The FND Society Podcast
Welcome to the FND Society Podcast, a series tailored for clinicians and researchers in the field of Functional Neurologic Disorders.
The podcast covers a wide range of topics, from basic science aspects like neuroimaging and biomarkers to clinical practice issues such as diagnosis, treatments, and outcomes. It also explores how FND is understood and treated within the current medical and psychological paradigms, with a goal to enhance knowledge and awareness across the medical community.
Our goal is to make this a valuable and accessible resource for professionals, delivering the latest research in FND through engaging conversations with experts in the field. We aim for this series to be a practical and informative experience, connecting listeners directly with groundbreaking developments and insights in FND. It's our hope that each episode will contribute meaningfully to your professional knowledge and understanding.
For more information about the FND Society visit: www.fndsociety.org
The FND Society Podcast
Jeff Staab - Persistent Postural-Perceptual Dizziness (PPPD)
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Professor Jeffrey Staab from the Mayo clinic brings together balance and psychiatry in his academic and clinical practice. He joins Dr Cotton in this podcast to speak about PPPD, vestibular migraine and the impact of dizziness on quality of life. Listen in to find the most up to date understanding of the neuroscience of balance and stay to enjoy the useful information provided to take back to the clinic.
Welcome to the Functional Neurologic Disorder Society podcast. I'm your host, Erica Cotton, coming to you from Chicago, Illinois, with a special thanks to Michael Romeo, our production engineer, coming to us from Australia, and our content curator, Ingrid Hertzauer, from the UK. Jeffrey Scott, Professor and Chair of Psychiatry and Psychology at Neoclinks, is the leading expert in persistent pastoral perceptual business, Triple PD, and affiliated with the Verity Society, the International Society for Neurocology, Diplomatic and Cassipular Research. We discuss triple PD prevalence, diagnostic gaps, recognition rights, mechanisms, common overlap and comorbidities, triple TD and the biopsychosocial models, treatments, treatment gaps, and possible solutions, and better integration of triple TD within the major academic medical centers, particularly F treatment programs. Without further ado, here's my discussion with Dr. Stopp. Oh, thank you so much for joining me today, Jeff. I am so thrilled to have you here. Why don't we start with you telling our listeners a little bit about your background, especially how you got into the work of FND? It's always so interesting how people find their way into this specialty. And I'm really eager to hear about your pathway into this great condition.
SPEAKER_02Well, thanks, Erica. It's a pleasure to join you today. So currently I'm a professor and chair of the Department of Psychiatry and Psychology at Mayo Clinic in Rochester, Minnesota. But as you mentioned, the sort of the route to here, the route to being involved in F and D, particularly with functional vestibular disorders, took a lot of twists and turns. When I was in medical school, that's 40 years ago now, the concept of conversion disorder was really prominent in neurology, psychiatry, psychology, as the only explanation for patients who had symptoms and signs in neurology that just did just really didn't fit with known structural diseases, structural metabolic diseases. And so that's how everyone was taught and had been taught for the better part of a century. And the thing that bothered me about it then, but I couldn't really sort of put our finger on it, is that is the thing that we're really grappling with now. And that is why is it why was it a psychiatric diagnosis just because nobody else had an idea what it could be? Um because there were times in which we certainly could find kind of the classic acute or chronic stressors that would lead to various symptoms in patients, and by addressing those, um see things, see their neurologic signs and symptoms get better. But that really was the minority of people and still is. So that was the first connection to the clinical side of work in um vestibular medicine. Uh and um, you know, again, the concepts at the time were very much um like the rule-out approach, and that is this concept of psychogenic dizziness, which was defined by what it wasn't. Um and uh the the wonderful thing about the team that I was working with at Penn was that um the neurologists and even the ENT surgeons were willing to sort out what was there. What was this thing in this bucket that was called psychogenic dizziness? And that's that's really where the the the genesis of our work in in sort of sorting things out. Um the other thing at that time, vestibular migraine hadn't yet been defined. That was in that bucket. Um, unless there were some neurologists who've been around long enough to know that vertigo and dizziness could come with migraine. And even though it wasn't a defined subtype, we're still willing to make that diagnosis back before it was really uh a full a formal thing. Um, so you know, we set about work trying to understand the psychological parts that that occurred in patients with dizziness and what what then sort of turned into um what we now call 3PD. You know, the the uh um German group in Munich had been at that for a decade before us. Um and so um with the concept of phobic postural vertigo, um, and similarly, you know, um Adolfo Bronstein's group in London with with visual vertigo and visually induced dizziness, and and the group at the University of Pittsburgh um with spatial motion phobia. So there were a lot of people that were, you know, kind of looking at this problem from different directions. And um, as I was recruited to Mayo Clinic, um the Berenice Society, which is uh sort of the equivalent of our FND Society for neurotology, um, well, well, it's it's a it's in the International Neurotology uh Um Society, um, you know, was developing diagnostic criteria and said, and and asked those of us who'd been involved in this if we could get together and really sort out what was going on and whether we were dealing with a single problem that we could define, or were there different pieces to it? And that's sort of what set in in process the um the um the work to define um persistent postural perceptual dizziness or 3PD. Uh and and then from that, um, once I was here at Mayo and the neurologists learned that I was interested in doing functional things, then you kind of expanded that into working in collaborations with um with the epilepsy group and with the movement disorders group.
