral therapy and they're not doing well, that doesn't help anybody. Dr Nevel: One hundred percent. As providers, obviously we all want to help our patients and having the correct diagnosis, you know, is the first step. What is most interesting to you about paroxysmal movement disorders? Dr Mahajan: So outside of the above, there are some unanswered questions that I find very interesting. Specifically, the overlap with epilepsy is very interesting, including shared genes, the episodic nature, presence of triggers, therapeutic response to anti-seizure drugs. All of this I think deserves further study. In the clinic, you may find that epilepsy and prognosis for movement disorders may occur in the same individual or in a family. Episodic ataxia has been associated with seizures. Traditionally this dichotomy of an ictal focus. If it's cortical then it's epilepsy, if it's subcortical then it's prognosis for movement disorders. This is thought to be overly simplistic. There can be co-occurrence of seizures and paroxysmal movement disorders in the same patient and that has led to this continuum between these two that has been proposed. This is something that needs to be looked into in more detail. Our colleagues in Epilepsy may scoff this, but there's concept of basal ganglia epilepsy manifesting as paroxysmal movement disorders was proposed in the past. And there was this case report that was published out of Italy where there was ictal discharge from the supplementary sensory motor cortex with a concomitant discharge from the ipsilateral coordinate nucleus in a patient with paroxysmal kinesigenic cardioarthidosis. So again, you know, basal ganglia epilepsy, no matter what you call it, the idea is that there is a clear overlap between these two conditions. And I think that is fascinating. Dr Nevel: Really interesting stuff. Well, thank you so much for chatting with me today. Dr Mahajan: Thank you, Kait. And thank you to the Continuum for inviting me to write this article and for this chance to speak about it. I'm excited about how it turned out, and I hope readers enjoy it as well. Dr Nevel: Today again, I've been interviewing doctor Abhi Mahajan about his article on diagnosis and management of paroxysmal movement disorders, which appears in the August 2025 Continuum issue on movement disorders. I encourage all of our listeners to be sure to check out the Continuum Audio episodes from this and other issues. As always, please read the Continuum articles where you can find a lot more information than what we were able to cover in our discussion today. And thank you for our listeners for joining today. And thank you, Abhi, so much for sharing your knowledge with 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.

Tics are movements or sounds that are quick, recurrent, and nonrhythmic. They fluctuate over time and can be involuntary or semivoluntary. Although behavioral therapy remains the first-line treatment, modifications to comprehensive behavioral intervention have been developed to make treatment more accessible. In this episode, Casey Albin, MD, speaks with Jessica Frey, MD, author of the article “Tourette Syndrome and Tic Disorders” in the Continuum® August 2025 Movement Disorders issue. Dr. Albin is a Continuum® Audio interviewer, associate editor of media engagement, and an assistant professor of neurology and neurosurgery at Emory University School of Medicine in Atlanta, Georgia. Dr. Frey is an assistant professor of neurology, Movement Disorders Fellowship Program Director, and Neurology Student Clerkship Director at the Rockefeller Neuroscience Institute in the department of neurology at West Virginia University in Morgantown, West Virginia. Additional Resources Read the article: Tourette Syndrome and Tic Disorders Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @caseyalbin Transcript 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 Albin: Hi all, this is Dr Casey Albin. Today I'm interviewing Dr Jessica Frey about her article Tourette Syndrome and Tic Disorders, which appears in the August 2025 Continuum issue on movement disorders. Dr Frey, thank you so much for being here, and welcome to the podcast. I'd love for you to briefly introduce yourself to our audience. Dr Frey: Thank you for having me here today. My name is Jessica Frey, and I am a movement disorder specialist at West Virginia University. I'm also the movement disorder fellowship director, as well as the neurology clerkship student director. Dr Albin: Dr. Frey, I feel like this was one of the things I actually had no exposure to as a resident. For trainees that kind of want to get a better understanding of how these are managed, what kind of counseling you do, what kind of interventions you're using, how can they get a little bit more exposure? Dr Frey: That's a great question, and I actually had a similar experience to you. I did not see that many patients with Tourette syndrome while I was in my residency training. I got a lot more exposure during my fellowship training, and that's when I actually fell in love with that patient population, caring for them, seeing them be successful. I think it depends on the program that you're in. During the pediatric neurology rotation might be your best bet to getting exposure to patients with Tourette syndrome, since a lot of them are going to be diagnosed when they're quite young, and sometimes they'll even continue to follow through young adulthood in the pediatric neurology clinic. However, up to 20% of patients with Tourette syndrome will have persistent tics during adulthood. And so, I think it is important for neurology trainees to understand how to manage them, understand what resources are out there. So, if you have an interest in that, absolutely try to follow either in the pediatric neurology department, or if you have a movement disorder program that has a Tourette clinic or has a movement disorder specialist who has an interest in Tourette syndrome, definitely try to hang out with them. Get to know that patient population, and educate yourself as much as you're able to educate the patients as well. Dr Albin: Yeah, I think that's fantastic advice. You wrote a fantastic article, and it covers a lot of ground. And I think let's start at some of the basics. When I think of Tourette syndrome and tics, I think of Tourette syndrome having tics, but maybe not all patients who have tics have Tourette syndrome. And so, I was wondering, A, if you could confirm that's true; and then could you tell us a little bit about some of the diagnostic criteria for each of these conditions? Dr Frey: Sure. So, a tic is a phenomenological description. So basically, what you're seeing is a description of a motor or phonic tic, which is a particular type of movement disorder. Tourette syndrome is a very specific diagnosis, and the diagnostic criteria for Tourette syndrome at this point in time is that you need to have had at least one phonic tic and two or more motor tics over the course of at least a year before the age of eighteen. Dr Albin: Got it. So, there's certainly more specific and a lot more criteria for having Tourette syndrome. I was struck in reading your article how many myths there are surrounding Tourette syndrome and tic disorders kind of in general. What's known about the pathophysiology of Tourette syndrome, and what are some common misconceptions about patients who have this disorder? Dr Frey: Yeah, so I think that's a really excellent question because for so many years, Tourette syndrome and tic disorders in general were thought to be psychogenic in origin, even dating back to when they were first described. The history of Tourette syndrome is quite interesting in that, when Tourette---who, you know, it's named after---was working with Charcot, a lot of the initial descriptors were of actual case reports of patients who had more psychogenic descriptions, and eventually they became known as tic disorders as well. It wasn't until the discovery of Haldol and using Haldol as a treatment for tic disorders that people started to change their perception and say, okay, maybe there is actually a neurologic basis for Tourette syndrome. So, in terms of the pathophysiology, it's not completely known, but what we do know about it, we think that there is some sort of hyperactivity in the corticostriatal-thalamocortical circuits. And we think that because of this hyperactivity, it leads to the hyperactive movement disorder. We think similar circuitry is involved in conditions like OCD, or obsessive compulsive disorder; as well as ADHD, or attention deficit hyperactivity disorder. And because of that, we actually do tend to see an overlap between all three of these conditions in both individuals and families. Dr Albin: And hearing all of that, does this all come back to, sort of, dopamine and, sort of, behavioral motivation, or is it different than that? Dr Frey: It's probably more complex than just dopamine, but there is the thought that dopamine does play a role. And even one of the hypotheses regarding the pathophysiology is actually that these tics might start as habits, and then when the habits become more common, they actually reshape the dopaminergic pathways. And each time a tic occurs, there's a little bit of a dopaminergic reward. And so over time, that reshapes those hyperactive pathways and changes the actual circuitry of the brain, leading it to be not just a habit but part of their neurologic makeup. Dr Albin: It's fascinating to hear how that actually might play into our neural circuitry and, over time, rewire our brain. Fascinating. I mean, this is just so interesting how movement disorders play into such behavioral regulation and some comorbid conditions like ADHD and OCD. I thought it would be really helpful, maybe, to our listeners to kind of think through a case that I suspect is becoming more common. So, if it's okay with you, I'll present sort of a hypothetical. Dr Frey: Absolutely. Dr Albin: This is a father bringing in his seventeen-year-old daughter. She's coming into the clinic because she's been demonstrating, over the past four to six weeks, some jerking movement in her right arm. And it's happened multiple times a day. And it was a pretty sudden onset. She had not had any movement like this before, and then several weeks ago, started moving the right hand. And then it became even more disruptive: her right leg was involved, she had some scrunching her face. This is all happening at a time where she was dealing with some stress, maybe a little bit of applications around college that she was having a lot of anxiety about. How do you sort of approach this case if this is someone who comes to your office? Dr Frey: Sure. So, I think the first thing that you want to get is a good solid history, trying to understand, what is the origin of these abnormal movements and what led to the abnormal movements. Now, a key thing here is that in Tourette syndrome, and most physiologic tic syndromes, there's a pretty early onset. So, in Tourette syndrome, the expected age of onset is between the ages of five and seven years old. So, to have kind of acute new abnormal movements as a seventeen-year-old would be very unusual for a new-onset diagnosis of Tourette syndrome. However, there's a couple of things from the history that could help you. One would be, were there ever tics in the past? Because sometimes, when you think retrospectively, a lot of these patients might have had a simple eye-blinking tic or a coughing tic when they were a child. And perhaps they did have Tourette syndrome, a very mild case of it. But because the tics were never that pronounced, they never went to see anyone about it and it was never known that they had Tourette syndrome in the first place. If there is no history like that and the movements are completely new, out of the blue, of course you want to rule out anything acute that could be going on that could be causing that. Looking at the phenomenology of the movements can also be very helpful. When you're looking at abnormal tic movements, you would expect most cases of something like Tourette syndrome to occur first in the midline and go in a rostrocoidal distribution. So, you mostly see things happening with eye blinking, throat clearing, sniffling, neck snapping. These are some of the immediate tics that start to happen. We also usually start to see simple tics, as opposed to complex tics, at the beginning. Now, over the course of time, many patients do develop more complex tics that might involve the arms or the extremities, but that would be unusual to see this as a presenting feature of new-onset Tourette syndrome. Dr Albin: Got it. So, I'm hearing that the history really matters and that sometimes, like those, like, first-onset seizures, I imagine as a neurointensivist, we see a lot of patients who've had seizures who think that they're presenting the first time. And then we go back and we say, well, actually they have had some abnormal movements at night. Sounds like it's very similar with these movement disorders where you have to really go back and ask, well, was there some sniffling? Did they go through a phase where they were grunting frequently? Because I can imagine that many children make those behaviors, and that it may not have registered as something that was cause for concern. Dr Frey: Absolutely. Dr Albin: And then the other thing I heard from you was that the phenomenology really matters and that there is a typical presentation, starting from sort of the face and working the way down. And that can be really helpful. But in this case, the family is quite clear. No, no, no. She's never had movements like this before. This is- nothing like this. We promise you, did not go through a phase where she was coughing or blinking, or, this is all totally new. And the phenomenology, they say, no, no, she did not start with blinking. It definitely started in the arm and then progressed in its complex movements. So, knowing that about her, how does that sort of shape how you move forward with the diagnosis? Dr Frey: Yeah. So, really good question. And this is something that I think really peaked during the Covid-19 pandemic. We saw an influx of patients, especially teenage girls or young adult girls, who basically would come in and have these new, acute-onset, abnormal movements. We weren't sure what to call them initially. There was some discussion of calling them “explosive tic disorder” and things like that. A lot of these actually looked very similar to psychogenic nonepileptic seizures, where they would come into the emergency department and have many abnormal movements that were so severe, that they were having a “tic attack” and couldn't stop the abnormal movements from occurring. And we saw so many of these cases during the Covid-19 pandemic that it eventually became known as a distinctive diagnostic criteria with the name of “functional ticlike behavior”, or FTLB. When we think about functional ticlike behavior, we think that these tics are driven more by anxiety and stress. A lot of times, the backstory of these patients, they were in a very stressful situation, and that's when the abnormal movement started. So, a very similar kind of backstory to patients that might develop psychogenic nonepileptic seizures. These tics were popularized, for lack of a better term, via social media during the Covid-19 pandemic. One article is out there that even has called these functional ticlike behaviors as “a pandemic within a pandemic”, because there was such a strong showing of ticlike behavior in the clinics during the Covid-19 pandemic. Although social media was thought to play a big role in these functional ticlike behaviors, we think that there's probably a little bit more complexity and nuance to why these functional ticlike behaviors develop. There is probably a little bit of a genetic predisposition. There's probably some other psychosocial factors at play. And when we see cases like this, the best thing that you can do is educate your patients about the differences between functional ticlike behaviors and tics that we see associated with conditions like Tourette syndrome. And then the best types of treatments that we have seen thus far are treating any underlying stressors, if any of those exist, as well as cognitive behavioral therapy has been shown to be somewhat helpful. As the Covid-19 pandemic has wound down, we have actually seen a lot less cases in our clinic. And one reason we think is less stressors, less uncertainty for the future, which we think was a driving precipitant of some of these cases. But it also is not as popularized in the media as well. There were a lot of TikTok users in particular, which lent itself to the name “TikTok tic”. These videos are not as viewed or not as popular as they were during the Covid-19 pandemic. One reason being that because we are not all relegated to our homes, constantly looking to online sources of information---just in general, we have kind of not been on the Internet as much as we were during the Covid-19 pandemic---as a society as a whole. Dr Albin: This is really fascinating how the environmental milieu, for lack of a better word, like, really influenced how patients were experiencing, sort of, functional neurologic disorders. In your article you describe really these three baskets of primary tic---which can then be a part of Tourette syndrome---,functional ticlike behaviors---which really were a unique manifestation of stress and anxiety specifically during the Covid-19 pandemic---, and then tics as a manifestation of some either different underlying etiology or medication side effect. So, when do you get concerned about that secondary etiology? Dr Frey: So secondary tics can occur in a variety of instances. I think some of the more common examples would be in genetic disorders. So, Huntington's disease is a really good example. I think we all associate chorea with Huntington's disease. That's probably the most commonly associated phenomenology that we see with Huntington's disease. But we can see a variety of movement disorders in Huntington's, and one of them is tics. So, when we see tics in association with other types of movement disorders, we should be thinking about a possible genetic etiology. If we see tics in association with other neurologic symptoms, such as seizures or cognitive changes, we should be thinking that this is something besides a primary tic disorder. You also mentioned medication use, and it's really important to think about tardive tics. I know we often think about tardive dyskinesia, and the first kind of phenomenology that jumps into our brain is usually chorea because it's those abnormal lip movements, finger movements, toe movements that we see after a patient has been on, for example, an antipsychotic or an antiemetic that has antidopaminergic properties. However, we can see a variety of abnormal movement disorders that occur secondary to antidopaminergic medications, especially after abrupt withdrawal of these antidopaminergic medications. And tics are one of them. There have been cases reported where people that have tardive tics will still report that they have a premonitory urge, as well as a sense of relief after their tics. So, it actually can seem very similar to Tourette syndrome and the tics that people with Tourette syndrome experience on a regular basis. The key here is that the treatment might differ because if it's due to an antidopaminergic medication or abrupt withdrawal of that antidopaminergic medication, you might need to treat it a little bit differently than you would otherwise. Dr Albin: I love that you bring in, it's not just looking at their specific movement disorder that they may be coming to clinic with, that tic disorder, but are there other movement disorders? Has there been a change in their medication history? Have they had cognitive changes? So really emphasizing the importance of that complete and comprehensive neurologic history, neurologic physical exam, to really get the complete picture so that it's not honing in on, oh, this is a primary tic. That's all there is to it, because it could be so much more. I know we're getting close to sort of the end of our time together, but I really wanted to switch to end on talking about treatment. And your article does such a beautiful job of talking about behavioral interventions and really exciting new medical interventions. But I would like to, if you don't mind, have you focus on, what behavioral counseling and what education do you provide for patients and their families? Because I imagine that the neurologist plays a really important role in educating the patient and their family about these disorders. Dr Frey: Absolutely. When we think about treatment, one of the most important things you can do for patients with Tourette syndrome or other primary tic disorders is educate them. This remains true whether it's a primary tic disorder that we see in Tourette syndrome or the functional ticlike behavior that we've discussed here. A lot of times, because there is such a stigma against people with tic disorders and Tourette syndrome, when they hear that they have Tourette syndrome or they are diagnosed with that, sometimes that can be an upsetting diagnosis. And sometimes you have to take time explaining what exactly that means and debunking a lot of the myths that go along with the stigmas associated with Tourette syndrome. I think a lot of times people are under the false assumption that people with Tourette syndrome cannot lead normal lives and cannot hold down jobs and cannot be productive members of society. None of that is true. Most of my patients have great lives, good quality of life, and are able to go about their day-to-day life without any major issues. And one of the reasons for that is we do have a lot of great treatment options available. Another important stigma to break down is that people with tic disorders are doing this for attention or doing this because they are trying to get something from someone else. That is absolutely false. We do think that the tics themselves are semivolitional because people with Tourette syndrome have some degree of control over their tics. They can suppress them for a period of time. But a lot of people with tic disorders and Tourette syndrome will describe their tics as if you're trying to hold onto a sneeze. And you can imagine how uncomfortable it is to hold in a sneeze. We're all able to do it for a period of time, but it's much easier to just allow that sneeze to occur. And a lot of times that's what they are experiencing, too. So, although there is some degree of control, it's not complete control, and they're certainly not doing these tics on purpose or for attention. So that's another important myth to debunk when you're counseling patients and their families. I think the dynamic between young patients that are presenting with their parents or guardians, sometimes that dynamic is a little bit challenging because another faulty assumption is that parents feel they are responsible for having this happen to their child. There used to be a really strong sense that parents were responsible for the tics that occurred in their children, and that is also absolutely not true. Parenting has nothing to do with having the tics or not. We know that this is a neurodevelopmental disorder. The brain is indeed wired differently and it's important to counsel that with the parents, too, so that they understand what tools they need to be successful for their children as well. Dr Albin: I love that. So, it's a lot of partnership with patients and their families. I really like that this is just a wire different, and I hope over time that working together we as neurologists can help break down some of that stigmatization for these patients. This has been an absolutely phenomenal discussion. I have so enjoyed learning from your article. For the listeners out there, there are some really phenomenal tables that go into sort of how to approach this from the office perspective, how to approach it from the treatment perspective. So, thank you again, Dr Jessica Frey, for your article on Tourette syndrome and tic disorders, which appears in the August 2025 Continuum issue on movement disorders. 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 Frey: Thank you for having me. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use 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.

Ataxia is a neurologic symptom that refers to incoordination of voluntary movement, typically causing gait dysfunction and imbalance. Genetic testing and counseling can be used to identify the type of ataxia and to assess the risk for unaffected family members. In this episode, Katie Grouse, MD, FAAN, speaks with Theresa A. Zesiewicz, MD, FAAN, author of the article “Ataxia” in the Continuum® August 2025 Movement 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. Zesiewicz is a professor of neurology and director at the University of South Florida Ataxia Research Center, and the medical director at the University of South Florida Movement Disorders Neuromodulation Center at the University of South Florida and at the James A. Haley Veteran's Hospital in Tampa, Florida. Additional Resources Read the article: Ataxia 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 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 Grouse: This is Dr Katie Grouse. Today I'm interviewing Dr Theresa Zesiewicz about her article on ataxia, which appears in the August 2025 Continuum issue on movement disorders. Welcome to the podcast, and please introduce yourself to our audience.  Dr Zesiewicz: Well, thank you, Dr Grouse. I'm Dr Theresa Zesiewicz, otherwise known as Dr Z, and I'm happy to be here. Dr Grouse: I have to say, I really enjoyed reading your article. It was a really great refresher for myself as a general neurologist on the topic of ataxia and a really great reminder on a great framework to approach diagnosis and management. But I wanted to start off by asking what you feel is the key message that you hope our listeners will take away from reading your article. Dr Zesiewicz: Yes, so, thanks. I think one of the key messages is that there has been an explosion and renaissance of genetic testing in the past 10 years that has really revolutionized the field of ataxia and has made diagnosis easier for us, more manageable, and hopefully will lead to treatments in the future. So, I think that's a major step forward for our field in terms of genetic techniques over the last 10 years, and even over the last 30 years. There's just been so many diseases that have been identified genetically. So, I think that's a really important take-home message. The other take-home message is that the first drug to treat Friedreich's ataxia, called omaveloxolone, came about about two years ago. This was also a really landmark discovery. As you know, a lot of these ataxias are very difficult to treat. Dr Grouse: Now pivoting back to thinking about the approach to diagnosis of ataxia, how does the timeline of the onset of ataxia symptoms inform your approach? Dr Zesiewicz: The timeline is important because ataxia can be acute, subacute or chronic in nature. And the timeline is important because, if it's acute, it may mean that the ataxia took place over seconds to hours. This may mean a toxic problem or a hypoxic problem. Whereas a chronic ataxia can occur over many years, and that can inform more of a neurodegenerative or more of a genetic etiology. So, taking a very detailed history on the patient is very important. Sometimes I ask them, what is the last time you remember that you walked normal? And that can be a wedding, that can be a graduation. Just some timeline, some point, that the patient actually walked correctly before they remember having to hold onto a railing or taking extra steps to make sure that they didn't fall down, that they didn't have imbalance. That sometimes that's a good way to ask the patient when is the last time they had a problem. And they can help you to try to figure out how long these symptoms have been going on. Dr Grouse: I really appreciate that advice. I will say that I agree, it can sometimes be really hard to get patients to really think back to when they really started to notice something was different. So, I like the idea of referencing back to a big event that may be more memorable to them. Now, given that framework of, you know, thinking through the timeline, could you walk us through your approach to the evaluation of a patient who presents to your clinic with that balance difficulties once you've established that? Dr Zesiewicz: Sure. So, the first thing is to determine whether the patient truly has ataxia. So, do they have imbalance? Do they have a wide base gait? That's very important because patients come in frequently to your clinic and they'll have balance problems, but they can have knee issues or hip issues, neuropathy, something like that. And sometimes what we say to the residents and the students is, usually ataxia or cerebellar symptoms go together with other problems, like ocular problems are really common in cerebellar syndromes. Or dysmetria, pass pointing, speech disorder like dysarthria. So, not only do you need to look at the gait, but you should look at the other symptoms surrounding the gait to see if you think that the patient actually has a cerebellar syndrome. Or do they have something like a vestibular ataxia which would have more vertigo? Or do they have a sensory ataxia, which would occur if a person closes his eyes or has more ataxia when he or she is in the dark? So, you have to think about what you're looking at is the cerebellar syndrome. And then once we look to see if the patient truly has a cerebellar syndrome, then we look at the age, we look at---as you said before, the timeline. Is this acute, subacute, or chronic? And usually I think of ataxia as falling into three categories. It's either acquired, it's either hereditary, or it's neurodegenerative. It can be hereditary. And if it's not hereditary, is it acquired, or is it something like a multiple system atrophy or a parkinsonism or something like that? So, we try to put that together and start to narrow down on the diagnosis, thinking about those parameters. Dr Grouse: That's really a helpful way to think through it. And it is true, it can get very complex when patients come in with balance difficulties. There's so many things you need to think about, but that is a great way to think about it. Of course, we know that most people who come in to the Movements Disorders clinic are getting MRI scans of their brains. But I'm curious, in which cases of patients with cerebellar ataxia do you find the MRI to be particularly helpful in the diagnosis? Dr Zesiewicz: So, an MRI can be very important. Not always, but- so, something like multiple system atrophy type C where you may see a hot cross bun sign or a pontine hyperintensity on the T2-weighted image, that would be helpful. But of course, that doesn't make the diagnosis. It's something that may help you with the diagnosis. In FXTAS, which is fragile X tremor/ataxia syndrome, the patient may have the middle cerebellar peduncle sign or the symmetric hyperintensity in the middle cerebellar peduncles, which is often visible but not always. Something like Wernicke's, where you see an abnormality of the mammillary bodies. Wilson's disease, which is quite rare, T2-weighted image may show hyperintensities in the putamen in something like Wilson's disease. Those are the main MRI abnormalities, I think, with ataxia. And then we look at the cerebellum itself. I mean, that seems self-evident, but if you look at a sagittal section of the MRI and you see just a really significant atrophy of the cerebellum, that's going to help you determine whether you really have a cerebellar syndrome. Dr Grouse: That's really encouraging to hear a good message for all of us who sometimes feel like maybe we're missing something. It's good to know that information can always come up down the line to make things more clear. Your article does a great review of spinal cerebellar ataxia, but I found it interesting learning about the more recently described syndrome of SCA 27B. Would you mind telling us more about that and other really common forms of SCA that's good to keep in mind? Dr Zesiewicz: Sure. So, there are now 49 types of spinal cerebellar ataxia that have been identified. The most common are the polyglutamine repeat diseases: so, spinocerebellar ataxia type 3 or type 2, type 6, are probably the most common. One of the most recent spinocerebellar ataxias to be genetically identified and clinically identified is spinocerebellar ataxia 27B. This is caused by a GAA expansion repeat in the first intron of the fibroblast growth factor on chromosome 13. And the symptoms do include ataxia, eye problems, downbeat nystagmus, other nystagmus, vertical, and diplopia. It appears to be a more common form of adult-onset ataxia, and probably more common than was originally thought. It may account for a substantial number of ataxias, like, a substantial percentage of ataxias that we didn't know about. So, this was really a amazing discovery on SCA 27B. Dr Grouse: Now a lot of us I think feel a little anxious when we think about genetic testing for ataxia simply because there's so many forms, things are changing quickly. Do you have a rule of thumb or a kind of a framework that we can think of as we approach how we should be thinking about getting genetic testing for the subset of patients? Dr Zesiewicz: Sure. And I think that this is where age comes into play a lot. So, if you have a child who's 10, 11, or 12 who's having balance problems in the schoolyard, does not have a history of ataxia in the family, the teachers are telling you that the child is not running correctly, they're having problems with physical education, that is someone who you would think about testing for Friedreich's ataxia. A preteen or a child, that would be one thing that would be important to test. When you talk to your patient, it's important to really take a detailed family history. Not just mom or dad, but ethnicity, grandparents, etc. And sometimes, once in a while, you come up with a known spinal cerebellar ataxia. Then you can just test for that. So, if a person is from Portugal or has Portugal background and they have ataxia and the parents had ataxia, you would think of spinal cerebellar ataxia type 3. Or if they're Brazilian, or if the person is from a certain area of Cuba and mom and dad had ataxia and that person has ataxia, you would think of spinal cerebellar ataxia type 2. Or if a person has ataxia and their parent had blindness or visual problems, you may be more likely to think of spinal cerebellar ataxia type 7, for example. If they have that---either they have a known genetic cause in in the family, first degree family, or they come from an area of the world in which we can pinpoint what type we think it is---you can go ahead and get those tests. If not, you can take an ataxia comprehensive panel. Many times now, if you take the panel and the panel is negative, it will reflex to the whole exome gene sequencing, where we're finding really unusual and more rare types of ataxia, which are very interesting. Spinal cerebellar ataxia type 32, spinal cerebellar ataxia type 36, I had a spinal cerebellar ataxia type 15. So, I think you should start with the age, then the family history, then where the person is from. And then, if none of those work out, you can get a comprehensive panel, and then go on to whole exome gene sequencing. Dr Grouse: That's really, really useful. Thank you so much for breaking that down in a really simple way that a lot of us can take with us. Pivoting a little bit now back towards different types of acquired ataxias, what are some typical lab tests that you recommend for that type of workup? Dr Zesiewicz: Again, if there's no genetic history and the person does not appear to have a neurodegenerative disease, we do test for acquired ataxias. Acquired ataxias can be complex. Many times, they are in the autoimmune family. So, what we start with are just basic labs like a CBC or a CMP, but then we tried to look at some of the other abnormalities that could cause ataxia. So, celiac disease, stiff person syndrome. So, you would look at anti-glutamic acid decarboxylase antibodies, Hashimoto's---so, antithyroglobulin antibodies or antithyroperoxidase antibodies would be helpful. You know, in a case of where the patients may have an underlying neoplasm, maybe even a paraneoplastic workup, such as an anti-Hu, anti-Yo, anti-Ri. A person has breast cancer, for example, you may want to take a paraneoplastic panel. I've been getting more of the anti-autoimmune encephalitis panels in some cases, that were- that are very interesting. And then, you know, things that sometimes we forget now like the syphilis test, thyroid-stimulating test, take a B12 and folate, for example. That would be important. Those are some of the labs. We just have on our electronic chart a group of acquired labs for ataxia. If we can't find any other reason, we just go ahead and try to get those. Dr Grouse: Now, I'm curious what you think is the most challenging aspect of diagnosing a patient with cerebellar ataxia? Dr Zesiewicz: So, for those of us who see many of these patients a day, some of the hardest patients are the ones that---regardless of the workup that we do, we've narrowed it down, it's not hereditary. You know, they've been through the whole exome gene sequencing and we've done the acquired ataxia workup. It doesn't appear to be that. And then we've looked for parkinsonism and neurodegenerative diseases, and it doesn't appear to be that either; like, the alpha-synuclein will be negative. Those are the toughest patients, where we think we've done everything and we still don't have the answer. So, I've had patients in whom I've taken care of family members years and years ago, they had a presumed diagnosis, and later on I've seen their children or other family members. And with the advent of the genetic tests that we have, like whole exome gene sequencing, we have now been able to give the patient and the family a definitive diagnosis that they didn't have 25 years ago. So, I would say don't give up hope. Retesting is important, and as science continues and we get more information and we make more landmark discoveries in genetics, you may be better able to diagnose the patient. Dr Grouse: I was wondering if you had any recommendations regarding either some tips and tricks, some pearls of wisdom you can impart to us regarding the work of ataxia, or conversely, any big pitfalls that you can help us avoid? I would love to hear about it. Dr Zesiewicz: Yeah, there's no easy way to treat or diagnose ataxia patients. I've always felt that the more patients you see- and sounds easy, but the more patients you see, the better you're going to become at it, and eventually things are going to fall into place. You'll begin to see similarities in patients, etc. I think it's important not only to make sure that a person has ataxia, but again, look at the other signs and symptoms that may point to ataxia that you'll see in a cerebellar syndrome. I think it's important to do a full neuroexam. If a person has spasticity, that may point you more towards a certain type of ataxia than if a person has no reflexes, for example, that we see in Friedreich's ataxia. Some of the ocular findings are very interesting as well. It's important to know if a person has a tremor. I've seen several Wilson's disease cases in my life with ataxia. They're very important. I think a full neuroexam and also a very detailed history would be very helpful. Dr Grouse: Tell us about some promising developments in the diagnosis and management of ataxia that we should be on the lookout for. Dr Zesiewicz: The first drug for Friedreich's ataxia was FDA-approved two years ago, which was an NRF2 activator, which was extremely exciting and promising. There are also several medications that are now in front of the FDA that may also be very promising and have gone through long clinical trials. There's a medication that's related to riluzole, which is a medication used for amyotrophic lateral sclerosis, that has been through about seven years of testing. That is before the FDA as well for spinal cerebellar ataxia. Friedreich's ataxia has now completed the first cardiac gene therapy program with AAV vectors, which- we're waiting for full results, but that's a cardiac test. But I would assume that in the future, neurological gene therapy is not far behind if we've already done cardiac gene therapy and Friedreich's ataxia. So, you know, some of these AAV vector-based genetic therapies may be very helpful, as well as ASO, antisense oligonucleotides, for example. And I think in the future, other things to think about are the CRISPR/Cas9 technology for potential treatment of ataxia. It is a very exciting time, and some major promising therapies have been realized in the past 2 to 3 years. Dr Grouse: Well, that's really exciting, and we'll all look forward to seeing these becoming more clinically applicable in the future. So, thank you so much for coming to talk with us today. Dr Zesiewicz: Thank you. Dr Grouse: Again, today I've been interviewing Dr Theresa Zesiewicz about her article on ataxia, which appears in the August 2025 Continuum issue on movement 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, 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.

Chorea describes involuntary movements that are random, abrupt, and unpredictable, flowing from one body part to another. The most common cause of genetic chorea in adults is Huntington disease, which requires comprehensive, multidisciplinary care as well as support for care partners, who may themselves be diagnosed with the disease. In this episode, Aaron Berkowitz, MD, PhD FAAN speaks with Kathryn P. L. Moore, MD, MSc, author of the article “Huntington Disease and Chorea” in the Continuum® August 2025 Movement Disorders 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 in San Francisco, California. Dr. Moore is an assistant professor and director of the Parkinson's Disease and Movement Disorders Fellowship in the department of neurology at Duke University in Durham, North Carolina. Additional Resources Read the article: Huntington Disease and Chorea Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @AaronLBerkowitz Guest: @KatiePMooreMD 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 with Continuum Audio, and today I'm interviewing Dr Kathryn Moore about her article on diagnosis and management of Huntington disease and chorea, which appears in the August 2025 Continuum issue on movement disorders. Welcome to the podcast, Dr Moore. Could you please introduce yourself to our audience? Dr Moore: Yeah, thank you so much. I'm so excited to be here. I'm Dr Moore. I'm an assistant professor of neurology at Duke University, where I work as a movement disorder specialist. I run our fellowship there and help with our residency program as well. So, I'm excited to speak with our listeners about chorea today. Dr Berkowitz: Fantastic. And we're excited to talk to you about chorea. So, as a general neurologist myself, I only see chorea pretty rarely compared to other movement disorders like tremor, myoclonus, maybe the occasional tic disorder. And like anything I don't see very often, I always have to look up the differential diagnosis and how to evaluate a patient with chorea. So, I was so glad to read your article. And next time I see a patient with chorea, I know I'll be referring to your article as a great reference to have a framework for how to approach it. I hope our readers will look at all these helpful tables on differential diagnosis based on distribution of chorea in the body, potential etiologies, time course of onset and evolution, associated drug-induced causes, what tests to send. So, I highly recommend our listeners read the article. Keep those tables handy for when a patient comes in with chorea. I'm excited to pick your brain about some of these topics today. First, how do you go about distinguishing chorea from other hyperkinetic movement disorders when you see a patient that you think might have chorea? Dr Moore: One of the wonderful things about being a movement disorder specialist is we spend a lot of time looking at movements and training our brain to make these distinctions. The things that I would be looking out for chorea is involuntary, uncontrolled movements that appear to be brief and flowing from one part of the body to another. So, if you can watch a patient and predict what movements they're going to do, this probably isn't chorea. And it should be flowing from one part of the body to another. So, not staying just in one part of the body or having sustained movements. It can be difficult to distinguish between a tic or dystonia or myoclonus. Those things tend to be more predictable and repetitive than the chorea, which tends to be really random and can look like dancing. Dr Berkowitz: That's very helpful. So, once you've decided the patient has chorea, what's your framework for thinking about the differential diagnosis of the cause of the patient's chorea? Dr Moore: Well, that could be really challenging. The differential for chorea is very broad, and so the two things that I tend to use are age of the patient and acuity of onset. And so, if you're thinking about acute onset of chorea, you're really looking at a structural lesion like a stroke or a systemic issue like infection, hyperglycemia, etc. Where a gradually progressive chorea tends to be genetic in nature. When you're thinking about the difference between a child and an adult, the most common cause of chorea in a child is Sydenham's chorea. And actually, the most common cause of chorea that I tend to see is Parkinson's disease medication. So, if anybody's seen dyskinesia in Parkinson's disease, you've seen chorea. But it's those two things that I'm using, the age of the patient and the acuity. Somewhere in the middle, though---so, if you have subacute onset of chorea---it's important to remember to think about autoimmune conditions or paraneoplastic conditions because these are treatable. Dr Berkowitz: That's very helpful. So, like in any chief concern in neurology, we're using the context like the age and then the time course. And then a number of other helpful points in your article about the distribution of chorea in the body. Any comments you'd like to make about- we have this very helpful table that I thought was very interesting. So, you really get deep into the nuances of chorea and the movement disorder specialist expert level. Are there any aspects of parts of the body affected by chorea or distribution of chorea across the body that help you hone your differential diagnosis? Dr Moore: Certainly. I think where the chorea is located in the body can be helpful, but not as helpful as other conditions where you're localizing a lesion or that sort of thing. Because you can have a systemic cause of chorea that causes a hemichorea; that you can have hyperglycemia causing a hemichorea, or even Sydenham's chorea being a hemichorea. But things that we think about, if the forehead is involved, I would think about Huntington's disease, although this is not pathognomonic. And if it's involving the face or the mouth, you can think about neuroacanthocytosis or, more commonly, tardive dyskinesia. Hemichorea would make me think about some of those systemic issues like hyperglycemia, Sydenham's chorea, those sorts of things, but I would rely more on the historical context and the acuity of presentation than the distribution itself. Dr Berkowitz: Got it. That's very helpful. So those can be helpful features, but not sort of specific for any particular condition. Dr Moore: Exactly. Dr Berkowitz: Yeah, I often see forehead chorea mentioned as sort of specific to Huntington's disease. Since I don't see much Huntington's disease myself, what does forehead chorea look like? What is the forehead doing? How do you recognize that there is chorea of the forehead? It's just sort of hard for me to imagine what it would look like. Dr Moore: It's really tricky. I think seeing the eyebrows go up and down or the brows furrow in an unpredictable way is really what we're looking for. And that can be hard if you're having a conversation. My forehead is certainly animated as we're talking about one of my favorite topics here. One of the tricks that I use with the fellows is to observe the forehead from the side, and there you can see the undulation of the forehead muscles. And that can be helpful as you're looking for these things. I think where it's most helpful to use the forehead is if you're trying to determine if someone with a psychiatric history has tardive dyskinesia or Huntington's disease, because there can be quite a lot of overlap there. And unfortunately, patients can have both conditions. And so, using the forehead movement can be helpful to maybe direct further testing for Huntington's disease. Dr Berkowitz: Oh, wow, that's a very helpful pearl. So, if you see, sort of, diffuse chorea throughout the body and the forehead is involved, to my understanding it may be less specific. But in the context of wondering, is the neuropsychiatric condition and movement disorder related by an underlying cause in the case of seeing orofacial dyskinesias, is the relationship a drug having caused a tardive dyskinesia or is the whole underlying process Huntington's, the absence of forehead might push you a little more towards tardive dyskinesia, presuming there is an appropriate implicated drug and the presence of forehead chorea would really clue you in more to Huntington's. Did I understand that pearl? Dr Moore: That's exactly right, and I'm glad you brought up the point about making sure, if you're considering tardive dyskinesia, that there has been an appropriate drug exposure. Because without that you can't make that diagnosis. Dr Berkowitz: That's a very helpful and interesting pearl, looking at the forehead from the side. That is a movement disorders pearl for sure. Sort of not just looking at the forehead from one angle and trying to figure out what it's doing, but going to look at the patient in profile and trying to sort it out. I love that. Okay. So, based on the differential diagnosis you would have crafted based on whether this is sort of acute, subacute, chronic, the age of the patient, whether it's unilateral, bilateral, which parts of the body. How do you go about the initial evaluation in terms of laboratory testing, imaging, etc.? Dr Moore: Well, certainly in an acute-onset patient, you're going to get a number of labs---and that's listed out for you in the paper---and consider imaging as well, looking for an infarct. One thing our learners will know is that sort of the typical answer to what's the infarct causing hemichorea would be the subthalamic nucleus. But really, those infarcts can be almost anywhere. There are case reports for infarcts in a wide variety of places in the brain leading to hemichorea. So, I think some general blood work and an MRI of the brain is a good place to start. For someone who has a more chronic course of the development of chorea, there are certain labs that I would get---and an MRI, because if you get an MRI and there's heavy metal deposition or other disease, structurally, that indicates a certain condition, that can help you pretty considerably. But otherwise, I'm looking for inflammatory markers, heavy metals, HIV, some general other things that are outlined, to help make sure that I'm not missing something that's treatable before I go down the route of genetic testing. And we may talk about this in a little bit, but if you start out with genetic testing and then you sort of have to back up and do more systemic testing, that can be very disjointed when it comes to good patient care. Dr Berkowitz: That's very helpful. So yeah, if it's acute, obviously this is the most straightforward scenario, acute and unilateral. We're imagining something lesional, as you said, either a stroke or---not sort of sudden, but fast, but not sudden---you might think of another structural lesion. Toxoplasmosis, right, has an affinity for the basal ganglia if you were seeing this in a patient who is immunocompromised. But in a case that, probably as you alluded to, sort of what we would see most commonly in practice, those still relatively rare, sort of subacute to chronic symmetric chorea. There's a long list of tests that are recommended. In your article and in other texts, I've read lupus testing, anti-phospholipid antibodies… but the list is long. I'll refer readers to your article. Out of curiosity as a specialist, how often do you see any of these labs come back revealing any underlying diagnosis in a patient who's otherwise healthy and just has developed chorea and comes to you with that chief concern? I feel like I've sent that mega-workup a few times; I'm obviously a general neurologist, but not nearly as many times as you have been. It's- I can't remember a time where something has come up, maybe an ANA one to forty or something like this that we don't think is relevant. But in your practice, how often do you end up finding a reversible cause in the laboratory testing versus ending up starting to go down the genetic testing route, which we'll talk about in a moment? Dr Moore: It's not common, but it is important that we capture these things. Because for a lot of those laboratory tests, there are treatments that are available, or other health implications if those come back positive. So, the case I think of is a polycythemia vera patient who had diffused subacute onset chorea and was able to be treated, was temporarily managed with medication for her chorea, and as her PV improved, she was able to come off those medications. As I was alluding to before---and I'm sure we'll talk about genetic testing---if you test for HD and it's negative, do you go down the route of additional expensive genetic testing, or do you then circle back and go, oops, I missed this treatable condition? As we talk about genetic testing as well, getting HD testing is a pretty involved process. And so, we want to make sure we are checking all those boxes before we move forward. So, it's not common, but we do catch some treatable conditions, and that's really important not to miss. Dr Berkowitz: That's very interesting. So, you diagnosed that polycythemia vera by blood smear, is that how you make the diagnosis? Dr Moore: Yes. Dr Berkowitz: And is that a once-in-a-career-so-far type of thing, or does that happen time to time? Dr Moore: For me, that's a once-so-far, but I don't doubt that I'll see it again. Dr Berkowitz: Great. And how about lupus and some of these other things we look for in the absence of other systemic features? Have you picked up any of these or heard of colleagues picking up something on laboratory testing? They said, oh, this patient came in for a referral for genetic testing, negative Huntington's disease. And good news, we found polycythemia vera; good news, we found undiagnosed lupus and we reversed it. I'm just curious, epidemiologically, seeing these long lists and not having the subspecialty practice that you do, how often you find a reversible cause like we do for neuropathy all the time, right? Oh, it's diabetes, it's B12---maybe not reversible, but preventing progression---or reversible dementia work up. You get so excited when you find low B12 and you replete the patient's B12, and they get better when they had been concerned they were developing an irreversible condition. How often does one in your subspecialty find a reversible cause on that initial mega-lab screen? Dr Moore: I think it's really uncommon, and maybe the folks that do are caught by someone else that never make it to Huntington's clinic, but I don't tend to see those cases. There are, of course, case reports and well-described in the literature about lupus and movement disorders and things of that nature, but that doesn't come to our clinic on a regular basis for sure. Dr Berkowitz: Got it. That's helpful to hear. Well, we've alluded to genetic testing a number of times now, so let's go ahead and talk about it. A lot of your article focuses on Huntington disease, and I was thinking about---in the course of our medical training in medical school, and then neurology residency, for those of us who don't become movement disorder experts like yourself---we learn a lot about Huntington disease. That's sort of the disease that causes chorea, until we later learned there are a whole number of diseases, not just the reversible causes we've been talking about, but a number of genetic diseases which you expertly reviewing your article. So, what are some of the red flags that suggest to you that a patient with chronically progressive chorea---and whom you're concerned for Huntington's or another genetic cause---what are some things you notice about the history, about the exam, the symptoms, the signs, the syndrome, that suggest to you that, actually, this one looks like it might not turn out to be HD. I think this patient might have something else. And as you have alluded to, how do you approach this? Do you send HD testing, wait for it to come back, and then go forward? Are there genetic panels for certain genetic causes of chorea? Do you skip just a whole exome sequencing, or will you miss some of the trinucleotide repeat conditions? How do you approach this in practice? Dr Moore: I'll try to tackle all that. One thing I will say is that a lot of patients with chorea, regardless of the cause, can look very similar to one another. So, if you're looking at chronic onset chorea, perhaps with some neuropsychiatric features, I'm going to most often think about HD because that's the most common cause. Certainly, as we mentioned before, if there's a lot of tongue protrusion, I would think about the acanthocytic conditions, neurocanthocytosis and McCloud syndrome. But generally in those conditions, we're looking at HD as the most likely cause. Certainly, if there is epilepsy or some other syndromic types of things going on, I may think more broadly. But it's important to know that while HD, as you mentioned, is the cause of chorea, many of our patients will have parkinsonism, tics, dystonia, a whole host of other movement phenomenologies. So, that wouldn't dissuade me from thinking about HD. When we think about the kind of patients that you're describing, upwards of 95% of those people will have Huntington's disease. And the process for genetic testing is fairly involved. The Huntington's Disease Society of America has organized a set of recommendations for providers to go about the process of genetic testing in a safe and supportive way for patients and their families. And so that's referred to in the article because it really is important and was devised by patients and families that are affected by this disease. And so, when we're thinking about genetic testing for HD, if I reveal that you have HD, this potentially affects your children and your parents and your siblings. You can have a lot of implications for the lives and health and finances of your family members. We also know that there is high suicidality in patients with HD, in patients who are at risk for HD; and there's even a higher risk of suicidality in patients who are at risk but test negative for HD. So, we do recommend a supportive environment for these patients and their families. And so, for presymptomatic patients or patients who are at risk and don't have chorea, this involves making sure we have, sort of, our ducks in a row, as it were, when we think about life insurance, and, do you have somebody supportive to be with you through this journey of genetic testing, no matter what the results are? So, oftentimes I'll say to folks, you know, there's this 20-page policy that I encourage you to look at, but there are Huntington's Disease Centers of Excellence across the country that are happy to help you with that process, to make sure that the patients are well supported. This is an individual genetic test because, as you mentioned, it is a CAG repeat disorder. And unfortunately, there is no chorea panel. So, if an HD test comes back negative, what we'll do then is think about what's called the HD phenocopies. As I mentioned before, some of these patients who look like they have HD will have a negative HD test. And so, what do you do then? Well, there's a handful of phenocopies---so, other genetic mutations that cause a very similar presentation. And so, we try to be smart, since there's not a panel, we try to be smart about how we choose which test to do next. So, for instance, there's a condition called DRPLA that is present in an African-American family here in my area, in North Carolina, as well as in Japan. And so, if someone comes from those backgrounds, we may decide that that's the next test that we're going to do. If they are white European descent, we may consider a different genetic test; or if they're sub-Saharan African, we may choose a different one from that. However, even if you do a really thorough job, all those blood tests, all those genetic tests, you will occasionally get patients that you can't find a diagnosis for. And so, it's important to know even when you do a good job, you may still not find the answer. And so, I think trying to do things with this complex of the presentation in a systematic way for yourself so you're not missing something. So, going back to our answer about, how do I look at lupus and polycythemia vera and all of that, to think about it in a systematic way. That when you get to the end and you say, well, I don't have an answer, you know you've tried. Dr Berkowitz: That's very helpful to hear your approach to these challenging scenarios, and also how to approach the potential challenging diagnosis for patients and their families getting this diagnosis, particularly in the presymptomatic phase. And your article touches on this with a lot of nuance and thoughtfulness. So, I encourage our listeners to have a read of that section as well. So, last here, just briefly in our final moments, you discuss in your article the various symptomatic treatments for chorea. We won't have time to go into all the details of all the many treatments you discussed, but just briefly, how do you decide which medication to start in an individual patient with chorea for symptomatic management? What are some of the considerations related to the underlying condition, potential side effect profiles of the particular medications, or any other considerations just broadly, generally, as you think about choosing one of the many medications that can be used to treat chorea? Dr Moore: Certainly. So, there is a group of FDA-approved medications, VMAT2 inhibitors, that we can choose from, or the off-label use of neuroleptics. And so, there's a lot of things that go into that. Some of that is insurance and cost and that sort of thing, and that can play a role. Others are side effects. So, for the VMAT2 inhibitors, they all do have a black box warning from the FDA about suicidality. And so, if a patient does struggle with mental health, has a history of suicidality, psychiatric admissions for that sort of thing, then I would be more cautious about using that medication. All patients are counseled about that, as are their families, to help us give them good support. So, the neuroleptics do not tend to have that side effect and can help with mood as well as the chorea and can be helpful in that way. And some of them, of course, will have beneficial side effects. So, olanzapine may help with appetite, which can be important in this disease. So, the big considerations would be the black box warning and suicidality, as well as, are we trying to just treat chorea or are we treating chorea and neuropsychiatric issues? Dr Berkowitz: Fantastic. Thank you for that overview. And again, for our listeners, there's a lot more detail about all of these medications, how they work, how they're used in different patient populations, their side effects, etc, to be reviewed in your excellent article. Again, today, I've been interviewing Dr Kathryn Moore about her article on diagnosis and management of Huntington's disease in chorea, which appears in the August 2025 Continuum issue on movement disorders. Be sure to check out Continuum Audio episodes from this and other issues. And thank you so much to our listeners for joining today. And thank you again, Dr Moore. Dr Moore: Thanks for having me. Dr Monteith: This is Dr Teshamae Monteith, associate editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use 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.

The first updated Footprints article requires two guests to do it justice - Dr Dakota Peacock and Dr Darius Ebrahimi-Fakhari join Eva Morava to discuss movement disorders in Inherited Metabolic Disease. Read the referenced paper here: https://doi.org/10.1016/j.ymgme.2025.109084 Find IMDs associated with psychiatric presentations at: https://www.iembase.org/gamuts/store/docs/Movement_disorders_update.pdf

We are discussing perspective changes in neurology genetics with the crossover of the APOE gene in neuro and cardio as well as telehealth for neurology predictive testing. Segment 1: Is it time for a paradigm shift? Inclusion of APOE  on genetic dyslipidemia panels.   Emily Brown is a certified genetic counselor at the Center for Inherited Heart Disease at Johns Hopkins Hospital. She graduated from the University of Maryland Genetic Counseling Program in 2014 and has practiced in cardiology for the past 10 years. Her main areas of interest include dyslipidemias, and she is a member of the National Lipid Association.   Hannah Ison is a cardiovascular genetic counselor at the Stanford Center for Inherited Cardiovascular Disease. She received her Master's in Medical and Molecular Genetics from Indiana University in 2018, and returned home to California to begin her career. Her primary clinical interest includes working with patients who have inherited lipid conditions in both the adult and pediatric setting. A large part of her role has been focused on developing a Pediatric Lipid Clinic at the Stanford Children's Hospital, allowing her to care for patients across the generations. Hannah was the co-chair of the Dyslipidemia Working Group through the cardiovascular SIG from 2020-2024 where she worked with members to develop dyslipidemia resources. In addition to her work in the lipid space, she also provides inpatient and outpatient genetic counseling to patients with isolated congenital heart disease, and enjoys participating in various research opportunities.    In this segment we discuss: - APOE's relevance in both Alzheimer's and cardiovascular disease - Counseling strategies for APOE alleles (ε2, ε3, and ε4), including penetrance, lifestyle modification, and exploration of risk for conditions and symptoms external to Alzheimer's - Case studies highlighting APOE's diagnostic, variant, and treatment insights - The need for standardization, education, and reframing of APOE testing in practice Segment 2: Patient-reported outcomes for remote and in-person visits for genetic counseling in adult neurology.   Rachel A. Paul, MS, CGC and Laynie Dratch, ScM, CGC are board-certified genetic counselors who specialize in adult neurogenetics and work with the Penn Neurogenetics Therapy Center team in Philadelphia, PA (https://www.linkedin.com/company/penn-neurogenetics-therapy-center).   Rachel provides clinical and research genetic counseling services for the Division of Movement Disorders at the University of Pennsylvania. Her research interests include genetic screening for clinical trials access, remote/telemedicine genetic services, and motivations/barriers for genetics utilization. She graduated cum laude from Temple University in Philadelphia, previously worked as a genetic counseling assistant (GCA) for the Penn neurogenetics program, and completed her training with the Arcadia University (now University of Pennsylvania) Genetic Counseling Program.   Laynie's clinical focus includes frontotemporal degeneration (FTD) spectrum disorders, amyotrophic lateral sclerosis (ALS), and other neurodegenerative conditions. Her research interests include the lived experiences of at-risk individuals, predictive genetic testing considerations, and genetic counseling access and service delivery. She graduated summa cum laude from Colgate University with a BA in neuroscience and a minor in psychology, and completed her genetic counseling masters training at the Johns Hopkins University and the National Institutes of Health.   In this segment we discuss: - How COVID-19 pushed neurogenetics counseling from in-person to telehealth. - Why patient satisfaction stayed high across both formats, with video outperforming phone. - What drives visit preferences—travel, tech comfort, privacy, and clinical needs. - Future research to refine protocols, improve access, and explore broader applications.   Would you like to nominate a JoGC article to be featured in the show? If so, please fill out this nomination submission form here. Multiple entries are encouraged including articles where you, your colleagues, or your friends are authors.   Stay tuned for the next new episode of DNA Dialogues! In the meantime, listen to all our episodes Apple Podcasts, Spotify, streaming on the website, or any other podcast player by searching, “DNA Dialogues”.    For more information about this episode visit dnadialogues.podbean.com, where you can also stream all episodes of the show. Check out the Journal of Genetic Counseling here for articles featured in this episode and others.    Any questions, episode ideas, guest pitches, or comments can be sent into DNADialoguesPodcast@gmail.com.    DNA Dialogues' team includes Jehannine Austin, Naomi Wagner, Khalida Liaquat, Kate Wilson and DNA Today's Kira Dineen. Our logo was designed by Ashlyn Enokian. Our current intern is Stephanie Schofield.

Progressive supranuclear palsy and corticobasal syndrome are closely related neurodegenerative disorders that present with progressive parkinsonism and multiple other features that overlap clinically and neuropathologically. Early recognition is critical to provide appropriate treatment and supportive care. In this episode, Teshamae Monteith, MD, FAAN speaks with Nikolaus R. McFarland, MD, PhD, FAAN, author of the article “Progressive Supranuclear Palsy and Corticobasal Syndrome” in the Continuum® August 2025 Movement Disorders issue. Dr. Monteith is the associate editor of Continuum® Audio and an associate professor of clinical neurology at the University of Miami Miller School of Medicine in Miami, Florida. Dr. McFarland is an associate professor of neurology at the University of Florida College of Medicine at the Norman Fixel Institute for Neurological Diseases in Gainesville, Florida. Additional Resources  Read the article: Progressive Supranuclear Palsy and Corticobasal Syndrome Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @headacheMD 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 Monteith: Hi, this is Dr Teshamae Monteith. Today I'm interviewing Dr Nikolaus McFarland about his article on progressive supranuclear palsy and cortical basilar syndrome, which appears in the August 2025 Continuum issue on movement disorders. Welcome, how are you? Dr Farland: I'm great. Thank you for inviting me to do this. This is a great opportunity. I had fun putting this article together, and it's part of my passion. Dr Monteith: Yes, I know that. You sit on the board with me in the Florida Society of Neurology and I've seen your lectures. You're very passionate about this. And so why don't you first start off with introducing yourself, and then tell us just a little bit about what got you interested in this field. Dr Farland: I'm Dr Nicholas McFarlane. I'm an associate professor at the University of Florida, and I work at the Norman Fixel Institute for Neurological Diseases. I am a director of a number of different centers. So, I actually direct the cure PSP Center of Care and the MSA Center of Excellence at the University of Florida; I also direct the Huntington's clinic there as well. But for many years my focus has been on atypical parkinsonisms. And, you know, I've treated these patients for years, and one of my focuses is actually these patients who suffer from progressive supranuclear palsy and corticobasal syndrome. So that's kind of what this review is all about. Dr Monteith: You probably were born excited, but I want to know what got you interested in this in particular? Dr Farland: So, what got me interested in this in particular was really the disease and the challenges that's involved in it. So, Parkinson's disease is pretty common, and we see a lot of that in our clinic. Yet many times, roughly about 10 to 15% of my patients present with these atypical disorders. And they're quite fascinating. They present in different ways. They're fairly uncommon. They're complex disorders that progress fairly rapidly, and they have multiple different features. They're sort of exciting to see clinically as a neurologist. I think they're really interesting from an academic standpoint, but also in the standpoint of really trying to bring together sort of a team. We have built a multidisciplinary team here at the University of Florida to take care of these patients. They require a number of folks on that team to take care of them. And so, what's exciting, really, is the challenge of treating these patients. There are very limited numbers of therapies that are available, and the current therapies that we have often really aren't great and over time they fail. And so, part of the challenge is actually doing research. And so, there's actually a lot of new research that's been going on in this field. Recently, there's been some revisions to the clinical criteria to help diagnose these disorders. So, that's really what's exciting. The field is really moving forward fairly rapidly with a number of new diagnostics, therapeutics coming out. And hopefully we can make a real difference for these patients. And so that's what really got me into this field, the challenge of trying to treat these patients, help them, advocate for them and make them better. Dr Monteith: And so, tell me what the essential points of this article. Dr Farland: So, the essential points, really, of this article is: number one, you know, just to recognize the new clinical criteria for both PSP and corticobasal syndrome, the diagnosis for these disorders or the phenotypic spectrum has really expanded over the years. So, we now recognize many different phenotypes of these disorders, and the diagnosis has gotten fairly complicated. And so, one of the goals of this article was to review those new diagnostic criteria and the different phenotypic ways these diseases present. I wanted to discuss, also, some of the neuropathology and clinicopathological overlap that's occurred in these diseases as well as some of the new diagnostic tests that are available. That's definitely growing. Some of the new studies that are out, in terms of research and clinical trials. And then wanted to review some of the approaches for treatment for neurologists. Particularly, we're hoping that, you know, this article educates folks. If you're a general neurologist, we're hoping that recognizing these diseases early on will prompt you to refer these patients to specialty clinics or movement disorder specialists early on so they can get appropriate care, confirm your diagnosis, as well as get them involved in trials if they are available. Dr Monteith: And how has the clinical criteria for PSP and cortical basilar syndrome changed? Dr Farland: I think I already mentioned there's been an evolution of the clinical criteria for PSP. There's new diagnostic criteria that were recently published, and it recognizes the multiple clinical phenotypes and the spectrum of the disease that's out there, which is much broader than we thought about. Corticobasal clinical criteria are the Dr Armstrong criteria from 2013. They have not been updated, but they are in the works of being updated. But it does recognize the classic presentation of corticobasal syndrome, plus a frontal executive predominant and then a variant that actually overlaps with PSP. So, there's a lot more overlap in these two diseases than we originally recognized. Dr Monteith: And so, you spoke a bit about FTD spectrum. So why don't you tell us a little bit about what that is? I know you mentioned multiple phenotypes. Dr Farland: What I really want to say is that both PSP and corticobasal syndrome, they're relatively rare, and what- sort of as to common features, they both are progressive Parkinson disorders, but they have variable features. While they're commonly associated with Parkinson's, they also fit within this frontotemporal lobar spectrum, having features that overlap both clinically and neuropathologically. I just want folks to understand that overlap. One of this pathological overlap here is the predominant Tau pathology in the brain, an increasing recognology- recognition of sort of the pathological heterogeneity within these disorders. So, there's an initial description, a classic of PSP, as Richardson syndrome. But now we recognize there are lots of different features to it and there are different ways it presents, and there's definitely a lot of clinical pathological overlap. Dr Monteith: Why don't we just talk about some red flags for PSP? Dr Farland: Yeah, sure. So, some of the red flags for PSP and even corticobasal syndrome are: number one is rapid progression with early onset of falls, gait difficulty, falling typically backwards, early speech and swallow problems that are more prominent than you see in Parkinson's disease, as well as eye gaze issues. So, ocular motor features, particularly vertical gaze palsy. In particular what we talk about is the supranuclear gaze palsy, and one of the most sensitive features that we've seen with these is downgaze limitation or slowed downgaze, and eventually a full vertical gaze palsy and followed supranuclear gaze palsy. So, there's some of the red flags that we see. So, while we think about the lack of response to levodopa frequently as something that's a red flag for Parkinson's, there are many times that we see Parkinson's patients, and about a quarter of them don't really respond. There's some features that don't respond to levodopa that may not be so specific, but also can be helpful in this disease. Dr Monteith: And what about the red flags for cortical basilar syndrome? Dr Farland: So, for cortical basilar syndrome, some of the red flags again are this rapidly depressive syndrome tends to be, at least in its classical present presentation, more asymmetric in its presentation of parkinsonism, with features including things like dystonic features, okay? For limb dystonia and apraxias---so, inability to do a learned behavior. One of those red flags is a patient who comes in and says, my hand doesn't work anymore, which is something extremely uncommon that you hear in Parkinson's disease. Most of those patients will present, say, I might have a tremor, but they very rarely will tell you that I can't use my hand. So look out for that sign. Dr Monteith: And let's talk a little bit about some of the advances in the fields you mentioned, evolving biomarker and imaging capacities. So, how are these advances useful in helping us understand these conditions, especially when there's so much heterogeneity? Dr Farland: I might start by talking a little bit about some of the clinical criteria that have advanced. Why don't we start there and just discuss some of the advances? I think in PSP, I think, originally we had both probable and possible diagnoses of PSP, and the diagnostic criteria were basically focused on what was what's called “classical PSP” or “Richardson syndrome”. But now we recognize that there are multiple phenotypes. There's an overlap with Parkinsonism that's slower in progression and morphs into PSP, the classical form. There's a frontal behavioral variant where patients present with that frontal behavioral kind of thing. There's a speech-language variant that can overlap with PSP. So they have prominent speech language, potentially even apraxia speech. So, recognition of these different phenotypes is sort of a new thing in this field. There's even overlap with cortical basal syndrome and PSP, and we note that the pathology can overlap as well. So, I think that's one of the things that have changed over time. And these were- recently came out in 2017 in a new publication in the Movement Disorders Society. So, in terms of diagnostic tests as well---and there's been quite a bit of evolution---really still to date, our best diagnostic test is imaging. MRI is really one of our best tests currently. Currently blood tests, spinal fluid, there's new biomarkers in terms of skin… they're still in the research phase and not necessarily very specific yet. So, we rely heavily on imaging still; and for PSP, what we're looking for largely are changes in the brain stem, and particularly focused on the midbrain. So disproportionate midbrain atrophy compared to the pons and the rest of the midbrain is a fairly specific intensive sign for PSP. Whereas in MSA we see more of a pontine atrophy compared to the midbrain. So that can be really helpful, and there are lots of different new measurements that can be done. PET scans are also being used as well. And there are new PET markers, but they still remain kind of research-based, but are becoming more and more prevalent and may be available soon for potential use. Although there's some overlap with PET tracers with Alzheimer's disease and different Tau isoforms. So, something to be wary about, but we will be seeing some of these soon coming out as well. More kind of up-to-date things include things like the spinal fluid as well as even some of the skin biopsies. And I think we've heard some word of recent studies that have come out that potentially in the very near future we might actually have some Tau protein tests that we can look at Tau either in spinal fluid or even in a skin biopsy. But again, still remains research-based and, we still need more information as to whether these tests can be reproducible and how sensitive or specific they are. Dr Monteith: It sounds like, when really approaching these patients, still, it's a lot of back to the history, back to the clinical and some basic imaging that we should be able to identify to distinguish these types of patients, and we're not quite where we need to be yet for biomarker. Dr Farland: I totally agree with you. I think it starts, really, with the clinical exam and that's our main focus here; and understanding some of the new clinical criteria which are more sensitive, but also specific, too. And they're really useful to look at. So, I think reviewing those; patients do progress, following them over time can be really useful. And then for diagnosis, getting imaging if you suspect a patient has an atypical presentation of parkinsonism, to look for signs or features that might be specific for these different disorders. Dr Monteith: Why don't we take a typical case, a typical patient that you would see in clinic, and walk us through the thought process---especially, maybe they presented somewhat early---and the different treatment approaches to helping the patient, and of course their family. Dr Farland: Yeah, sure. So, a typical patient might be someone who comes in with, like, a three year history of progressive gait problems and falling. And let's say the patient says, I'm falling backwards frequently. They may have had, like, a rib fracture, or they hit their head once, and they're describing some speech issues as well. Now they're relying on a walker and family members saying they rarely let them be by themselves. And there may be some slowing of their cognitive function and maybe a bit of withdrawal. So that's a typical patient. So, the approach here is really, what are some of the red flags? I think already you hear a red flag of a rapidly progressive disease. So, Parkinson's disease patients rarely have frequent falls within the first five years. So, this is within three years or less. You're already hearing early onset of gait problems and falling, and particularly falling backwards rather than forwards as often Parkinson's disease patients do. You're hearing early speech problems and maybe a subtle hint of cognitive slowing and some withdrawal. So, a lot of things that sort of are red flags. So, our approach really would be examining this patient really closely. Okay? We'd be listening to the history, looking at the patient. One thing is that some of these patients come in, they may be in a wheelchair already. That's a red flag for us. If they're wearing sunglasses---sometimes we see that patients, they have photosensitivity and they're in a chair and they're wearing sunglasses---you take the glasses off and you look at their face and they have that sort of a facial stare to them---not just the masked face, but the stare---and their eyes really aren't moving. So, another kind of clue, maybe this is probably something atypical, particularly PSP is what I'm thinking about. So, the approach is really, do a thorough exam. I always recommend looking at eye movements and starting with volitional saccades, not giving them a target necessarily, but asking them to look up and then look down. And then particularly look at the speed of downgaze and whether they actually have full versions down, are able to do that. That's probably your most sensitive test for a patient who has PSP. Not the upgaze, which can be- upgaze impairment in older patients can be nonspecific. So, look for that down gaze. So, if I can get out one message, that's one thing that can be easily done and examined fairly quickly for diagnosis of these patients. And then just look for signs of rigidity, bradykinesia, maybe even some myelopraxia, and then look at their gait carefully so that there's a high suspicion. Again, if there's some atypical features, imaging is really important. So, my next step would be probably getting an MRI to evaluate whether- do they have brain somatrophy or other widespread atrophy or other signs? You need to think about your differential diagnosis for some of these patients as well. So, common things are common; vascular disease, you can't have vascular parkinsonism or even signs of NPH. Both of those can present with progressive gait difficulty and falls. So, the gait may look more like Parkinson's rather than ataxic gait that we see in classic PSP, but still they have early gait issues, and that can be a mimicker of PSP, So looking for both of those things in your imaging. Think about sort of autoimmune potentially causes. So, if they have a really rapid progressive cause, there are some rare autoimmune things. There have been recent reports of things like IgLON5, although there's limited cases, but we're doing more screening for some of those autoimmune causes. And then even some infectious causes like Whipples, that are rarely present like this. Okay? And have other signs and features. Dr Monteith: So, let's say you diagnose this patient with PSP and you're assessing the patients to see how you can improve their quality of life. So, what are some potential symptomatic managements that will help our patient? Dr Farland: I recommend for most all of these patients… while the literature indicates that many patients with PSP, and especially corticobasal syndrome, don't respond well to levodopa. So, the classic treatment for parkinsonism. However, we all recommend a trial of levodopa. These patients may respond partially to doses of levodopa, and we try to push the doses a bit higher. So, the recommended trial is usually a dose up to roughly 1000 milligrams of levodopa per day. And give it some time, at least two, if not actually three months of a trial. If not well-tolerated, you can back off. If there's no response at all or no improvement, then slowly back off and taper patients off and ask them to tell you whether they feel like they're actually worsening. So, many patients, sometimes, don't recognize the improvements, or family members don't recognize it until we actually taper them back off. And they may end up saying there are some other things that even recognize. Even some nonmotor benefits can be seen with levodopa. In some cases, we do keep them on levodopa, but levodopa's our best therapy for this. Dopamine agonists, MAO inhibitors, have all been sort of tried and they've been studied, but often don't really help or fail to help benefit these patients and could be fraught with some other side effects. I think many people do also turn to Amantadine as a treatment for Parkinson's, gait problems, freezing, if you see it in these disorders. Yet Amantadine is fraught with issues of side effects, including cognitive issues, and I think is not well-tolerated. But there are the rare patient who actually does respond to this or claims they respond to this. By and large, these patients relentlessly progress, unfortunately. So, beside treatment of other symptoms, I think it's really important to recognize that they require supportive cares and therapy. So, starting those early on and getting your allied healthcares kind of involved. So that includes people like physical, occupational therapy for the gait issues, the falls, occupational therapy for doing daily activities. Speech language pathology can be really a critical player for these because of the early speech and language issues, as well as swallow difficulties. Swallow is compared quickly in these patients. And so, we do recommend the screening evaluation, then often following patients either every six- or even annually, at least, with a swallow evaluation. And we recommend the fluoroscopic-guided kind of modified barium swallow for these patients.  Dr Monteith: And how does that differ if, let's say, the patient had cortical basilar syndrome? What are some of the symptomatic treatments that would be high on your consideration? Dr Farland: So actually, these patients also have a very similar approach, and they often have some overlapping features. Maybe a little bit of difference in terms of the level of apraxia and some dystonic features that you see in corticobasal syndrome. So, as I mentioned earlier that these patients have a more typ- when they present, typically have a more asymmetric presentation. And one of the biggest issues is this limb apraxia. They may have abnormal movements as well as, like, the alien limb-type phenomena as well. So, the focus of therapy, while similar in the sense we focus on the parkinsonism, I do always try levodopa and try to ramp up the doses to see if it benefits. It does often fail, but it's definitely worth trying. The other focus of these patients is trying to treat symptoms. Dystonia, those features… in some cases, we can help; if it's painful or uncomfortable, muscle relaxants can be used. If it's vocal, things like Botox can be really helpful. Often times it is more palliative than actually restorative in terms of function, but still can be really helpful for patients who ask about pain and discomfort and trying to treat. And then of course, again, the focus on our supportive care. We need to build that network and build that team of folks, the therapists, the physical, occupational, and the speech therapist to help them. If they have language problems---like either in PSP or corticobasal---I'll also include my request to a speech language pathologist to work on cognitive function. That's a special, additional thing you have to ask for and then specifically request when you make a referral to a speech language pathologist. Dr Monteith: That is so important. I think keeping the simulation, keeping the social support, and I would probably guess that you would also include screening for sleep and mood disorder. Dr Farland: Absolutely. Mood disorders are really big in these diseases. Patients are suffering terribly. You do hear about labile mood in both of these diseases, particularly PSP; and even what's called pseudobulbar palsy, where the mood is not always congruent with the affect. So they may laugh or cry inappropriately, and particularly the crying can be very disturbing to family and caregivers to see that. And so, treating those things can be really important. So always asking about the mood issues. Depression in particular is something that we're very sensitive about, and there is a higher incidence of suicidal ideations. Asking about that and feeling and making sure that they are in a safe environment can be really important. Dr Monteith: Thank you so much. Dr Farland: Thank you. Dr Monteith: Today I've been interviewing Dr Nikolaus McFarland about his article on progressive supranuclear palsy and cortical basilar syndrome, which appears in the August 2025 Continuum issue on movement 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, 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.

Multiple system atrophy is a rare, sporadic, adult-onset, progressive, and fatal neurodegenerative disease. Accurate and early diagnosis remains challenging because it presents with a variable combination of symptoms across the autonomic, extrapyramidal, cerebellar, and pyramidal systems. Advances in brain imaging, molecular biomarker research, and efforts to develop disease-modifying agents have shown promise to improve diagnosis and treatment. In this episode, Casey Albin, MD speaks with Tao Xie, MD, PhD, author of the article “Multiple System Atrophy” in the Continuum® August 2025 Movement Disorders issue. Dr. Albin is a Continuum® Audio interviewer, associate editor of media engagement, and an assistant professor of neurology and neurosurgery at Emory University School of Medicine in Atlanta, Georgia. Dr. Xie is director of the Movement Disorder Program, chief of the Neurodegenerative Disease Section in the department of neurology at the University of Chicago Medicine in Chicago, Illinois. Additional Resources Read the article: Multiple System Atrophy 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: @caseyalbin 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 Albin: Hello everyone, this is Dr Casey Albin. Today I'm interviewing Dr Tao Xie about his article on diagnosis and management of multiple system atrophy, which appears in the August 2025 Continuum issue on movement disorders. Welcome to the podcast, and please introduce yourself to our audience. Dr Xie: Thank you so much, Dr Albin. My name is Tao Xie, and sometimes people also call me Tao Z. I'm a mood disorder neurologist, professor of neurology at the University of Chicago. I'm also in charge of the mood disorder program here, and I'm the section chief in the neurodegenerative disease in the Department of Neurology at the University of Chicago Medicine. Thank you for having me, Dr Albin and Dr Okun and the American Academy of Neurology. This is a great honor and pleasure to be involved in this education session. Dr Albin: We are delighted to have you, and thank you so much for the thoughtful approach to the diagnosis and management. I really want to encourage our listeners to check out this article. You know, one of the things that you emphasize is multiple system atrophy is a fairly rare condition. And I suspect that clinicians and trainees who even have a fair amount of exposure to movement disorders may not have encountered that many cases. And so, I was hoping that you could just start us off and walk us through what defines multiple system atrophy, and then maybe a little bit about how it's different from some of the more commonly encountered movement disorders. Dr Xie: This is a really good question, Dr Albin. Indeed, MSA---multisystem atrophy----is a rare disease. It is sporadic, adult-onset, progressive, fatal neurodegenerative disease. By the name MSA, multisystem atrophy. Clinically, it will present with multiple symptoms and signs involving multiple systems, including symptoms of autonomic dysfunction and symptoms of parkinsonism, which is polyresponsive to the levodopa treatment; and the symptom of cerebellar ataxia, and symptom of spasticity and other motor and nonmotor symptoms. And you may be wondering, what is the cause- underlying cause of these symptoms? Anatomically, we can find the area in the basal ganglia striatonigral system, particularly in the putamen and also in the cerebellar pontine inferior, all of the nuclear area and the specific area involved in the autonomic system in the brain stem and spinal cord: all become smaller. We call it atrophy. Because of the atrophy in this area, they are responsible for the symptom of parkinsonism if it is involved in the putamen and the cerebral ataxia, if it's involved in the pons and cerebral peduncle and the cerebellum. And all other area, if it's involved in the autonomic system can cause autonomic symptoms as well. So that's why we call it multisystem atrophy. And then what's the underlying cellular and subcellular pathological, a hallmark that is in fact caused by misfolded alpha-synuclein aggregate in the oligodontia site known as GCI---glial cytoplasmic increasing bodies---in the cells, and sometimes it can also be found in the neuronal cell as well in those areas, as mentioned, which causes the symptom. But clinically, the patient may not present all the symptoms at the same time. So, based on the predominant clinical symptom, if it's mainly levodopa, polyresponsive parkinsonism, then we call it MSAP. If it's mainly cerebellar ataxia, then we call it MSAC. But whether we call it MSP or MSC, they all got to have autonomic dysfunction. And also as the disease progresses, they can also present both phenotypes together. We call that mixed cerebellar ataxia and parkinsonism in the advanced stage of the disease. So, it is really a complicated disease. The complexity and the similarity to other mood disorders, including parkinsonism and the cerebellar ataxia, make it really difficult sometimes, particularly at the early stages of disease, to differentiate one from the other. So, that was challenging not only for other professionals, general neurologists and even for some movement disorder specialists, that could be difficult particularly if you aim to make an accurate and early diagnosis. Dr Albin: Absolutely. That is such a wealth of knowledge here. And I'm going to distill it just a little bit just to make sure that I understand this right. There is alpha-synuclein depositions, and it's really more widespread than one would see maybe in just Parkinson's disease. And with this, you are having patients present with maybe one of two subtypes of their clinical manifestations, either with a Parkinson's-predominant movement disorder pattern or a cerebellar ataxia type movement disorder pattern. Or maybe even mixed, which really, you know, we have to make things quite complicated, but they are all unified and having this shared importance of autonomic features to the diagnosis. Have I got that all sort of correct? Dr Xie: Correct. You really summarize well. Dr Albin: Fantastic. I mean, this is quite a complicated disease. I would pose to you sort of a case, and I imagine this is quite common to what you see in your clinic. And let's say, you know, a seventy-year-old woman comes to your clinic because she has had rigidity and poor balance. And she's had several falls already, almost always from ground level. And her family tells you she's quite woozy whenever she gets up from the chair and she tends to kind of fall over. But they noticed that she's been stiff,and they've actually brought her to their primary care doctor and he thought that she had Parkinson's disease. So, she started levodopa, but they're coming to you because they think that she probably needs a higher dose. It's just not working out very well for her. So how would you sort of take that history and sort of comb through some of the features that might make you more concerned that the patient actually has undiagnosed multiple systems atrophy? Dr Xie: This is a great case, because we oftentimes can encounter similar cases like this in the clinic. First of all, based on the history you described, it sounds like an atypical parkinsonism based on the slowness, rigidity, stiffness; and particularly the early onset of falls, which is very unusual for typical Parkinson disease. It occurs too early. If its loss of balance, postural instability, and fall occurred within three years of disease onset---usually the motor symptom onset---then it raises a red flag to suspect this must be some atypical Parkinson disorders, including multiple system atrophy. Particularly, pou also mentioned that the patient is poorly responsive to their levodopa therapy, which is very unusual because for Parkinson disease, idiopathic Parkinson disease, we typically expect patients would have a great response to the levodopa, particularly in the first 5 to 7 years. So to put it all together, this could be atypical parkinsonism, and I could not rule out the possibility of MSA. Then I need to check more about other symptoms including autonomic dysfunction, such as orthostatic hypertension, which is a blood pressure drop when the patient stands up from a lying-down position, or other autonomic dysfunctions such as urinary incontinence or severe urinary retention. So, in the meantime, I also have to put the other atypical Parkinson disorder on the differential diagnosis, such as PSP---progressive supranuclear palsy---and the DLBD---dementia with Lewy body disease.---Bear this in mind. So, I want to get more history and more thorough bedside assessment to rule in or rule out my diagnosis and differential diagnosis. Dr Albin: That's super helpful. So, looking for early falls, the prominence of autonomic dysfunction, and then that poor levodopa responsiveness while continuing to sort of keep a very broad differential diagnosis? Dr Xie: Correct. Dr Albin: One of the things that I just have to ask, because I so taken by this, is that you say in the article that some of these patients actually have preservation of smell. In medical school, we always learn that our Parkinson's disease patients kind of had that early loss of smell. Do you find that to be clinically relevant? Is that- does that anecdotally help? Dr Xie: This is a very interesting point because we know that the loss of smelling function is a risk effect, a prodromal effect, for the future development of Parkinson disease. But it is not the case for MSA. Strange enough, based on the literature and the studies, it is not common for the patient with MSA to present with anosmia. Some of the patients may have mild to moderate hyposmia, but not to the degree of anosmia. So, this is why even in the more recent diagnosis criteria, the MDS criteria published 2022, it even put the presence of anosmia in the exclusion criteria. So, highlight the importance of the smell function, which is well-preserved for the majority in MSA, into that category. So, this is a really interesting point and very important for us, particularly clinicians, to know the difference in the hyposmia, anosmia between the- we call it the PD, and the dementia Lewy bodies versus MSA. Dr Albin: Fascinating. And just such a cool little tidbit to take with us. So, the family, you know, you're talking to them and they say, oh yes, she has had several fainting episodes and we keep taking her to the primary care doctor because she's had urinary incontinence, and they thought maybe she had urinary tract infections. We've been dealing with that. And you're sort of thinking, hm, this is all kind of coming together, but I imagine it is still quite difficult to make this diagnosis based on history and physical alone. Walk our listeners through sort of how you're using MRI and DAT scan and maybe even some other biomarkers to help sort of solidify that diagnosis. Dr Xie: Yeah, that's a wonderful question. Yeah. First of all, UTI is very common for patients with MSA because of urinary retention, which puts them into a high risk of developing frequent UTI. That, for some patients, could be the very initial presentation of symptoms. In this case, if we check, we say UTI is not present or UTI is present but we treat it, then we check the blood pressure and we do find also hypertension---according to new diagnosis criteria, starting drop is 20mm mercury, but that's- the blood pressure drop is ten within three minutes. And also, in the meantime the patients present persistent urinary incontinence even after UTI was treated. And then the suspicion for MS is really high right at this point. But if you want increased certainty and a comfortable level on your diagnosis, then we also need to look at the brain MRI mark. This is a required according to the most recent MDS diagnosis criteria. The presence of the MRI marker typical for MSA is needed for the diagnosis of clinically established MSA, which holds the highest specificity in the clinical diagnosis. So then, we have- we're back to your question. We do need to look at the brain MRI to see whether evidence suggestive of atrophy around the putamen area, around the cerebellar pontine inferior olive area, is present or not. Dr Albin: Absolutely. That's super helpful. And I think clinicians will really take that to sort of helping to build a case and maybe recognizing some of this atypical Parkinson's disease as a different disease entity. Are there any other biomarkers in the pipeline that you're excited about that may give us even more clarity on this diagnosis? Dr Xie: Oh, yeah. This is a very exciting area. In terms of biomarker for the brain imaging, particularly brain MRI, in fact, today there's a landmark paper just published in the Java Neurology using AI, artificial intelligence or machine learning aid, diagnoses a patient with parkinsonism including Parkinson's disease, MSA, and PSP, with very high diagnostic accuracy ranging from 96% to 98%. And some of the cases even were standard for autopsy, with pathological verification at a very high accurate rate of 93.9%. This is quite amazing and can really open new diagnosis tools for us to diagnose this difficult disease; not only in an area with a bunch of mood disorder experts, but also in the rural area, in the area really in need of mood disorder experts. They can provide tremendous help to provide accurate, early diagnosis. Dr Albin: That's fantastic and I love that, increasing the access to this accurate diagnosis. What can't artificial intelligence do for us? That's just incredible. Dr Xie: And also, you know, this is just one example of how the brain biomarker can help us. Theres other---a fluid biomarker, molecular diagnostic tools, is also available. Just to give you an example, one thing we know over the past couple years is skin biopsy. Through the immunofluorescent reaction, we can detect whether the hallmark of abnormally folded, misfolded, and the phosphorate, the alpha-synuclein aggregate can be found just by this little pinch of skin biopsy. Even more advanced, there's another diagnosis tool we call the SAA, we call the seizure amplification assay, that can even help us to differentiate MSA from other alpha-synucleinopathy, including Parkinson disease and dementia with Lewy bodies. If we get a little sample from CSF, spinal cerebral fluids, even though this is probably still at the early stage, a lot of developments still ongoing, but this, this really shows you how exciting this area is now. We're really in a fast forward-moving path now. Dr Albin: It's really incredible. So, lots coming down the track in, sort of, MRI, but also with CSF diagnosis and skin biopsies. Really hoping that we can hone in some of those tools as they become more and more validated to make this diagnosis. Is that right? Dr Xie: Correct. Dr Albin: Amazing. We can talk all day about how you manage these in the clinic, and I really am going to direct our listeners to go and read your fantastic article, because you do such an elegant job talking about how this takes place in a multidisciplinary setting, if at all possible. But as a neurointensivist, I was telling you, we have so much trouble in the hospital. We have A-lines, and we have the ability to get rapid KUBs to look at Ilias, and we can have many people as lots of diagnosis, and we still have a lot of trouble treating autonomiclike symptoms. Really, really difficult. And so, I just wanted to kind of pick your brain, and I'll start with just the one of orthostatic hypotension. What are some of the tips that you have for, you know, clinicians that are dealing with this? Because I imagine that this is quite difficult to do without patients. Dr Xie: Exactly. This is indeed a very difficult symptom to deal with, particularly at an outpatient setting. But nowadays with the availability of more medication---to give an example, to treat patients with orthostatic hypertension, we have not only midodrine for the cortisol, we also have droxidopa and several others as well. And so, we have more tools at hand to treat the patient with orthostatic hypertension. But I think the key thing here, particularly for us to the patient at the outpatient setting: we need to educate the patient's family well about the natural history of the disease course. And we also need to tell them what's the indication and the potential side effect profile of any medication we prescribe to them so that they can understand what to expect and what to watch for. And in the meantime, we also need to keep really effective and timely communication channels, make sure that the treating physician and our team can be reached at any time when the patient and family need us so that we can be closely monitoring, their response, and also monitoring potential side effects as well to keep up the quality of care in that way. Dr Albin: Yeah, I imagine that that open communication plays a huge role in just making sure that patients are adapting to their symptoms, understanding that they can reach out if they have refractory symptoms, and that- I imagine this takes a lot of fine tuning over time. Dr Xie: Correct. Dr Albin: Well, this has just been such a delight to get to talk to you. I really feel like we could dive even deeper, but I know for the sake of time we have to kind of close out. Are there any final points that you wanted to share with our listeners before we end the interview? Dr Xie: I think for the patients, I want them to know that nowadays with advances in science and technology, particularly given a sample of rapid development in the diagnostic tools and the multidisciplinary and multisystemic approach to treatment, nowadays we can make an early and accurate diagnosis of the MSA, and also, we can provide better treatment. Even though so far it is still symptomatically, mainly, but in the near future we hope we can also discover disease-modifying treatment which can slow down, even pause or prevent the disease from happening. And for the treating physician and care team professionals, I just want them to know that you can make a difference and greatly help the patient and the family through your dedicated care and also through your active learning and innovative research. You can make a difference. Dr Albin: That's amazing and lots of hope for these patients. Right now, you can provide really great care to take care of them, make an early and accurate diagnosis; but on the horizon, there are really several things that are going to move the field forward, which is just so exciting. Again today, I've been really greatly honored and privileged to be able to talk to Dr Tao Xie about his article on diagnosis and management of multiple system atrophy, which appears in the August 2025 Continuum issue on movement disorders. Be sure to check out Continuum Audio episodes for this and other issues. And thank you again to our listeners for joining us today. Dr Xie: Thank you so much for having me. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use 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.

Essential tremor is the most common movement disorder, although it is often misdiagnosed. A careful history and clinical examination for other neurologic findings, such as bradykinesia, dystonia, or evidence of peripheral neuropathy, can reveal potential alternative etiologies. Knowledge about epidemiology and associated health outcomes is important for counseling and monitoring for physical impairment and disability. In this episode, Lyell Jones, MD, FAAN, speaks with Ludy C. Shih, MD, MMSc, FAAN, author of the article “Essential Tremor” in the Continuum® August 2025 Movement Disorders issue. Dr. Jones is the editor-in-chief of Continuum: Lifelong Learning in Neurology® and is a professor of neurology at Mayo Clinic in Rochester, Minnesota. Dr. Shih is clinical director of the Parkinson's Disease and Movement Disorders Center at Beth Israel Deaconess Medical Center in Boston, Massachusetts. Additional Resources Read the article: Essential Tremor Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Guest: @ludyshihmd 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 Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today, I'm interviewing Dr Ludy Shih, who recently authored an article on essential tremor for our latest issue of Continuum on movement disorders. Dr Shih is an associate professor of neurology at Harvard Medical School and the clinical director of the Parkinson's Disease and Movement Disorder Center at Beth Israel Deaconess Medical Center in Boston. Dr Shih, welcome, and thank you for joining us today. Why don't you introduce yourself to our listeners? Dr Shih: Thank you, Dr Jones, for having me. It's a real pleasure to be here on the podcast with you. I'm a neurologist, I trained in movement disorders fellowship, and I currently see patients and conduct clinical research. We offer a variety of treatments and diagnostic tests for our patients with movement disorders. And I have developed this interest, a clinical research interest in essential tremor. Dr Jones: And so, as an expert in essential tremor, the perfect person to write such a really spectacular article. And I can't wait for our listeners to hear more about it and our subscribers to read it. And let's get right to it. If you had, Dr Shih, a single most important message for our listeners about caring for patients with essential tremor, what would that message be? Dr Shih: Yeah, I think the takeaway that I've learned over the years is that people with essential tremor do develop quite a few other symptoms. And although we propose that essential tremor is this pure tremor disorder, they can experience a lot of different comorbidities. Now, there is some debate as to whether that is expected for essential tremor or is this some part of another syndrome, which we may talk about later in the interview. But the fact of the matter is, it's not a benign condition and people do experience some disability from it. Dr Jones: And I think that speaks to how the name of this disorder has evolved over time. right? You point out in your article, it used to be called benign essential tremor or benign familial tremor. But it's really not so straightforward as it. And fairly frequently these symptoms, the patient's tremor, can be functionally limiting, correct? Dr Shih: That is correct. In fact, the reason I probably started getting interested in essential tremor was because our center had been doing a lot of deep brain stimulation for essential tremor, which is remarkably effective, especially for tremor that reaches an amplitude that really no oral medication is going to satisfyingly treat. And if you have enough upper limb disability from this very large-amplitude tremor, a surgical option may make a lot of sense for a lot of patients. And yet, how did they get to that point? Do they continue to progress? These were the sort of interesting questions that got raised in my mind as I started to treat these folks. Dr Jones: We'll come back to treatment in just a minute here, because there are many options, and it sounds like the options are expanding. To start with the diagnosis- I mean, this is an extraordinarily common disorder. As you point out, it is the most common movement disorder in the US and maybe the world, and yet it seems to be underrecognized and frequently misdiagnosed. Why do you think that is? Dr Shih: Great question. It's been pretty consistent, with several case series over the decades showing a fairly high rate of quote/unquote “misdiagnosis.” And I think it speaks to two things, probably. One is that once someone sees a postural and kinetic tremor of the arms, immediately they think of essential tremor because it is quite common. But there's a whole host of things that it could actually be. And the biggest one that we also have to factor in is also the heterogeneity of the presentation of Parkinson's disease. Many people, and I think increasingly now these days, can present with not a whole lot of the other symptoms, but may present with an atypical tremor. And it becomes actually a little hard to sort out, well, do they have enough of these other symptoms for me to suspect Parkinson's, or is the nature of their tremor suspicious enough that it would just be so unusual that this stays essential tremor and doesn't eventually develop into Parkinson's disease? And I think those are the questions that we all still grapple with from time to time in some of our clinics. Dr Jones: Probably some other things related to it with, you know, our understanding of the pathophysiology and the availability of tests. And I do want to come back to those questions here in just a minute, but, you know, just the nomenclature of this disorder… I think our clinical listeners are familiar with our tendency in medicine to use words like essential or idiopathic to describe disorders or phenomena where we don't understand the precise underlying mechanism. When I'm working with our trainees, I call these “job-security terms” because it sounds less humbling than “you have a tremor and we don't know what causes it,” right? So, your article does a really nice job outlining the absence of a clear monogenic or Mendelian mechanism for essential tremor. Do you think we'll ever have a eureka moment in neurology for this disorder and maybe give it a different name? Dr Shih: It's a great question. I think as we're learning with a lot of our neurologic diseases---and including, I would even say, Parkinson's disease, to which ET gets compared to a lot---there's already now so much more known complexity to something that has a very specific idea and concept in people's minds. So, I tend to think we'll still be in an area where we'll have a lot of different causes of tremor, but I'm hopeful that we'll uncover some new mechanisms for which treating or addressing that mechanism would take care of the tremor in a way that we haven't been able to make as much progress on in the last few decades as maybe we would have thought given all the advances in in technology. Dr Jones: That's very helpful, and we'll be hopeful for that series of discoveries that lead us to that point. I think many of our listeners will be familiar with the utility---and, I think, even for most insurance companies, approval---for DAT scans to discriminate between essential tremor and Parkinsonian disorders. What about lab work? Are there any other disorders that you commonly screen for in patients who you suspect may have essential tremor? Dr Shih: Yeah, it's a great question. And I think, you know, I'm always mindful that what I'm seeing in my clinic may not always be representative of what's seen in the community or out in practice. I'll give an example. You know, most of the time when people come to the academic Medical Center, they're thinking, gosh, I've tried this or that. I've been on these medicines for the last ten years. But I've had essential tremor for twenty years. We get to benefit a little bit from all that history that's been laid down. And so, it's not as likely you're going to misdiagnose it. But once in a while, you'll get someone with tremor that just started a month ago or just started, you know, 2 or 3 months ago. And you have to still be thinking, well, I've got to get out of the specialist clinic mindset, and think, well, what else really could this be? And so, while it's true for everybody, moreso in those cases, in those recent onset cases, you really got to be looking for things like medications, electrolyte abnormalities, and new-onset thyroid disorder, for example, thyroid toxicosis. Dr Jones: Very helpful. And your article has a wonderful list of the conditions to consider, including the medications that might be used for those conditions that might result or unmask a tremor of a different cause. And I think being open-minded and not anchoring on essential tremor just because it's common, I think is a is a key point here. And another feature in your article that I really enjoyed was your step-by-step approach to tremor. What are those steps? Dr Shih: Well, I think you know first of all, tremor is such common terminology that even lay people, patients, nonclinicians will use the word “tremor.” And so, it can be tempting when the notes on your schedule says referred for tremor to sort of immediately jump to that. I think the first step is, is it tremor? And that's really something that the clinician first has to decide. And I think that's a really important step. A lot of things can look superficially like tremor, and you shouldn't even assume that another clinician knows what tremor looks like as opposed to, say, myoclonus. Or for example a tremor of the mouth; well, it actually could be orolingual or orobuccal dyskinesia, as in tardive dyskinesia. And another one that tremor can look like is ataxia. And so, I think- while they sound obvious to most neurologists, perhaps, I think that---especially in the area of myoclonus, where it can be quite repetitive, quite small amplitude in some conditions---it can really resemble a tremor. And so, there are examples of these where making that first decision of whether it's a tremor or not can really be a good sort of time-out to make sure you're going down the right path to begin with. And I think what's helpful is to think about some of the clinical definitions of a tremor. And tremor is really rhythmic, it's oscillatory. You should see an agonist and antagonist muscle group moving back and forth, to and fro. And then it's involuntary. And so, I think these descriptors can really help; and to help isolate, if you can describe it in your note, you can probably be more convinced that you're dealing with the tremor. The second step that I would encourage people to really consider: you've established it's a tremor. The most important part exam now becomes, really, the nontremor part of the exam. And it should be really comprehensive to think of what else could be accompanying this, because that's really how we make diagnosis of other things besides essential tremor. There really should be a minimum of evidence of parkinsonism, dystonia, neuropathy, ataxia- and the ataxia could be either from a peripheral or central nervous system etiology. Those are the big four or five things that, you know, I'm very keen to look for and will look pretty much in the head, neck, the axial sort of musculature, as well as the limbs. And I think this is very helpful in terms of identifying cases which turn out to have either, say, well, Parkinson's or even a typical Parkinson disorder; or even a genetic disorder, maybe even something like a fragile X tremor ataxia syndrome; or even a spinal cerebellar ataxia. These cases are rare, but I think if you uncover just enough ataxia, for example, that really shouldn't be there in a person, let's say, who's younger and also doesn't have a long history of tremor; you should be more suspicious that this is not essential tremor that you're dealing with. And then the last thing is, once you've identified the tremor and you're trying to establish, well, what should be done about the tremor, you really have to say what kind of tremor it is so that you can follow it, so you can convey to other people really what the disability is coming from the tremor and how severe the tremor is. So, I think an example of this is, often in the clinic, people will have their patients extend their arms and hands and kind of say, oh, it's an essential tremor, and that's kind of the end of the exam. But it doesn't give you the flavor. Sometimes you'll have a patient come in and have a fairly minimal postural tremor, but then you go out, take those extra few seconds to go grab a cup of water or two cups of water and have them pour or drink. And now all of a sudden you see this tremor is quite large-amplitude and very disabling. Now you have a better appreciation of what you really need to do for this patient, and it might not be present with just these very simple maneuvers that you have at bedside without props and items. And then the severity of it; you know, we're so used to saying mild, moderate, severe. I think what we've done in the Tremor Research Group to use and develop the Essential Tremor Rating Assessment Scale is to get people used to trying to estimate what size the tremor is. And you can do that by taking a ruler or developing a sense of what 1 centimeter, 2 centimeters, 3 centimeters looks like. I think it'd be tremendously helpful too, it's very easy and quick to convey severity in a given patient. Dr Jones: I appreciate you, you know, having a patient-centered approach to the- how this is affecting them and being quantitative in the assessment of the tremor. And that's a great segue to a key question that I run into and I think others run into, which is when to initiate therapy? You know, if you see a patient who, let's say they have a mild tremor or, you know, something that quantitatively is on the mild end of the spectrum, and you have, you know, a series of options… from a medication perspective, you have to say, well, when does this across that threshold of being more likely to benefit the patient than to harm the patient? How do you approach that question? What's your threshold for starting medication? Dr Shih: Yeah. You know, sometimes I will ask, because---and I know this sounds like a strange question---because I feel like my patients will come for a couple of different reasons. Sometimes it's usually one over the other. I think people can get concerned about a symptom of a tremor. So, I actually will ask them, was your goal to just get a sense for what this tremor is caused by? I understand that many people who develop tremor might be concerned it might be something like Parkinson's disease. Or is this also a tremor that is bothering you in day-to-day life? And often you will hear the former. No, I just wanted to get checked out and make sure you don't think it's Parkinson's. It doesn't bother me enough that I want to take medication. They're quite happy with that. And then the second scenario is more the, yeah, no, it bothers me and it's embarrassing. And that's a very common answer you may hear, may be embarrassing, people are noticing. It's funny in that many people with essential tremor don't come to see a doctor or even the neurologist for many years. And they will put up with it for a very long time. And they've adopted all sorts of compensatory strategies, and they've just been able to handle themselves very admirably with this, in some cases, very severe tremor. So, for some of them, it'll take a lot to come to the doctor, and then it becomes clear. They said, I think I'm at the point where I need to do something about this tremor. And so, I think those three buckets are often sort of where my patients fall into. And I think asking them directly will give you a sense of that. But you know, it can be a nice time to try some as-needed doses of something like Propranolol, or if it's something that you know that they're going to need something on day-to-day to get control of the tremor over time, there are other options for that as well. Dr Jones: Seems like a perfect scenario for shared decision-making. Is it bothersome enough to the patient to try the therapy? And I like that suggestion. That's a nice pearl that you could start with an a- needed beta blocker, right, with Propranolol. And this is a question that I think many of us struggle with as well. If you've followed a patient with essential tremor for some time and you've tried different medications and they've either lost effectiveness or have intolerable adverse effects, what is your threshold for referring a patient for at least considering a surgical neurostimulator therapy for their essential tremor? Dr Shih: Yeah, so surgical therapies for tremor have been around for a long time now, since 1997, which was when it was approved by the FDA for essential tremor and Parkinson tremor. And then obviously since then, we have a couple more options in the focus ultrasound thalamotomy, which is a lesioning technique. When you have been on several tremor medications, the list gets smaller and smaller. It- and then chance of likely satisfying benefit from some of these medications can be small and small as you pass through the first and second line agents and these would be the Propranolol and the primidone. And as you say, quite a few patients- it's estimated between 30 to 50% of these patients end up not tolerating these first two medications and end up discontinuing them. Some portion of that might also be due to the fact that some of our patients who have been living with essential tremor for decades now, to the point that their tremor is getting worse, are also getting older. And so, polypharmacy and/or some of the potential side effects of beta blockers and anticonvulsants like primidone may be harder to bear in an older adult. And then as you talk about in the article, there's some level of evidence for topiramate, and then from there a number of anticonvulsants or benzos, which have even weaker evidence for them. It's a personal decision. As I tell folks, look, this is not going to likely extend your life or save your life, but it's a quality of life issue. And of course, if there are other things going on in life that need to be taken care of and they need that kind of care and attention, then, you know, you don't need to be adding this to your plate. But if you are in the position where those other things are actually okay, but quality of life is really affected by your being unable to use your upper limbs in the way that you would like to… A lot of people's hobbies and applications are upper limb-based, and enjoying those things is really important. Then I think that this is something- a conversation that we begin and we begin by talking about yes, there are some risks involved, but fortunately this is the data we have on it, which is a fairly extensive experience in terms of this is the risk of, you know, surgery-related side effects. This is the risk of if you're having stimulation from DBS stimulation-related side effects, which can be adjustable. It's interesting, I was talking with colleagues, you know, after focused ultrasound thalamotomy was approved. That really led more people to come to the clinic and start having these discussions, because that seemed like a very the different sort of approach where hardware wasn't needed, but it was still a surgery. And so, it began that conversation again for a bunch of people to say, you know, what could I do? What could I tolerate? What would I accept in terms of risk and potential benefit? Dr Jones: Well, I think that's a great overview of a disorder where, you know, I think the neurologist's role is really indispensable. Right? I mean, you have to have this conversation not just once, this is a conversation that you have over time. And again, I really want to refer our listeners to this article. It's just a fantastic overview of a common disorder, but one where I think there are probably gaps where we can improve care. And Dr Shih, I want to thank you for joining us, and thank you for such a great discussion on essential tremor. I learned a lot from your article, and I learned even more from the interview today. I suspect our readers and listeners will too. Dr Shih: Well, thank you again for the invitation and the opportunity to kind of spread the word on this really common condition. Dr Jones: Again, we've been speaking with Dr Ludy Shih, author of a fantastic article on essential tremor in Continuum's latest issue on movement disorders. Please check it out, and thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. 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.

How do you prepare for your visit with your movement disorders specialist – your doctor, nurse practitioner, or PA? In this episode filled with practical guidance, Sherrie Gould, NP, CMRD, continues with her series about working with your medical care team.Bring your care partner, write everything down, have your questions ready. Sherrie looks at this and much more as you get ready for your Parkinson's appointment. 

Welcome to the NeurologyLive® Mind Moments® podcast. Tune in to hear leaders in neurology sound off on topics that impact your clinical practice. In this episode, "Improving Quality of Life in Movement Disorders Through Nonmotor Symptom Management" Alex Dessy, MD, clinical assistant professor in movement disorders at Jefferson Health, shares a comprehensive look at modern-day care strategies for patients with Parkinson disease and other movement disorders. Dessy discusses the foundational role of detailed history-taking, exam-based observation, and phenomenology in diagnosing complex conditions, along with the growing utility of genetic and imaging tools. She also explains the challenges of managing nonmotor symptoms—like sleep disturbance, fatigue, and constipation—and how lifestyle strategies and interdisciplinary collaboration are often as vital as medication. Lastly, she emphasizes the importance of clear and compassionate communication with patients and families as neurology becomes increasingly therapeutic. Looking for more Movement disorders discussion? Check out the NeurologyLive® Movement disorders clinical focus page. Episode Breakdown: 1:00 – How movement disorder diagnosis is approached through history, physical exam, and phenomenology 4:05 – What makes certain movement disorder cases complex and how diagnostics like genetics and imaging are used 6:20 – Neurology News Minute 8:45 – How nonmotor symptoms in Parkinson's (fatigue, constipation, sleep) are managed with lifestyle strategies 12:30 – Approaching therapeutic communication and expectation-setting with patients and families The stories featured in this week's Neurology News Minute, which will give you quick updates on the following developments in neurology, are further detailed here: Eisai Showcases Promising 4-Year Data for Alzheimer Therapy Lecanemab at AAIC 2025 IHL-42X to Enter Phase 3 Trials for Obstructive Sleep Apnea Following Positive Phase 2 Data FDA Approves Fremanezumab as First Anti-CGRP Preventive Therapy for Pediatric Episodic Migraine Thanks for listening to the NeurologyLive® Mind Moments® podcast. To support the show, be sure to rate, review, and subscribe wherever you listen to podcasts. For more neurology news and expert-driven content, visit neurologylive.com.

Parkinson disease is a neurodegenerative movement disorder that is increasing in prevalence as the population ages. The symptoms and rate of progression are clinically heterogenous, and medical management is focused on the individual needs of the patient. In this episode, Kait Nevel MD, speaks with Ashley Rawls, MD, MS, author of the article “Parkinson Disease” in the Continuum® August 2025 Movement 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. Rawls is an assistant professor at the University of Florida Health, Department of Neurology at the Norman Fixel Institute for Neurological Diseases in Gainesville, Florida Additional Resources Read the article:  Parkinson Disease Subscribe to Continuum®: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @IUneurodocmom Guest: @DrRawlsMoveMD Full episode transcript available here Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about earning CME, subscribing to the journal, and exclusive access to interviews not featured on the podcast. Dr Nevel: Hello, this is Dr Kait Nevel. Today I'm interviewing Dr Ashley Rawls about her article on Parkinson disease, which appears in the August 2025 Continuum issue on movement disorders. Ashley, welcome to the podcast, and please introduce yourself to the audience. Dr Rawls: Thank you, Kait. Hello everyone, my name is Dr Ashley Rawls. I am a movement disorder specialist at the University of Florida Fixel Institute for Neurologic Diseases in Gainesville, Florida. It's a pleasure to be here. Dr Nevel: Awesome. To start us off talking about your article, can you share what you think is the most important takeaway for the practicing neurologist? Dr Rawls: Yes. I would say that my most important takeaway for this article is that Parkinson disease remains a clinical diagnosis. I think the field has really been advancing and trying to find a biomarker to help with diagnosis through ancillary testing. For example, with the dopamine transporter, the DAT scan, an alpha-synuclein skin biopsy, an alpha-synuclein amplification assay that can happen in blood and CSF. However, I think it's so critical to make sure that you have a very strong history and a very thorough physical exam and use those biomarkers or other testing to help with, kind of, bolstering your thoughts on what's going on with the patient. Dr Nevel: Great. And I can't wait to talk a little bit more about the ancillary testing and how you use that. Before we get to that, can you review with us some of the components of the clinical diagnosis of Parkinson disease? Dr Rawls: Yes. So, when I think about a person that comes in that might have a neurodegenerative disease, I think about two different features, mainly: both motor and Manon motor. So, for my motor features, I'm thinking about resting tremor, bradykinesia---which is fullness of movement with decrement over time---rigidity, and then a specific gait disturbance, a Parkinsonian gait, involving stooped posture, decreased arm swing. They can also have reemergent tremor while walking if they do have tremor as part of their disease process, and also in-block turning as they are walking down the hallway. So, those are my motor features that I look for. So now, when we're talking about a specific diagnosis of Parkinson disease, the one motor feature that you need to have is bradykinesia. The reason why I make sure to speak about bradykinesia, which is slowness of movement with decrement over time, is because people can still have Parkinson disease without having tremor, a resting tremor. So even though that's one of the core cardinal features that most of us will be able to notice very readily, you don't have to necessarily have a resting tremor to be diagnosed with Parkinson' disease. When I talk about nonmotor features, those are going to be the three, particularly the prodromal features that can occur even ten years before people have motor features, can be very prominent early on in the disease process. For example, hyposmia or anosmia for decrease or lack of sense of smell. Another one that we really look for is going to be RBD, or rapid eye movement behavior disorder; or REM behavior disorder, the person acting out their dreams, calling out, flailing their limbs, hitting their bed partner. And then the other one is going to be severe constipation. So those three prodromal nonmotor symptoms of hyposmia/anosmia, RBD or REM behavior disorder, and severe constipation can also make me concerned as a red flag that there is a sort of neurodegenerative issue like a Parkinson disease that may be going on with the patient. Dr Nevel: Great, thank you so much for that overview. While we're talking about the diagnosis, do you mind kind of going back to what you mentioned in the beginning and talking about the ancillary tests that sometimes are used to kind of help, again, bolster that diagnosis of Parkinson disease? You know, like the DAT or the alpha-synuclein skin biopsy. When should we be using those? Should we be getting these on everyone? And what scenarios should we really consider doing one of those tests? Dr Rawls: The scenario in which I would order one of the ancillary testing, particularly like a DAT scan or a skin biopsy, looking for alpha-synuclein is going to be when there are potential red flags or a little bit of confusion in regard to the history and physical that I need to have a little bit more clarification on. For example, if I have a patient that has a history of using dopamine blocking agents, for example, for severe depression; or they have a history of cancer diagnosis and they've been on a dopamine agent like metoclopramide; those I want to be mindful because if they're coming in to see me and they're having the symptoms of Parkinsonism---which is going to be resting tremor, bradykinesia rigidity, or gait disturbance---I need to try to figure out is it potentially due to a medication effect, particularly if they're still on the dopamine blockade medication, or is it something where they're actually having a neurodegenerative illness underneath it, like a Parkinson disease? The other situation that would make me order a DAT skin or a skin biopsy is going to be someone who is coming in that maybe has elements of essential tremor, they have more of a postural or an intention tremor that's very flapping and larger amplitude, and maybe have some mild symptoms and Parkinsonism that might be difficult to distinguish between other musculoskeletal things like arthritis, other imbalance issues from, you know, hip problems or knee problems and what have you. Then I might say, okay, let's see if there is some sort of neurodegeneration underneath this; that may be- that there could be, you know, potentially two elements like a central tremor and Parkinson disease going on. Or is this someone who actually really has Parkinson disease, but there's other factors that are kind of playing into that. Dr Nevel: Great, thank you for that. Gosh, things have really changed over the past fifteen years or so where we have this ancillary testing that we're able to use more, because what you read in the textbook isn't always what you see in clinic. And as you described, there are patients who… it's not as clear cut, and these tests can be helpful. Could you tell us more about the levodopa challenge test? How is this useful in clinical practice? And what are some key points that we should know about when utilizing this strategy for patients who we think have Parkinson disease? Dr Rawls: So, before we had all this ancillary testing with the DAT scan, the skin biopsy, the alpha-synuclein amplification assay, many times if you had a suspicion that a person that had Parkinson disease, but you weren't entirely sure, you would say, hey, listen, let us give you back the dopamine that your body may be missing and see if you have an improvement, in particular in your motor symptom. So, when I talk with my patients, I say, listen, I might have a strong suspicion that you have Parkinson disease. Doing a levodopa trial can not only be diagnostic, but also can be therapeutic as well. So, with this levodopa trial, what I end up doing is saying, okay, we're going to start the medication at a low dose because we are looking to see if you have improvement in three of the main cardinal motor symptoms. Obviously, tremor is much easier for us to see if it gets better. It's very obvious on exam, and the patients are more readily able to see it. Whereas stiffness and slowness is much harder to quantify and try to figure out. Am I stiff and slow because of potential muscle tightness from Parkinson disease, or is it something that's more of a musculoskeletal issue? So, I will tell persons, okay, we're looking for improvement in these three cardinal motor symptoms, and things that we're looking for is getting into and out of a car, into and out of a chair, turning over in bed, seeing how do we navigate ourselves in our daily lives? I give people the example of going through the grocery store, going through a busy airport. Are we able to move better and respond better to different changes in our environment which can give us a better clue of if our stiffness and slowness in particular are being improved with the medication? The other part of this is talking about potential side effects of the carbidopa- of the levodopa in particular. One big thing that I think limits people initially is going to be the nausea, vomiting, potential GI upset when starting this medication initially. So, oftentimes I will find people coming in, oh, you know, my outside doctor started me immediately on one tab of carbidopa/levodopa three times per day. I got nauseous, I threw up, and I never took the medication again. So often times I will start low and go slow because once someone throws up my medication, they are not going to want to take it again---with good reason. So, often times I will ask the patient, hey listen, are you very sensitive to medications? If you are very sensitive, we might start one tablet per day for a week, one tablet twice a day, and then go up until we get to two tablets three times a day if we're talking about carbidopa/levodopa. If someone is not as sensitive then I might go up a little bit quicker. What do we mean when we talk about 600 milligrams per day? So usually, the amount that I use is carbidopa/levodopa, 25/100; so, 100 milligrams being the levodopa portion. Many people just start off at 1 tab 3 times a day, which gives you 300 milligrams of levodopa, and they say, oh, it didn't work, I must not have Parkinson or something else. Well, it just may have been that we did not give an adequate trial and adequate dose to the person. Now if they're not able to tolerate the medication because of the side effects, that's something different. But if they don't have side effects and don't notice a difference, there is room to increase the carbidopa/levodopa or the levodopa replacement that you are using so that you can give it, you know, a very good try to see, is it actually improving resting tremor, bradykinesia and rigidity? Dr Nevel: Yeah, great. Thanks for that. When you diagnose a patient with Parkinson disease, how do you counsel that patient? How do you break that difficult news? And how do you counsel them on what to expect in the future and goals of treatment? I know that's a lot in that question, but it also is a lot that you do in one visit, oftentimes, or at least introduce these kind of concepts to patients in a single visit. Dr Rawls: One thing that I think is helpful for me is trying to understand where the patients and their families are when they come in. Because some of the patients come in and have no prior inkling that they may have a neurodegenerative illness like Parkinson disease. Some of my patients come in and say, I'm here for a second opinion for Parkinson disease. So, then I have an idea of where we are in regard to potential understanding of how to start the conversation going forward. If it is someone who is coming in and has not heard about Parkinson disease, or their family has not been made aware that that's the one reason why they're coming to see a movement disorder specialist, then I will start at the beginning After we finish our history, do a very thorough physical exam, I will talk about things that I heard in the history and that I see on the physical exam that make me concerned for a disease like Parkinson disease. I make sure to tell them where I'm getting my criteria from and not just start off, I think you have Parkinson, here's your medication. I think that's very jarring when you're talking with patients and their families, particularly if they had no idea that this could be a potential diagnosis on the table. Like I said, I will start off with recounting, this is what I've heard in your history that makes me concerned. This is what I've seen on your physical exam that makes me concerned. And I think you have Parkinson disease and here is why. And I'll tell them about the tenants like we discussed about Parkinson disease, both the motor and nonmotor symptoms that we see. So that's kind of the first part is, I make sure to lay it out and then open the room up for some questions and clarification. The other portion of this is that, when I'm talking about counseling the patient, I say, we do not expect Parkinson disease to decrease your lifespan. However, over time, our persons, because it is a neurodegenerative illnesses will accumulate deficits over time. So, more stiffness, more slowness, more walking problems. They may, if they have tremor, the tremor may become worse. If they don't have tremor, they might develop tremor in the future. If we're talking about the nonmotor symptoms that we talk about, the main ones are going to be issues with urinary problems, issues with bowels, and then the other thing is going to be neuropsychiatric issues like anxiety and depression. And those things become more prominent, usually, the nonmotor symptoms later on in the disease process, and then also cognitive impairment as well. I really want to make sure that they have the information that I'm seeing, and if there's anything that they want to correct on their end, as in they're saying, oh wait, well, actually I noticed something else, then that's usually when that comes out around kind of the wrapping-up portion of the visit. So, I think that's really important to, one, be very clear in what I am seeing and if there's red flags, and then tell them, okay this is not going to shorten your lifespan. However, over time, we do have other issues and problems that will arise and we can support you as best as we can through that. The one thing I also been very open with people about is- because our patients will say, is there anything I can do? What can be done? Is there any medication to slow down or stop things? And I let people know that unfortunately, right now there's not an intervention that slows down, stops, or reverses disease progression, with the exception of exercise. Consistent exercise has been found to help to slow down disease progression, okay? And also, it can help to release the dopamine already being made innately in the brain. And also, it can help with our cardiovascular health in the big thing: being balanced. Core strength, quadricep strength. So that's also something that people can work on that they should. And I let people know that exercise is as important as the medications themselves. Dr Nevel: Absolutely. And it's incredible how much they incorporate exercise into their daily lives and get active, people who weren't active before their diagnosis, and how much that can help. One question that I think patients sometimes ask is, when they understand how carbidopa/levodopa works and what the expectations are for that medication, that it's not a disease-modifying medication, but that it can help with their symptoms. And then they kind of hear, well as time goes on, they need higher doses or, you know, it doesn't control their motor symptoms as well. They'll say, okay well, is it better to wait then? Should I wait to start carbidopa/levodopa? Like in my mind, I'm only maybe going to get X amount of time from carbidopa/levodopa. So, I'd rather wait to start it than start it now. What do you say to them and how do you counsel them through that? Dr Rawls: So that is a common question that I do get with my patients. So, I tell people, I'm here for you. And it really depends on how you feel at this time. Because you have to weigh the risks and benefits of the medication itself. If someone who's very, very mild decides to take the medication, they feel nauseous, they're just going to say, hey, listen, it's not for me right now. I don't feel like I need it, and then stop, which is with definitely within their right. But what I always counsel patients as well is to say, the dopamine-producing neurons in the substantia nigra are starting to die over time. That is why we are getting the signs and symptoms of Parkinson disease. At some point, your brain is not going to produce enough dopamine that is needed for you to move when you want to move and not move when you don't want to move. Okay? Giving you at least the motor symptoms of Parkinson disease. With this, it's not that the medication stops working, it's just that you need more dopamine to help replace the dopamine that's being lost. However, the dopamine that you are taking or levodopa that you're taking orally is not going to be released as consistently as it is in your brain on demand and shut off when you don't need it. Hence the reason we get more motor fluctuations. Also, potential side effects in the medication like orthostatic hypertension, hallucinations, impulse control disorders. Because you're having to take more escalating doses, those side effects can become more prominent and also lead us to have to balance between the side effects and the medication itself. So, it's not that the medication does not work, your body needs more of it. Some people will say, oh, well, I want to wait, and I say, that's completely fine. However, my cutoff is basically saying, if you are finding that you, as the person who's afflicted is not able to get up in the morning like you want to, you're avoiding going to walk your dog or working in your garden, you know, because you feel stiff and feel slow; you're avoiding, you know, going out to the community, having lunch with your friends or your family because you're embarrassed by your tremor; this is something that is keeping you from living your life. And that's the time that we need to strongly consider starting the medications. So, a person afflicted will accumulate deficits. However, it's how much the deficits are going to affect you. So, if it's really affecting your life, we have tools and ways to help mitigate that. Dr Nevel: Yeah, absolutely. Are there any aspects of Parkinson disease management that you feel are maybe underrecognized or perhaps underutilized? In other words, you know, are there things that we the listeners should be maybe more aware of or think about offering or recommending to our patients that you think maybe aren't as much as they could be? Dr Rawls: I will say the nonmotor symptoms---in particular the neuropsychiatric symptoms with the anxiety and depression, usually later on disease process but also can be earlier as well---I think that is going to be something that is recognized but maybe undertreated in a lot of our patient population. I think part of that is also the fluctuations in dopamine that are occurring naturally in the person, but also, our patients, oftentimes with their medication regimen, really have to be on the ball taking the medication. If they're even 15 minutes late, 10 minutes late, 5 minutes late, we're now off, and now we're waiting for it to kick in. And so that can cause a lot of anxiousness even throughout the day. And then knowing that slowly over time that they're going to accumulate these motor and nonmotor deficits can definitely be problematic as well. There is obvious reason for this underlying potential anxiety and depression. And while we do talk about that and bring that up, sometimes patients will say, oh well, I don't think it's a problem right now. I don't have to mess with this. But usually at some point it does become an issue that usually the family members will bring up and saying, hey, you know, my loved one is very anxious. Or I've noticed that they're just really disengaged from what's going on in their lives and they are not talking as much, they're not going out as much. Again, that could be a combination of depression/anxiety, but it also can be a physical- a combination of, I'm not physically able to do these things, or, they're much more difficult for me to initiate doing these activities. I always want to be mindful. If my patients come in and they already have a diagnosis of depression or anxiety and they're already being treated by a mental health counselor, provider, or a psychiatrist, then I will work with providers so that we can try to optimize their medication regimen. The other thing is, well, if this is the first time that they're really being seen by someone and talking about their anxiety and depression, then oftentimes I will have them go back to their primary care and see if maybe an SSRI or SNRI will be helpful to try to help with the neuropsychiatric symptoms they may be experiencing. So that's one big one. Another one that I think that might be a little bit underappreciated is going to be drooling. Sometimes I'll come in and see my patients and notice some drooling that's happening with the mouth being open, not being able to initiate the swallowing reflex consistently throughout the day. Or they may be patting their face a lot with a napkin or a towel and then bringing that up and bringing it to light. Oh yeah. I have a lot of drooling while I'm awake. It's on my shirt. It's embarrassing. I feel like it's a little bit too much for me or my family. We have to put a bib on because I'm just drooling all throughout the day. That can really be uncomfortable and cause skin breakdown. It can also be socially embarrassing. So, there are some tools that I talk to people about with drooling. One thing I start with is going to be using sugar-free gum or candy while the person is awake to help initiate the swallow reflex, and sometimes that's all that's needed. There are other agents that can be used---like glycopyrrolate, sublingual atropine drops, and scopolamine patches---that can help with decreasing saliva production. But there can be side effects of making the entire body feel dry, and then also potential cardiac arrhythmias. If those are not helpful or they're contraindicated with the patient, another thing is going to be botulinum toxin injections. So those can be done on the parotid and salivary glands to decrease the amount of saliva that's being produced. So oftentimes people will come to me, because I'm also a botulinum toxin injector. I've been sent by some of my colleagues to inject our persons that have significant sialorrhea. Dr Nevel: Wonderful. Well, thank you so much for chatting with me today about your article. Again, today I've been interviewing Dr Ashley Rawls about her article on Parkinson disease, which appears in the August 2025 Continuum issue on movement disorders. Be sure to check out Continuum Audio episodes from this and other issues. And thank you to our listeners for joining today. And thank you, Ashley, for sharing all your knowledge with us today. Dr Rawls: Thank you, Kate, I appreciate your time. And have a great day, everyone. Dr Monteith: This is Dr Teshmae 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.

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In this episode, Lyell K. Jones Jr, MD, FAAN, speaks with Michael S. Okun, MD, FAAN, who served as the guest editor of the August 2025 Movement Disorders issue. They provide a preview of the issue, which publishes on August 1, 2025. 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. Okun is the director at Norman Fixel Institute for Neurological Diseases and distinguished professor of neurology at University of Florida in Gainesville, Florida. Additional Resources Read the issue: continuum.aan.com Subscribe to Continuum®: shop.lww.com/Continuum Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the American Academy of Neurology: aan.com Social Media facebook.com/continuumcme @ContinuumAAN Host: @LyellJ Guest: @MichaelOkun Full episode transcript available here: Dr Jones: Our ability to move through the world is one of the essential functions of our nervous system. Gross movements like walking ranging down to fine movements with our eyes and our hands, our ability to create and coordinate movement is something many of us take for granted. So what do we do when those movements stop working as we intend? Today I have the opportunity to speak with one of the world's leading experts on movement disorders, Dr Michael Okun, about the latest issue of Continuum on Movement Disorders. Dr Jones: This is Dr Lyell Jones, Editor-in-Chief of Continuum. Thank you for listening to Continuum Audio. Be sure to visit the links in the episode notes for information about subscribing to the journal, listening to verbatim recordings of the articles, and exclusive access to interviews not featured on the podcast. Dr Jones: This is Dr Lyle Jones, Editor-in-Chief of Continuum: Lifelong Learning in Neurology. Today, I'm interviewing Dr Michael Okun, who is Continuum's guest editor for our latest issue on movement disorders. Dr Okun is the Adelaide Lackner Distinguished Professor of Neurology at the University of Florida in Gainesville, where he's also the director of the Norman Fixel Institute for Neurological Diseases. Dr Okun, welcome, and thank you for joining us today. Why don't you introduce yourselves to our listeners?  Dr Okun: It's great to be here today. And I'm a neurologist. Everybody who knows me knows I'm pretty simple. I believe the patient's the sun and we should always orbit around the person with disease, and so that's how I look at my practice. And I know we always participate in a lot of research, and I've got a research lab and all those things. But to me, it's always the patients and the families first. So, it'll be great to have that discussion today.  Dr Jones: Yeah, thank you for that, Dr Oaken. Obviously, movement disorders is a huge part of our field of neurology. There are many highly prevalent conditions that fit into this category that most of our listeners will be familiar with: idiopathic Parkinson's disease, essential tremor, tic disorders and so on. And having worked with trainees for a long time, it's one of the areas that I see a lot of trainees gravitate to movement disorders. And I think it's in part because of the prevalence; I think it's in part because of the diversity of the specialty with treatment options and DBS and Botox. But it's also the centrality of the neurologic exam, right? That's- the clinical examination of the patient is so fundamental. And we'll cover a lot of topics today with some questions that I have for you about biomarkers and new developments in the field. But is that your sense too, that people are drawn to just the old-fashioned, essential focus on the neurologic encounter and the neurologic exam? Dr Okun: I believe that is one of the draws to the field of movement. I think that you have neurologists from all over the world that are really interested and fascinated with what things look like. And when you see something that's a little bit, you know, off the normal road or off the normal beaten path… and we are always curious. And so, I got into movement disorders, I think, accidentally; I think even as a child, I was looking at people who had abnormal movements and tremors and I was very fascinated as to why those things happened and what's going on in the brain. And, you know, what are the symptoms and the signs. And then later on, even as my own career developed, that black bag was so great as a neurologist. I mean, it makes us so much more powerful than any of the other clinicians---at least in my biased opinion---out on the wards and out in the clinic. And, you know, knowing the signs and the symptoms, knowing how to do a neurological examination and really walking through the phenomenology, what people look like, you know, which is different than the geno- you know, the genotypes, what the genes are. What people look like is so much more important as clinicians. And so, I think that movement disorders is just the specialty for that, at least in my opinion. Dr Jones: And it helps bring it back to the patient. And that's something that I saw coming through the articles in this issue. And let's get right to it. You've had a chance to review all these articles on all these different topics across the entire field of movement disorders. As you look at that survey of the field, Dr Okun, what do you think is the most exciting recent development for patients with movement disorders?  Dr Okun: I think that when you look across all of the different specialties, what you're seeing is a shift. And the shift is that, you know, a lot of people used to talk in our generation about neurology being one of these “diagnose and adios” specialties. You make the diagnosis and there's nothing that you can do, you know, about these diseases. And boy, that has changed. I mean, we have really blown it out of the water. And when you look at the topics and what people are writing about now and the Continuum issue, and we compare that the last several Continuum issues on movement disorders, we just keep accumulating a knowledge base about what these things look like and how we can treat them. And when we start thinking about, you know, all of the emergence of the autoimmune disorders and identifying the right one and getting something that's quite treatable. Back in my day, and in your day, Lyle, we saw these things and we didn't know what they were. And now we have antibodies, now we can identify them, we can pin them down, and we can treat many of them and really change people's lives. And so, I'm really impressed at what I see in changes in identification of autoimmune disorders, of channelopathies and some of the more rare things, but I'm also impressed with just the fundamental principles of how we're teaching people to be better clinicians in diseases like Parkinson's, Huntington's, ataxia, and Tourette. And so, my enthusiasm for this issue of Continuum is both on, you know, the cutting edge of what we're seeing based on the identification on our exams, what we can do for these people, but also the emergence of how we're shifting and providing much better care across a continuum for folks with basal ganglia diseases. Dr Jones: Yeah, I appreciate that perspective, Dr Okun. One of the common themes that I saw in the issue was with these new developments, right, when you have new tools like new diagnostic biomarker tools, is the question of if and when and how to integrate those into daily clinical practice, right? So, we've had imaging biomarkers for a while, DAT scans, etc. For patients with idiopathic Parkinson disease, one of the things that I hear a lot of discussion and controversy about are the seed amplification assays as diagnostic biomarkers. What can you tell us about those? Are those ready for routine clinical use yet?  Dr Okun: I think the main bottom-line point for folks that are out there trying to practice neurology, either in general clinics or even in specialty clinics, is to know that there is this movement toward, can we biologically classify a disease? One of the things that has, you know, really accelerated that effort has been the development of these seed amplification assays, which---in short for people who are listening---are basically, we “shake and bake” these things. You know? We shake them for like 20 hours and we use these prionlike proteins, and we learn from diseases like prion disease how to kind of tag these things and then see, do they have degenerative properties? And in the case of Parkinson's disease, we're able to do this with synuclein. That is the idea of a seed amplification assay. We're able to use this to see, hey, is there synuclein present or not in this sample? And people are looking at things like cerebrospinal fluid, they're looking at things like blood and saliva, and they're finding it. The challenge here is that, remember- and one of the things that's great about this issue of Continuum is, remember, there are a whole bunch of different synucleinopathies. So, Dr Jones, it isn't just Parkinson's disease. So, you've got Parkinson's disease, you've got Lewy body, you know, and dementia with Lewy bodies. You've got, you know, multiple system atrophy is within that synucleinopathy, you know, group primary autonomic failure… so not just Parkinson's disease. And so, I think we have to tap the brakes as clinicians and just say, we are where we are. We are moving in that direction. And remember that a seed amplification assay gives you some information, but it doesn't give you all the information. It doesn't forgive you looking at a person over time, examining them in your clinic, seeing how they progress, seeing their response to dopamine- and by the way, several of these genes that are associated with Parkinson; and there's, you know, less than 20% of Parkinson is genetic, but several of these genes, in a solid third---and in some cases, in some series, even more---miss the synuclein assay, misses, you know, the presence of a disease like Parkinson's disease. And so, we have to be careful in how we interpret it. And I think we're more likely to see over time a gemish: we're going to smush together all this information. We're going to get better with MRIs. And so, we're actually doing much better with MRIs and AI-based intelligence. We've got DAT scans, we've got synuclein assays. But more than anything, everybody listening out there, you can still examine the person and examine them over time and see how they do over time and see how they do with dopamine. And that is still a really, really solid way to do this. The synuclein assays are probably going to be ready for prime time more in choosing and enriching clinical trials populations first. And you know, we're probably 5, 10 years behind where Alzheimer's is right now. So, we'll get there at some point, but it's not going to be a silver bullet. I think we're looking at these are going to be things that are going to be interpreted in the context for a clinician of our examination and in the context of where the field is and what you're trying to use the information for. Dr Jones: Thank you for that. And I think that's the general gestalt I got from the articles and what I hear from my colleagues. And I think we've seen this in other domains of neurology, right? We have the specificity and sensitivity issues with the biomarkers, but we also have the high prevalence of copathology, right? People can have multiple different neurodegenerative problems, and I think it gets back to that clinical context, like you said, following the patient longitudinally. That was a theme that came out in the idiopathic Parkinson disease article. And while we're on Parkinson disease, you know, the first description of that was what, more than two hundred years ago. And I think we're still thinking about the pathophysiology of that disorder. We understand risk factors, and I think many of our listeners would be familiar with those. But as far as the actual cause, you know, there's been discussion in recent years about, is there a role of the gut microbiome? Is this a prionopathic disorder? What's your take on all of that?  Dr Okun: Yeah, so it's a great question. It's a super-hot area right now of Parkinson. And I kind of take this, you know, apart in a couple of different ways. First of all, when we think about Parkinson disease, we have to think upstream. Like, what are the cause and causes? Okay? So, Parkinson is not one disease, okay? And even within the genes, there's a bunch of different genes that cause it. But then we have to look and say, well, if that's less than 20% depending on who's counting, then 80% don't have a single piece of DNA that's closely associated with this syndrome. And so, what are we missing with environment and other factors? We need to understand not what happens at the end of the process, not necessarily when synuclein is clumping- and by the way, there's a lot of synuclein in the brains normally, and there's a lot of Tau in people's brains who have Parkinson as well. We don't know what we don't know, Dr Jones. And so when we begin to think about this disease, we've got to look upstream. We've got to start to think, where do things really start? Okay? We've got to stop looking at it as probably a single disease or disorder, and it's a circuit disorder. And then as we begin to develop and follow people along that pathway and continuum, we're going to realize that it's not a one-size-fits-all equation when we're trying to look at Parkinson. By the way, for people listening, we only spend two to three cents out of every dollar on prevention. Wouldn't prevention be the best cure, right? Like, if we were thinking about this disease. And so that's something that we should be, you know, thinking about. And then the other is the Global Burden of Disease study. You know, when we wrote about this in a book called Ending Parkinson's Disease, it looked like Parkinson's was going to double by 2035. The new numbers tell us it's almost double to the level that we expected in 2035 in this last series of numbers. So, it's actually growing much faster. We have to ask why? Why is it growing faster? And then we have lots of folks, and even within these issues here within Continuum, people are beginning to talk about maybe these environmental things that might be blind spots. Is it starting in our nose? Is it starting in our gut? And then we get to the gut question. And the gut question is, if we look at the microbiomes of people with Parkinson, there does seem to be, in a group of folks with Parkinson, a Parkinson microbiome. Not in everyone, but if you look at it in composite, there seems to be some clues there. We see changes in Lactobacillus, we see some bacteria going up that are good, some bacteria going down, you know, that are bad. And we see flipping around, and that can change as we put people on probiotics and we try to do fecal microbiota transplantations- which, by the way, the data so far has not been positive in Parkinson's. Doesn't mean we might not get there at some point, but I think the main point here is that as we move into the AI generation, there are just millions and millions and millions of organisms within your gut. And it's going to take more than just our eyes and just our regular arithmetic. You and I probably know how to do arithmetic really well, but this is, like, going to be a much bigger problem for computers that are way smarter than our brains to start to look and say, well, we see the bacteria is up here. That's a good bacteria, that's a good thing or it's down with this bacteria or this phage or there's a relationship or proportion that's changing. And so, we're not quite there. And so, I always tell people---and you know, we talk about the sum in the issue---microbiomes aren't quite ready for prime time yet. And so be careful, because you could tweak the system and you might actually end up worse than before you started. So, we don't know what we don't know on this issue.  Dr Jones: And that's a great point. And one of the themes they're reading between the lines is, we will continue to work on understanding the bio-pathophysiology, but we can't wait until that day to start managing the risk factors and treating patients, which I think is a good point. And if we pivot to treatment here a little bit, you know, one of the exciting areas of movement disorders---and really neurology broadly, I think movement disorders has led the field in many ways---is bioelectronic therapy, or what one of my colleagues taught me is “electroceutical therapy”, which I think is a wonderful term. Dr Okun, when our listeners are hearing about the latest in deep brain stimulation in patients who have movement disorders, what should they know? What are the latest developments in that area with devices? Dr Okun: Yeah. So, they should know that things are moving rapidly in the field of putting electricity into the brain. And we're way past the era where we thought putting a little bit of electricity was snake oil. We know we can actually drive these circuits, and we know that many of these disorders---and actually, probably all of the disorders within this issue of Continuum---are all circuit disorders. And so, you can drive the circuit by modulating the circuit. And it's turned out to be quite robust with therapies like deep brain stimulation. Now, we're seeing uses of deep brain stimulation across multiple of these disorders now. So, for example, you may think of it in Parkinson's disease, but now we're also seeing people use it to help in cases where you need to palliate very severe and bothersome chorea and Huntington's disease, we're seeing it move along in Tourette syndrome. We of course have seen this for various hyperkinetic disorders and dystonias. And so, the main thing for clinicians to realize when dealing with neuromodulation is, take a deep breath because it can be overwhelming. We have a lot of different devices in the marketplace and no matter how many different devices we have in the marketplace, the most important thing is that we get the leads. You know, where we're stimulating into the right location. It's like real estate: location, location, location, whether you've got a lead that can steer left, right, up, down and do all of these things. Second, if you're feeling overwhelmed because there are so many devices and so many settings, especially as we put these leads in and they have all sorts of different, you know, nodes on them and you can steer this way and that way, you are not alone. Everybody is feeling that way now. And we're beginning to see AI solutions to that that are going to merge together with imaging, and then we're moving toward an era of, you know, should I say things like robotic programming, where it's going to be actually so complicated as we move forward that we're going to have to automate these systems. There's no way to get this and scale this for all of the locales within the United States, but within the entire world of people that need these types of devices and these therapies. And so, it's moving rapidly. It's overwhelming. The most important thing is choosing the right person. Okay? For this, with multidisciplinary teams, getting the lead in the right place. And then all these other little bells and whistles, they're like sculpting. So, if you think of a sculpture, you kind of get that sculpture almost there. You know, those little adds are helping to maybe make the eyes come out a little more or the facial expression a little bit better. There's little bits of sculpting. But if you're feeling overwhelmed by it, everybody is. And then also remember that we're starting to move towards some trials here that are in their early stages. And a lot of times when we start, we need more failures to get to our successes. So, we're seeing trials of people looking at, like, oligo therapies and protein therapies. We're seeing CRISPR gene therapies in the laboratory. And we should have a zero tolerance for errors with CRISPR, okay? we still have issues with CRISPR in the laboratory and which ones we apply it to and with animals. But it's still pretty exciting when we're starting to see some of these therapies move forward. We're going to see gene therapies, and then the other thing we're going to see are nano-therapies. And remember, smaller can be better. It can slip across the blood brain barrier, you have very good surface area-to-volume ratios, and we can uncage drugs by shining things like focused ultrasound beams or magnets or heat onto these particles to turn them on or off. And so, we're seeing a great change in the field there. And then also, I should mention: pumps are coming and they're here. We're getting pumps like we have for diabetes and neurology. It's very exciting. It's going to be overwhelming as everybody tries to learn how to do this. So again, if you're feeling overwhelmed, so am I. Okay? But you know, pumps underneath the skin for dopamine, pumps underneath the skin for apomorphine. And that may apply to other disorders and not just Parkinson as we move along, what we put into those therapies. So, we're seeing that age come forward. And then making lesions from outside the brain with focused ultrasound, we're starting to get better at that. Precision is less coming from outside the brain; complications are also less. And as we learn how to do that better, that also can provide more options for folks. So, a lot of things to read about in this issue of Continuum and a lot of really interesting and beyond, I would say, you know, the horizon as to where we're headed.  Dr Jones: Thank you for that. And it is a lot. It can be overwhelming, which I guess is maybe a good reason to read the issue, right? I think that's a great place to end and encourage our listeners to pick up the issue. And Dr Okun, I want to thank you for joining us today. Thank you for such a great discussion on movement disorders. I learned a lot. I'm sure our listeners will as well, given the importance of the topic, your leadership in the field over many years. I'm grateful that you have put this issue together. So, thank you. And you're a busy person. I don't know how we talked you into doing this, but I'm really glad that we did.  Dr Okun: Well, it's been my honor. And I just want to point out that the whole authorship panel that agreed to write these articles, they did all the work. I'm just a talking head here, you know, telling you what they did, but they're writing, and the people that are in the field are really, you know, leading and helping us to understand, and have really put it together in a way that's kind of helped us to be better clinicians and to impact more lives. So, I want to thank the group of authors, and thank you, Dr Jones. Dr Jones: Again, we've been speaking with Dr Michael Okun, guest editor of Continuum's most recent issue on movement disorders. Please check it out. And thank you to our listeners for joining today. Dr Monteith: This is Dr Teshamae Monteith, Associate Editor of Continuum Audio. If you've enjoyed this episode, you'll love the journal, which is full of in-depth and clinically relevant information important for neurology practitioners. Use the link in the episode notes to learn more and subscribe. Thank you for listening to Continuum Audio.

If you have Parkinson's, should you see a neurologist who is a movement disorders specialist? A general neurologist? An advanced practice provider –  nurse practitioner or PA? Or your primary care physician.Although this may seem like an obvious series of questions, in this episode nurse practitioner Sherrie Gould unpacks some of the differences between these medical professionals and some of your options if you are facing a long wait to get an appointment to see a clinician.

Episode #115 is all about diving into the midlife woman's brain—your most vital, complex, and vulnerable organ—and why protecting it matters more than ever. Here's a fact that doesn't get enough attention: two out of three people with Alzheimer's are women. And this isn't just about old age. The seeds of cognitive decline can start as early as your 40s—or even sooner.We'll talk about:• Why women are at greater risk for Alzheimer's and dementia• The brain-hormone connection during menopause and midlife• What you can do now to preserve memory, focus, and cognitive resilience• How genes like APOE4 interact with lifestyle—and what that means• How belly fat, or visceral fat. Affect cognition and brain health• And the power of early, personalized preventionMy guest, Dr. Kellyann Niotis, MD, is the first fellowship-trained preventive neurologist in the world, specializing in risk reduction strategies for neurodegenerative disorders such as Alzheimer's Disease, Lewy Body Dementia, and Parkinson's Disease. Dr. Niotis led the preventive neurology program within Dr. Peter Attia's medical practice, Early Medical, and managed the country's first Alzheimer's Prevention Clinic at Weill Cornell Medical College/NewYork-Presbyterian Hospital, where she developed research programs for Parkinson's and Lewy Body Dementia prevention. Her work has been published in several medical journals, including Neurology, Nature Mental Health, Frontiers of Aging Neuroscience, Aging and Disease, Movement Disorders, Journal of Alzheimer's Disease, Alzheimer's & Dementia, and Journal of the Prevention of Alzheimer's Diseas,e and has been presented at national and international conferences.She is passionate about the budding medical space of preventive neurology, in particular pertaining to the advocacy of preventive neurology policy changes and making treatment & education more accessible to the masses. She has received numerous honors and awards, and her opinions have been featured in popular media outlets, including CNN.Whether you're looking for tools to sharpen your brain today or you're thinking long-term about protecting yourself and your loved ones, this conversation is full of insight and hope.Medical Disclaimer:By listening to this podcast, you agree not to use this podcast as medical advice or to make any lifestyle changes to treat any medical condition in yourself or others. Consult your own physician for any medical issues that you may be having. This entire disclaimer also applies to any of my guests on my podcast.Learn more about Dr. Niotis:Website: https://drkellyannniotis.com/IG: @drkellyannniotisFB: @drkellyannniotisResources:Lancet Commission Modifiable Risk Factor list:https://www.thelancet.com/infographics-do/dementia-riskStay connected with JFW:Watch on my YouTube channel: https://www.youtube.com/@jillfooswellness/videosFollow me on Instagram: https://www.instagram.com/jillfooswellness/Follow me on Facebook: https://www.facebook.com/jillfooswellnessGrab discounts on my favorite biohacking products: https://www.jillfooswellness.com/health-productsEnjoy 20% savings and free shipping at Fullscript for your favorite supplements by leading brands:https://us.fullscript.com/welcome/jillfooswellnessSubscribe to the JFW newsletter at www.jillfooswellness.com and receive your FREE Guide on How To Increase Your Protein in 5 Easy Steps and your free Protein Powder Recipe Ebook. Schedule your complimentary 30-minute Zoom consultation here:https://calendly.com/jillfooswellness/30-minute-zoom-consultations

In this episode, Prof. Tiago Outeiro interviews Prof. William Langston on the intriguing history of drug addicts manifesting parkinsonism in the 1980s, and how MPTP became a tool compound for modeling certain aspects of Parkinson's disease.

Ever consider specializing deeper into an aspect of neuro? Wonder what it's like to dive deep into a subset of the neuro population and sharpen your practice? In today's show, host Erin Gallardo, PT, DPT, NCS interviews Andrew Doubek, PT, DPT, GCS, NMD about his recent experience going through an accredited movement disorders fellowship program at the Ohio State. In the show we talk about the details of what the fellowship was like from the schedule, mix of experiences, requirements and types of patients. Andrew shares his insights and words of wisdom to anyone considering a fellowship.   Plus, with documentation efficiency being top of mind for so many clinicians, Andrew generously shares his handout of smart phrases crafted from the Clinical Practice Guidelines that you can plug into your assessments and progress notes to ensure you're targeting the key aspects needed in your notes in less time. Download the smart phrase guides here! PD CPG smartphrase.docx FND smartphrase.docx Core outcomes smart phrases.docx

In this episode of the Scope of Things, host Deborah Borfitz brings you the news on a precision medicine initiative in Sweden integrating research with healthcare, newly available cardiometabolic clinical data registries for real world evidence projects, updates to guidelines on the reporting of clinical trials, AI improving the monitoring of movement disorders, and the best-yet biomarker for stroke and dementia risk. Joining the conversation is Briony Swire-Thompson, director of the Psychology of Misinformation Lab at Northeastern University Network Science Institute, to discuss the current misinformation epidemic and how clinical trials and sites can best deal with it. News Roundup   Precision Omics Initiative Sweden (PROMISE) Correspondence in Nature Medicine  Article in Clinical Research News  Cardiometabolic clinical data registries Article in Clinical Research News New CONSORT reporting guidelines  Article in JAMA VisionMD for analyzing motor function Article in Nature Best-yet biomarker for stroke and dementia risk Article in Diagnostics World News  The Scope of Things podcast explores clinical research and its possibilities, promise, and pitfalls. Clinical Research News senior writer, Deborah Borfitz, welcomes guests who are visionaries closest to the topics, but who can still see past their piece of the puzzle. Focusing on game-changing trends and out-of-the-box operational approaches in the clinical research field, the Scope of Things podcast is your no-nonsense, insider's look at clinical research today.

In observance of Parkinson's disease awareness month, we are excited to speak with special guests Michael S. Fitts and Dr. Reversa Joseph.Michael S. Fitts recent retiree, served as assistant dean for user access and diversity at The University of Alabama at Birmingham (UAB Libraries). He was diagnosed with Parkinson's disease in 2011 at age 38. In 2001 he became the first African American faculty member of the Lister Hill Library of the Health Sciences and later went on to become both the first African American assistant director and assistant dean. In 2015, Michael was appointed to the UAB/Lakeshore Research Collaborative — an organization whose primary goal is to promote the health and wellness of people with disabilities. In addition to his nearly 30-year career with UAB, he actively serves as an advocate for the education of those with early-onset Parkinson's by being an example of living successfully and productively with the disease. Since 2018, Michael has served on the Board of Directors for the Parkinson Association of Alabama, contributing to outreach across the state. Additionally, he actively contributes to the Michael J. Fox Foundation Patient Council and serve as a Research Advocate for the Parkinson's Foundation, supporting research and patient engagement.Dr. Reversa Joseph began her journey into medicine with a passion for solving problems and seeking answers, which naturally led me to neuroscience. However, witnessing my father, a Vietnam veteran, struggle with Parkinson's disease (PD) became the pivotal moment that directed her toward Neurology and ultimately specializing in Movement Disorders. This deeply personal experience profoundly shaped her life and her family's.One unforgettable experience was transitioning her practice from an academic institution to the U.S. Department of Veterans Affairs (VA) to address the unmet needs of veterans with movement disorders. Driven by her father's condition, this shift was both uplifting and challenging. This significant transition was driven by a clear unmet need and her desire to serve our veterans, honoring my father's condition and his service to our country.At the VA, Dr. Joseph developed and leads a Movement Disorders Clinic, directing a Multidisciplinary Care Team to provide comprehensive, integrative care to veterans with Parkinson's disease and other neurological disorders. This endeavor has been deeply fulfilling and reinforced her commitment to serving vulnerable populations and improving healthcare access.Dr. Joseph's involvement with the Parkinson's Foundation began in 2018 as a board member for the Great Lakes Chapter. Throughout the years, she has supported the Foundation by giving various presentations on topics such as PD 101, Women and Parkinson's Disease, and Integrative Therapies and PD. She also participates in Moving Day with her team, Vets on the Move.Dr. Joseph is particularly proud of our efforts to mitigate health inequities in people living with Parkinson's through targeted and tailored training in research advocacy. One of hermost rewarding contributions has been to help develop a novel Learning Institute using culturally responsive pedagogy to train African Americans living with Parkinson's and their care partners to collaborate with researchers and scientists as primary partners in the drug development process.Additionally, Dr. Joseph has given national lectures for the Parkinson's Foundation to raise awareness about Parkinson's disease and the Black community, addressing issues such as late and misdiagnosis, treatment and overall care. Dr. Joseph works to provide a framework on how to mitigate these disparities. She has also participated in various podcasts to raise awareness that Parkinson's also affects African Americans. Her volunteer work is driven by a desire to make a tangible difference, to support an organization that supports so many, and to contribute to t

Send us a textSeason 2 - Episode 31In the ring withParkinson's diseaseThe boys are out on their travels again but this time they are visiting a Centre set up for people battling Parkinson's Disease through a Boxercise session.Parkinson's disease is a progressive brain condition that affects movement, balance, and coordination. It's caused by the death of nerve cells in the brain, which leads to symptoms that can worsen over time. After years of progress, a disease that was once considered untreatable has come to show promising advancements when placed in the right hands of Movement Disorders specialists. Equipped with the right tools and an increased understanding, specialists now have the power to vastly improve the quality of life for the patients affected. Dopamine plays a vital role in regulating the movement of the body. A reduction in dopamine is responsible for many of the symptoms of Parkinson's disease. Exactly what causes the loss of nerve cells is unclear. Most experts think that a combination of genetic and environmental factors is responsible.Today the boys have the opportunity to speak with Head coach Carl Ambrose about the valuable boxercise sessions he provides for people with Parkinson's Disease and the impact it has on their lives.The Boy's also speak to two participants of the class today,  Lisa and David who both have differing levels of Parkinson's disease, they tell us about their illness, their coping mechanisms and what the Boxercise class means to them.This was an eye opening experience for both Martin & Patrick and certainly reinforces how exercise in any form can help illness and just as importantly the mind helping to have a positive mental attitude.#Leemack#Stoma#HeartTransplant#EbsteinsAnomaly#RareCondition#HealthJourney#LifeChangingDiagnosis#MentalHealth#Vulnerability#SelfCompassion#PostTraumaticGrowth#MedicalMiracle#BBCSports#Inspiration#Cardiology#Surgery#Podcast#Healthcare#HeartHealth#MedicalBreakthrough#EmotionalJourney#SupportSystem#HealthcareHeroes#PatientStories#CardiologyCare#MedicalJourney#LifeLessons#MentalWellness#HealthAwareness#InspirationalTalk#LivingWithIllness#RareDiseaseAwareness#SharingIsCaring#MedicalSupport#BBCReporter#HeartDisease#PodcastInterview#HealthTalk#Empowerment#Wellbeing#HealthPodcast#ChronicIllnessCheck out our new website at www.whostomanddick.comwww.milestonefitness>ukCheck out our website at www.whostomanddick.com

In this episode, Brain & Life Podcast co-hosts Dr. Daniel Correa and Dr. Katy Peters answer some listener-submitted questions. Then, Dr. Correa is then joined by Dr. Michael Okun, co-director of the Center for Movement Disorders and Neurorestoration, and the Adelaide Lackner Professor of Neurology at the University of Florida. Dr. Okun sheds light on the increasing rates of Parkinson's disease diagnosis in our communities, environmental factors that may contribute to the disease, and important considerations for those diagnosed with Parkinson's.   Additional Resources Parkinson Secrets Skin Problems May Be Early Signs of a Neurologic Condition Factors That May Increase the Risk of Parkinson's Disease Parkinson's Disease Won't Extinguish This Firefighter's Passion   Other Brain & Life Podcast Episodes Ed Begley Jr. on Utilizing a Healthy Lifestyle to Thrive with Parkinson's Disease How American Ninja Warrior Jimmy Choi Rose Above Parkinson's Comedy and Courage: Comedian Richard Lewis on Living with Parkinson's Disease   We want to hear from you! Have a question or want to hear a topic featured on the Brain & Life Podcast? ·       Record a voicemail at 612-928-6206 ·       Email us at BLpodcast@brainandlife.org   Social Media:  Dr. Michael Okun @michaelokun @fixelinstitute Hosts: Dr. Daniel Correa @neurodrcorrea; Dr. Katy Peters @KatyPetersMDPhD

Dr. Michele Matarazzo interviews Dr. Victor Fung, President of the International Parkinson and Movement Disorder Society and lead author of the recent viewpoint published in the Movement Disorders journal. Together, they explore the biological definition and classification of Parkinson's disease, discussing its key insights, future prospects, and the implications of recent advances in the field. Read the article.

In this enlightening episode of Join the Docs, the ever-curious Professor Jonathan Sackier and the delightfully witty Doctor Nigel Guest dive deep into the gray matter (pun absolutely intended) to untangle the mysteries of the human brain and its trusty sidekick, the nervous system. Who are the guests this week? Joining this week is the insightful Ione Georgakis, an Occupational Therapist and Advocacy Manager for Tourette Action and Dr. Ed Palmer, a fellow Tourette expert and psychiatrist.. Ione and Ed bring a synapse-worthy amount of knowledge and compassion to the discussion, shedding light on the challenges faced by individuals with Tourette syndrome and other movement disorders. Their expertise in therapeutic interventions and advocacy adds a crucial nerve center to the conversation, underscoring the importance of holistic care and patient empowerment.  How does the brain orchestrate movement? The dynamic trio pirouettes straight into the topic, exploring the brain's role as the maestro of movement. Tremors are likened to an over-caffeinated squirrel, while rigidity gets compared to the Tin Man pre-lube job, adding just the right amount of levity to complex concepts.  When Parkinson's disease is discussed, The Docs examine it with a careful and informed approach. Diagnosing the condition, they explain, requires a balance of scientific knowledge and clinical judgment, as the symptoms can be subtle and vary from person to person. Treatment options are diverse, including medications and deep brain stimulation, a procedure that involves implanting a device to help regulate brain activity and manage symptoms more effectively. The laughs don't come at the expense of insight. Stories pepper the episode like synaptic sparks. Ione and Ed  add their own heartwarming anecdotes of resilience and triumph, illustrating how tailored therapies and supportive communities provide vital nourishment for those living with movement disorders.What will you take away from this episode? By the episode's end, listeners will have a newfound appreciation for the pun-damental intricacies of the human brain, a smile on their faces, and perhaps an irresistible urge to break out into dance—just remember to thank your motor neurons!  —--DISCLAIMER: The views and opinions expressed on Join the Docs are those of Dr. Nigel Guest, Jonathan Sackier and other people on our show. Be aware that Join the Docs is not intended to be medical advice, it is for information and entertainment purposes only - please, always take any health concerns to your doctor or other healthcare provider. We respect the privacy of patients and never identify individuals unless they have consented. We may change details, dates, place names and so on to protect privacy. Listening to Join the Docs, interacting on our social media, emailing or writing to us does not establish a doctor patient relationship.To Contact Us: For a deeper dive on this episode's issue, merchandise and exclusive content, head to www.jointhedocs.comFollow us on youtube.com/JoinTheDocs Follow us on instgram.com/JoinTheDocsFollow us on tiktok.com/JoinTheDocsFollow us on: facebok.com/JoinTheDocsFollow us on: x.com/JoinTheDocs

Dr. Sara Schaefer interviews Dr. Jaclyn Martindale on stigma in the experiences of individuals with pediatric movement disorders and tic disorders. They discuss the reasons behind stigma, types of stigma, and ways that stigma is perpetuated and mitigated in this special episode for World Movement Disorders Day 2024.

Dr. Indu Subramanian shares her view on stigma affecting people with Parkinson's disease, along with some practical tips on how to fight it as doctors and as a society.

Today's episode is a look into a condition that affects millions every day, epilepsy. While it's impact and triggers can be overwhelming, the latest advancements in medicine offer much hope for patients and their families alike. Host:Willard ShepardAward-Winning JournalistExperts:Dr. Pooja Patel, M.D.Neurologist Director of the epilepsy monitoring unit at Marcus Neuroscience InstituteDr. Luis Felipe Tornes, M.D.NeurologistDirector of the epilepsy program at Baptist Health Miami Neuroscience Institute

Dr. Natasha Fothergill-Misbah discusses stigma in movement disorders with Dr. Sara Schaefer, including the origins, types, and consequences of stigma, and how stigma may be perpetuated and combatted around the world.

To help meet the growing global need for more movement disorders specialists, The Michael J. Fox Foundation created the Edmond J. Safra Fellowship in Movement Disorders in collaboration with longtime partner the Edmond J. Safra Foundation. This program supports the training of movement disorders specialists who will provide expert care and drive advances in Parkinson's research. The program is positively impacting early-career clinician-researchers, as well as the centers where they train. These impacts will continue to grow over the years as more fellows are trained. In this episode, Dr. Marcelo Merello and Dr. Sergio Castillo-Torres share their insights and perspectives as a Fellowship Director and a Fellow in the program, respectively. Marcelo is Director of the Department of Neurosciences and Chief of the Movement Disorders Clinic at the Institute for Neurological Research or Fleni Hospital. He is fellowship Director at Fleni and the University of Buenos Aires. In addition, Marcelo is Principal Investigator with the National Council for Scientific and Technical Research and Professor of Neurodegenerative Diseases at the Pontifical Catholic University of Argentina. Sergio is an Associate Professor in Neurology and Internal Medicine at the Dr. Jose E. Gonzales University Hospital of the Autonomous University of Nuevo Leon. He was an Edmond J. Safra Fellow in Movement Disorders at Fleni Hospital. Visit michaeljfox.org/fellowship to learn more about the Edmond J. Safra Fellowship in Movement Disorders.This podcast is geared toward researchers and clinicians. If you live with Parkinson's or have a friend or family member with PD, listen to The Michael J. Fox Foundation Parkinson's Podcast. Hear from scientists, doctors and people with Parkinson's on different aspects of life with the disease as well as research toward treatment breakthroughs at https://www.michaeljfox.org/podcasts.

To help meet the growing global need for more movement disorders specialists, The Michael J. Fox Foundation created the Edmond J. Safra Fellowship in Movement Disorders in collaboration with longtime partner the Edmond J. Safra Foundation. This program supports the training of movement disorders specialists who will provide expert care and drive advances in Parkinson's research. The program is positively impacting early-career clinician-researchers, as well as the centers where they train. These impacts will continue to grow over the years as more fellows are trained. In this episode, Dr. Marcelo Merello and Dr. Sergio Castillo-Torres share their insights and perspectives as a Fellowship Director and a Fellow in the program, respectively. Marcelo is Director of the Department of Neurosciences and Chief of the Movement Disorders Clinic at the Institute for Neurological Research or Fleni Hospital. He is fellowship Director at Fleni and the University of Buenos Aires. In addition, Marcelo is Principal Investigator with the National Council for Scientific and Technical Research and Professor of Neurodegenerative Diseases at the Pontifical Catholic University of Argentina. Sergio is an Associate Professor in Neurology and Internal Medicine at the Dr. Jose E. Gonzales University Hospital of the Autonomous University of Nuevo Leon. He was an Edmond J. Safra Fellow in Movement Disorders at Fleni Hospital. Visit michaeljfox.org/fellowship to learn more about the Edmond J. Safra Fellowship in Movement Disorders.This podcast is geared toward researchers and clinicians. If you live with Parkinson's or have a friend or family member with PD, listen to The Michael J. Fox Foundation Parkinson's Podcast. Hear from scientists, doctors and people with Parkinson's on different aspects of life with the disease as well as research toward treatment breakthroughs at https://www.michaeljfox.org/podcasts.

Dr. Alexander Lehn breaks down functional movement disorders; what is happening in the brain, what are the potential risk factors and what future treatments and clinical trials we have to look forward to.

Dr. Sara Schaefer interviews Dr. Jennifer Goldman about her systematic review and meta-analysis on subjective cognitive complaints in Parkinson's disease, including the prevalence, epidemiology, and correlation with objective cognitive findings and neuropsychiatric disease. The article was recently named the Movement Disorders journal Review Article of the Year.

Autoimmune cerebellar ataxia and other autoimmune movement disorders encompass a broad spectrum of different clinical syndromes, antibodies, and immunopathophysiologic mechanisms. Given the overlap between phenotypes and antibodies, panel testing in serum and CSF is recommended. In this episode, Gordon Smith, MD, FAAN, speaks with Bettina Balint, MD, author of the article “Autoimmune Movement Disorders,” 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. Balint is an assistant professor for clinical research on complex movement disorders and Parkinson's diseases, a consultant neurologist, the head of the Department of Movement Disorders, and co-lead for the Centre for Movement Disorders and Functional Neurosurgery in the Department of Neurology at the University Hospital Zurich in Zurich, Switzerland. Additional Resources Read the article: Autoimmune Movement Disorders Subscribe to Continuum: shop.lww.com/Continuum Earn CME (available only to AAN members): continpub.com/AudioCME Continuum® Aloud (verbatim audio-book style recordings of articles available only to Continuum® subscribers): continpub.com/Aloud More about the 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, 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: This is Dr Gordon Smith. Today, I'm interviewing Dr Bettina Balint about her article on ataxia and other autoimmune movement disorders, which appears in the August 2024 Continuum issue on autoimmune neurology, which is a highly anticipated and exciting issue. Dr Balint, welcome to the podcast, and, perhaps, you can just introduce yourself to our audience and tell us a little bit about your practice and how you became interested in this topic.   Dr Balint: Thank you, Gordon, for having me. I am an assistant professor for clinical research in complex movement disorders and Parkinson's disease at the University of Zurich and the Head of the Movement Disorders Department at the University Hospital in Zurich. So while I'm originally German (from Heidelberg), I have now been to Switzerland since end of 2021.   Dr Smith: So, you know, how many movement disorder chiefs have a focus on autoimmune movement disorders? I found that really interesting. Most of the movement disorder folks I interact with, their primary interest is in neurodegeneration.   Dr Balint: Very good question. Even so, I never asked myself that question, really, but I think I'm the only one with this designated focus as such. Many people come from the neurology angle - most of them. Even so, movement-disorder people really welcome this field and are interested, but I think somebody who has dedicated their interest and time to it? I think I can't actually think of many other people.   Dr Smith: Yeah, I think it's really cool, and, of course, autoimmune neurology is the flavor of the day these days, right? I mean, I remember when I was at the University of Utah, we were recruiting Stacy Clardy (who I think many of our listeners will know). I remember thinking, you know, she's never going to be busy. How many of these autoimmune problems are there, really? And she was, like, deluged when she came. These are really common problems. I guess that was one question I had for you. You know, we think of these as rare disorders, and when we look at the article, you have these tables of these antibodies, and a lot of them are pretty uncommon – but, cumulatively, how common are autoimmune movement disorders?   Dr Balint: It's a very difficult question, because we don't have good epidemiological data. And if you look at series, I mean, most papers addressing this issue come actually from the ataxia field. And then, depending on where you look at, you might find varying numbers, and they might be also influenced by the fact that they come from ataxia centers with own certain biases. Even so, it's very close to my heart, but, I also still think it's overall very rare. So, in my practice, I see all sorts of movement disorders, and overall, they're still quite rare, but the point is that they are treatable and have important management implications, so you want to be sure not to miss any of them.   Dr Smith: Well, maybe we can go to that next. Part of the challenge here, of course, is there's just so many of these different syndromes and antibodies. Are there pearls that you can provide our listeners that would help them guide when they should be thinking about these disorders when they confront a patient with a particular phenotype? Like ataxia, for instance - you know, there are certain aspects of the clinical scenario that should trigger, “Wow, this might be an autoimmune problem”.   Dr Balint: So, in general, I would say there are certain scenarios where you would want to think of an autoimmune etiology in your differential. One is a very characteristic phenotype. So, speaking broadly in terms of movement disorders, stiff-person spectrum disorders have a very characteristic phenotype which you need to recognize, and then you will be able to see it when a patient enters. Important phenotypes to know which are very characteristic are faciobrachial dystonic seizures, for example, with anti-GA1 antibodies, or pseudofinalistic movements in non-REM sleep is IgLON5 antibodies, leg myoclonus is CASPR2 antibodies. I don't want to necessarily enumerate all the scenarios. The point here is there are some characteristic phenotypes where you would think of autoimmune neurology. Another scenario where you would think of autoimmune, for example, the context of late-onset paroxysmal movement disorders. So, classically, when we think of paroxysmal dyskinesia, we think of a group of genetic disorders, but if somebody develops a paroxysmal movement disorder later in life in adulthood, then you would think of autoimmune neurology, and this applies also in the context of episodic ataxias. Another red flag might be a propensity to autoimmunity. For example, somebody with type one diabetes and vitiligo coming in for cerebellar ataxia, of course, you would think of anti-GAD ataxia. And, similarly, if somebody has recently been diagnosed with a cancer and develops a rapidly disabling syndrome, of course, then you would think of a paraneoplastic autoimmune disorder. And with autoimmune syndrome, there are some symptoms which are also like tell-tale signs. So, for example, somebody with a stiff-person spectrum disorder, an ataxia with long-lasting diarrhea over months, losing weight - investigations haven't found anything, then you would think of DPPX antibodies or celiac disease. Or, if you have, like, a neuropathic pain which is otherwise not explained, then you might think of CASPR2 antibodies in somebody with a cerebellar ataxia. So, there are some features of some antibodies. (Again, I will not now list all of them which might point you to a diagnosis.) Then, of course, another scenario which is important, I think, is if you have a hemisyndrome without a structural lesion on imaging. Classically, neurologists are trained to think of a hemisyndrome - we look for a lesion on the contralateral side. But if you have, like, for example, a hemichorea without a lesion or a hemiataxia without a lesion, one should also think of an autoimmune disorder with antibodies. And then, more generally, of course, if you have changes on brain MRI or information on CSF, of course, if the clinical cause is more rapidly progressive - and last, but not least, if somebody does not really fit into our categories of the degenerative symptoms or metabolic syndromes or functionality disorders, then, of course, one should just take a step back and think, could it be something autoimmune? Having said that, if I may, I just want to say that, I mentioned that rapid disease course, and on the other hand, it's important to stress that a slowly progressive disease cause does not exclude an autoimmune etiology.   Dr Smith: So, that was a great summary. Thank you. I don't know if you're familiar with the term “Aunt Minnie” (something I learned in medical school and radiology). There are certain findings that are “Aunt Minnie”, you know what “Aunt Minnie” looks like, and if you see these particular findings, you should really think about a specific disease - and I think you gave a lot of pearls in that answer, so I appreciate that. This may seem like a bit of a random question, but it's interesting that there are some of these phenotypes that do replicate genetic phenotypes, and you used episodic ataxia, which, in a younger individual, we think of a spectrum of various genetic disorders. Is that random, or are there instances where the underlying mutation in a genetic disorder actually serves as a target for autoimmunity in a later-onset autoimmune problem? Not that the mutation causes autoimmunity, but are there shared targets - in one disease it's the mutation, and another, there's an antibody that binds to the protein, for instance?   Dr Balint: That's an excellent topic, and even though it's not addressed in the Continuum article, I actually covered this in an article in Brain from 2018, where we also discuss parallels (immunogenetic parallels) with targets seen in genetic disease or in autoimmune disease, and there are actually some examples for cerebellar ataxia, and some of the targets are, indeed, the same for the antibodies and mutation. And some targets are a little bit more difficult, because for those, the antibodies would probably not be pathogenic, but it's more like an autoimmune overall target but it's T-cell mediated. But, for example, water-gated, um, calcium channels - we have antibodies and we have mutations. Or, another example would be glycine receptor antibodies give you acquired hyperekplexia, whereas the mutations give you hereditary hyperekplexia. So, there is, indeed, a bit of an overlap between autoimmune and genetic disorders, but often, also, like, the age at onset (because that might be the next question, the age at onset), and maybe family history and associated features, should help to distinguish the two. I think more from the pathophysiological point interesting, rather than clinically too confusing.   Dr Smith: Wow, that's really cool. So, another question I have is regarding antibody panels, right? And so, I think, oftentimes (at least around here), folks confronting an unusual phenotype will send the Mayo panel - they'll send autoimmune encephalitis or a paraneoplastic panel – and, you know, I think one of the challenges I have thinking about the spectrum of phenotypes that you described, I mean, if you recognize “Aunt Minnie”, then you know where to go, but it seems to me that there's a lot of these that maybe folks don't recognize “Aunt Minnie”. What is the diagnostic utility and pearls and pitfalls of ordering these panels when you're not really certain? In other words, is there a risk of a false positive if the pretest probability is low? So, I guess that's a long question, but do you have guidance about when we should and maybe when we should not be ordering these panels? So, you know, undifferentiated ataxia that's chronically progressive - should we be sending a panel or not? Patients who are later-onset acute, maybe so. So, what's the guidance on when to order the panel?   Dr Balint: It's a tricky topic also for many people in our practice, because, of course, as you said, we don't want to miss something, but, indeed, with any test which you order with a low pretest probability and which is not quite appropriate, you might have false positives, and that might cause much additional trouble in security, or maybe unnecessary and invasive immunotherapy with adverse effects – so, it's really important to think well about antibody testing. And, generally speaking, like always in medicine, we shouldn't order random tests, and antibody panels and neuronal antibodies are not designed as a screening test, so you need to have a phenotype and a reasonable suspicion - and clinical acumen is really key, and that's why also the article is so much focused on the phenotype. It's clearly not that any movement disorder patient who enters the outpatient clinic should get a blood test for antibodies that will likely cause harm, and it has been shown that these antibodies can be falsely positive, both in other diseases but also in healthy controls, and much depends also on which tests you use (but, let's not go into too much detail over here) - so, generally speaking, I would say if you have a suspicion of an autoimmune disease clinically (I mentioned some scenarios where you would think of an autoimmune disorder). And then, ataxias are, of course, a bit tricky, because often, we don't have too many other handles there, and there's still also a significant number of acquired late-onset ataxia where we don't know what the cause is. I think in the ataxia scenario, if I don't have a good answer or explanation, I would order antibody tests a bit more freely - I mean, if you do it properly, you do the serum and the CSF, and that also increases your sensitivity but also the specificities, so I wouldn't then just do the serum, but then go for serum and CSF. In other movement disorders, it depends also a little bit on the phenotype. So, somebody with a phenotype fitting well with Parkinson's disease, I wouldn't do any testing. Somebody with clear PSP phenotype without any red flags or not-fitting features, it is very unlikely to have an antibody finding, and this has been shown also in cohorts. But, if you have something which is not fitting in the phenotypes - for example, you have somebody where you think it might be a PSP phenotype with predominantly axial Parkinsonism falls, but you notice that the oculomotor disturbance is not a vertical gaze palsy, but a horizontal gaze palsy – so, it's not really fitting phenotype as you know it. That's a scenario where would probably think of antibody testing. Then, if you do the testing theorem - and CSF, in general, is gold standard - there are some antibodies where theorem is good enough (like, for example, with aquaporin-4 antibodies), but the reason why we do serum and CSF, as I mentioned, is the increased sensitivity and specificity. And nowadays, in the antibody world, we have something similar to the genetics - we have the variant of unknown significance and in the neurology world, we coin the term “antibody of unknown significance” to also give a name to the problem that, sometimes, we get a test result and it is difficult to interpret. Another handle over there would be to try to confirm the test result in another test method. So for example, if you have a cell-based assay with an antibody finding, you would like to confirm that on immunohistochemistry - the staining pattern is in keeping with that.   Dr Smith: So, Bettina, that was a really great and comprehensive answer to the question with a lot of pearls packed into it, and I think the idea that, you know, oftentimes, it's helpful to do both serum and CSF testing is important - also looking for staining to further confirm the diagnosis. And, I think one of the things that I was struck by in your response was the example of a PSP patient who instead of vertical gaze palsy had horizontal gaze palsy as a red flag, and I think a lot of our listeners are probably familiar with the idea that maybe hyperkinetic movement disorders might be autoimmune, or certainly rapidly progressive ataxia, but at least I don't think of Parkinsonian syndromes as often. I know there are some that we need to consider. Maybe you can give us some pearls about when we should consider antibody testing in a patient who has a Parkinson syndrome?   Dr Balint: So, I will not cover now the paraneoplastic Parkinsonian syndromes (because they typically develop as rapidly that you would anyway think about it, hopefully), but go more into those conditions which might mimic degenerative disease - and one of the most interesting antibodies in this regard is IgLON5, and you will be aware that it has been discovered in 2014 in patients who shared a characteristic sleep movement disorder (non-REM parasomnia). The spectrum has broadened a lot, and one possible manifestation is that it could come into the differential of Parkinsonian syndromes - so, for example, if you have axial Parkinsonism and a gaze palsy, you are in a PSP phenotype, but the red flag would be maybe if the eye movement disorders are not really fitting with the PSP phenotype. Also, in PSP patients, we don't expect parasomnias at night. If the bed partner is, for example, complaining that the patient is moving in his sleep and doing movements, then this would be a red flag, and in this context, you would think of IgLON5. IgLON5 could also give you Parkinsonism and cerebellar ataxia, and they might have dysautonomia, and, of course, with a sleep movement disorder, you are now in the ballpark of MSA phenotypes; however, if there are additional features (like, for example, fasciculations) which you don't expect in MSA, that would be, again, the red flag. So, typically, even in those differentials, there are some red flags on handles which would point you to the diagnosis - it is not that it completely mimics the phenotype of our default degenerative disease, but, sometimes, you need to hunt a little bit for those handles.   Dr Smith: So, Bettina, that's really interesting. I wanted to ask you about IgLON5, and in particular, the sleep phenotype, but, you know, I wonder whether there's a risk of just confusing this with REM sleep behavior disorder and a chronic Parkinsonian syndrome - what's the time course of this, and any other wisdom in terms of how to differentiate it from, you know, a more common neurodegenerative problem?   Dr Balint: So, the spectrum of sleep disorders in IgLON5 is actually a bit broad. The characteristic thing is the non-REM sleep parasomnia with the finalistic fine movements, but classic REM sleep behavior disorder has also been reported in these patients. And one of the tricky things is IgLON5 is a slowly progressive disease (some patients had symptoms for a decade prior to diagnosis), so it's really an important differential of autoimmune disease - but as mentioned, the features not fitting in, and they are typically also the cardinal features. So, gaze palsies are very frequent, ptosis, bulbar symptoms, vocal cord palsy, sleep movement disorders which might not fit to the original phenotype, and breathing problems (for example) so severe that they require a tracheostoma – so, these are some red flags which would alert you to this diagnosis of anti-IgLON5 disease.   Dr Smith: I'm curious, Bettina, how do you keep up on all of this and keep it all straight? Right, there's a lot of information, and as I was reading your article, you've got these wonderful tables - and in fact, this whole issue for our listeners feels that way. I've read several of these articles now, and I'm just curious what your strategy is to stay up to date and stay organized. You have to be very organized to be an autoimmune neurologist, it seems to me.   Dr Balint: And having a little bit of OCD helps clearly, as always, in neurology. I think it is just that I started to be interested in this area for a while and I have in my head the clinical phenotype to most important associated antibodies, and as the field continues, I just add up on that panel. But, I don't want people to be discouraged - you're right, many antibodies, but I think the point is not to know each and every antibody but to know in which scenario to think of an autoimmune syndrome and then to know where to look it up.   Dr Smith: Well, I think that's a great way of ending our conversation, Bettina. I think your article does a great job of that, and one of the things I love about Continuum is these articles serve as point-of-care tools. I think our conversation will also serve as a useful framework, because I think you've talked a lot about how to organize your thinking, and, you know, pearls for when we should be thinking about these disorders which are uncommon, but you certainly don't want to miss one because the therapy can be very effective. So, Bettina, thank you so much for joining me. This has been a really great conversation.   Dr Balint: Thank you so much, Gordon. Thank you very much for your good questions.   Dr Smith: So, again, today, I've had the great pleasure of interviewing Dr Bettina Balint, whose article on ataxia and other autoimmune movement disorders appears in the most recent issue of Continuum, which is on autoimmune neurology. Be sure to check out Continuum Audio episodes from this and other issues. And thanks 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.

Though existing evidence supports that dysfunction in the clearing of cellular debris plays an important role in the development of Parkinson's disease, many unanswered questions remain regarding the mechanisms of the autophagy-lysosomal pathway involved in this process. In particular, research in the field has been limited by a lack of reliable, quantitative tests for monitoring autophagy-lysosome activity. In this interview, Dr. Zhenyu Yue describes his research investigating the cellular and molecular mechanisms for Parkinson's disease and other neurodegenerative diseases, focusing on their work examining the regulation of the autophagy-lysosomal pathway, potential therapeutic targets, and MJFF-funded research that aims to develop sensitive, robust autophagy-lysosome assays to facilitate the discovery of biomarkers for PD using stem cell-derived neurons and biofluids. Zhenyu is the Aidekman Research Professor in the Department of Neurology and Friedman Brain Institute at the Icahn School of Medicine at Mount Sinai. He is also the Director of the Center of Parkinson's Disease Neurobiology and Director of Basic Research of Movement Disorders at Mount Sinai.This podcast is geared toward researchers and clinicians. If you live with Parkinson's or have a friend or family member with PD, listen to The Michael J. Fox Foundation Parkinson's Podcast. Hear from scientists, doctors and people with Parkinson's on different aspects of life with the disease as well as research toward treatment breakthroughs at https://www.michaeljfox.org/podcasts.

Though existing evidence supports that dysfunction in the clearing of cellular debris plays an important role in the development of Parkinson's disease, many unanswered questions remain regarding the mechanisms of the autophagy-lysosomal pathway involved in this process. In particular, research in the field has been limited by a lack of reliable, quantitative tests for monitoring autophagy-lysosome activity. In this interview, Dr. Zhenyu Yue describes his research investigating the cellular and molecular mechanisms for Parkinson's disease and other neurodegenerative diseases, focusing on their work examining the regulation of the autophagy-lysosomal pathway, potential therapeutic targets, and MJFF-funded research that aims to develop sensitive, robust autophagy-lysosome assays to facilitate the discovery of biomarkers for PD using stem cell-derived neurons and biofluids. Zhenyu is the Aidekman Research Professor in the Department of Neurology and Friedman Brain Institute at the Icahn School of Medicine at Mount Sinai. He is also the Director of the Center of Parkinson's Disease Neurobiology and Director of Basic Research of Movement Disorders at Mount Sinai.This podcast is geared toward researchers and clinicians. If you live with Parkinson's or have a friend or family member with PD, listen to The Michael J. Fox Foundation Parkinson's Podcast. Hear from scientists, doctors and people with Parkinson's on different aspects of life with the disease as well as research toward treatment breakthroughs at https://www.michaeljfox.org/podcasts.

August 8, 2024 - Mental Health Association of New York State CEO Glenn Liebman talks about legislation addressing drug-induced movement disorders, which can be caused by older medications used to treat severe mental health conditions.

In the last episode of this three-part series, Dr. Jeff Ratliff discusses how to approach patients presenting with emergent rigidity and difficulty moving.

In the second episode of this three-part series, Dr. Jeff Ratliff provides a rapid overview of hyperkinetic disorders that require urgent attention.

In the first episode of this three-part series, Dr. Jeff Ratliff discusses a few key points to help recognize and initiate treatment for patients with movement disorder emergencies, focusing on the initial approach to these disorders. It is important to consider medications, labs, and imaging as part of the evaluation process.

Dr. Eduardo Fernández and Dr. Daniel Weintraub discuss whether subjective cognitive complaints can predict future incident cognitive impairment and other questions related to early cognitive impairment in people with Parkinson's disease, referencing Dr. Weintraub's recent article, "Association between subjective cognitive complaints and incident functional impairment in Parkinson's disease" published in Movement Disorders. Read article »

On this episode, we discuss the management of a few different movement disorders. We review the pharmacotherapy options for restless leg syndrome, Tourette's syndrome, and tardive dyskinesea.  Cole and I are happy to share that our listeners can claim ACPE-accredited continuing education for listening to this podcast episode! We have continued to partner with freeCE.com to provide listeners with the opportunity to claim 1-hour of continuing education credit for select episodes. For existing Unlimited (Gold) freeCE members, this CE option is included in your membership benefits at no additional cost! A password, which will be given at some point during this episode, is required to access the post-activity test. To earn credit for this episode, visit the following link below to go to freeCE's website: https://www.freece.com/ If you're not currently a freeCE member, we definitely suggest you explore all the benefits of their Unlimited Membership on their website and earn CE for listening to this podcast. Thanks for listening! We want to give a big thanks to our sponsor, High-Powered Medicine. HPM is a book/website database of summaries for over 150 landmark clinical trials. You can get a copy of HPM, written by Dr. Alex Poppen, PharmD, at the links below:  Purchase a subscription or PDF copy - https://highpoweredmedicine.com/ Purchase the paperback and hardcover - Barnes and Noble website We want to give a big thanks to our main sponsor Pyrls. Try out their drug information app today. Visit the website below for a free trial: www.pyrls.com/corconsultrx If you want to support the podcast, check out our Patreon account. Subscribers will have access to all previous and new pharmacotherapy lectures as well as downloadable PowerPoint slides for each lecture. You can find our account at the website below:  www.patreon.com/corconsultrx If you have any questions for Cole or me, reach out to us on any of the following: Text - 415-943-6116 Mike - mcorvino@corconsultrx.com Cole - cswanson@corconsultrx.com Instagram and other social media platforms - @corconsultrx  This podcast reviews current evidence-based medicine and pharmacy treatment options. This podcast is intended to be used for educational purposes only and is intended for healthcare professionals and students. This podcast is not for patients and not intended as advice or treatment.

In this Hot Topic, Dr. Sarah Lidstone moderates a discussion with Dr. Mark Hallett and Prof. Mark Edwards on the limitations of phenomenology in movement disorders. Drawn from a recent viewpoint by Prof. Edwards and using functional movement disorder as an example, they discuss the benefits and drawbacks of a phenotype equaling disease paradigm, the voluntary vs. involuntary movement disorder, and what we can learn from functional movement disorders.

Demand for movement disorder specialists continues to grow, but not enough neurologists are receiving focused training in Parkinson's and related conditions in order to meet the current and projected needs in the U.S. and around the world. In collaboration with longtime partner the Edmond J. Safra Foundation, The Michael J. Fox Foundation created the Edmond J. Safra Fellowship in Movement Disorders with the goal of growing the global base of movement disorders specialists. In this episode Dr. Rachel Dolhun shares more about this fellowship program, the application process, and how the program supports the training of movement disorders clinician-researchers who will become leaders in Parkinson's care and advance science in the field. Rachel is Senior Vice President of Medical Communications at The Michael J. Fox Foundation for Parkinson's Research. Visit michaeljfox.org/funding to learn more about the Edmond J. Safra Fellowship in Movement Disorders. This podcast is geared toward researchers and clinicians. If you live with Parkinson's or have a friend or family member with PD, listen to The Michael J. Fox Foundation Parkinson's Podcast. Hear from scientists, doctors and people with Parkinson's on different aspects of life with the disease as well as research toward treatment breakthroughs at https://www.michaeljfox.org/podcasts.

In this Hot Topic episode, Dr. Michele Matarazzo interviews Dr. Raul Martinez on the recent evidence and future applications of focused ultrasound-based ablations in movement disorders, such as Parkinson's disease and essential tremors. Discover how this innovative approach is improving patient care and what it could mean for the future of medical treatment.

Award-winning actor Michael J. Fox was diagnosed with Parkinson's disease in 1991 at just 29 years of age. It's a progressive brain disorder that can strip away a person's movement and speech over time. There's been some headway since Mr. Fox created his foundation on Parkinson's research in 2000. But what's the latest and what more can be done for the estimated one million Americans who have this disease? Host: David Jeannot Guests: Diego Torres-Russotto, M.D., Chief of Movement Disorders at Baptist Health Miami Neuroscience Institute Ana Velasco, Parkinson's Patient

Grab your Neuro Rapid Review Questions Grab your Neuro Rapid Review Questions More Neuro for the PANCE 122 Peripheral Nerve Disorders & how to keep getting better at what you do 121 Movement Disorders – Best episode ever 120 Movement Disorders 119 Headaches – Get These Right! 118: Brain Trauma & Memorizing Medication tip The post 123 Seizures & Cognitive Disorders – Last episode of 2023 appeared first on Physician Assistant Exam Review.

www.physicianassistantexamreview.com/blackfriday to find out more about getting in on the 75% off deal Click here to get the active study guide for movement disorders – It’s amazing! Essential Tremor Clinical Presentation Labs, Studies, and Physical Exam Findings Treatment Huntington's Disease Clinical Presentation Labs, Studies, and Physical Exam Findings Treatment Parkinson's Disease Clinical Presentation Labs, Studies, […] The post 121 Movement Disorders – Best episode ever appeared first on Physician Assistant Exam Review.

I created an Active Study Guide for this episode with Sticky Stories, PANCE questoins and more. Click here to get it. Cerebral Palsy Risk Factors Clinical Presentation Labs, Studies, and Physical Exam Findings Treatment Differential Diagnosis Multiple Sclerosis (MS) Risk Factors Clinical Presentation Labs, Studies, and Physical Exam Findings Treatment Options Differential Diagnosis Myasthenia Gravis […] The post 120 Movement Disorders appeared first on Physician Assistant Exam Review.

For the second time this summer the top Republican in the Senate, Minority Leader Mitch McConnell, abruptly went silent at a news conference. He was about to answer a question from a reporter when he suddenly froze up. He seemed unable to speak. An aide then stepped in, trying to keep things moving along.The senator's silences have raised concerns about his mental fitness – and larger questions about an aging Congress.NPR's Mary Louise Kelly speaks with Dr. Ann Murray, the Movement Disorders division chief at the Rockefeller Neurosciences Institute at West Virginia University.