SPEAKER_03That's such a wonderful trajectory. And I like the the early start where it just so happened that there was a vestibular, the vestibular lab that happened to have an opening. And so then that just worked out that way. You know, and I hear that in so many people's stories is well, I got into it because someone suggested it, or there was an opening, and I did it and I liked it, and here I am.
SPEAKER_02Yeah, I think you're right. I think that there's um uh I think I think that the just the idea that this that we don't know what we don't know in this field, and that's not quite right, um, and then just opportunities to come together with other like-minded folks. There's a that I think there's a lot of those stories. I agree with you about that.
SPEAKER_03Yeah, it's so fascinating. And I think it takes maybe a certain personality, a certain mind to go, oh, we don't know a lot about this. Sure, I'll work in that, right? And which is that often gray area of there's not rules yet. There isn't there's not full mechanisms known. We're kind of building things out as we go. I think you know, certain personalities maybe gravitate more towards that sort of career condition than others that are saying, nope, we know everything about it. Here's the rules, here's what we know, here's the the things to do. So that's wonderful. It's more trailblazing approach, which is great. Awesome. So, first question, and something that really struck me as I was reviewing um all the wonderful literature you've published on triple PD is about the prevalence rate. And I was shocked just how high the prevalence rate of triple PD is, and that it is, I believe, and I was just so shocked, that it is the most prominent or most um frequent functional neurologic disorder. And I just given all the hype around functional seizures and functional movements and which clinics we see more commonly, I was just shocked at that. So I'd love to hear your thoughts about why that's the case and actual base rates of this condition.
SPEAKER_02Yeah, so let's start with that. I I don't think we know which which of the neural functional neurologic disorders are the most common because, like what you said, the the numbers are coming from different places. Um and so um, but in neurotology, it is the most common cause of chronic dizziness. Um people who have day in and day out vestibular symptoms. Um, so after we published the definition of 3PD in 2017, several groups around the world look at prevalence rates. And the prevalence rates that we know about come from clinical populations. So there's not yet been a good study in the general, in the general public. Um, there have been some some work in in um in the general population about sensitivity to some of the provocative factors of 3PD, like how sensitive people are to motion, their own movements or visual motion. So some of those data are around, but not about 3PD itself. Um so the two largest studies came from Asia, one from China and one from Korea, both involving over 10,000 patients. Um, so not small numbers. And these were both in general um referral neurology clinics, so hospital or or university-based neurology clinics. And um they those those prevalence that prevalence came in at 20%. So one out of five patients presenting to a neurology clinic with complaints of dizziness, unsteadiness, or vertigo um end up with a diagnosis of 3 PD. Um, there was a smaller study of a few hundred patients done in Japan in an internal medicine clinic. And again, among people who presented with dizziness, it was about 14%. Um, smaller studies in neurology clinics in Europe also came in at that 20% number for neurology. Um, and um another group in Canada, um, and this is an interesting group in Ottawa that runs both an acute dizziness clinic, so sees patients within just a few days of initial presentation and then has a clinic for chronic dizziness. And in the chronic dizziness side, um, half of their patients had 3 PD either as the primary diagnosis or much more commonly with something else. But in the acute in the acute phase, that you know, within the first week or two, um, the rates of functional or psychiatric causes of disease were very low. So that suggests that this is something that kind of evolved um following a a neurological, odologic, or other medical event. Um, it also can follow um a um uh psychiatric distress that causes a dizzy or unsteady kind of a sensation. Um, but that but that's where the, you know, so that's if we think about that, those studies come from three different continents and still come in around this, these numbers of, you know, one in seven in primary care, one in five in general neurology, and one in two in specialty dizziness centers.
SPEAKER_03Yeah, which is just massive, massive proportional numbers. Um, on that, on that note, it would be probably helpful for our listeners at this point who are less familiar with triple PD to introduce um basic diagnostic criteria. And then also if you could give um some common case exam, not case examples, but just common pathways that people develop triple PD, like you mentioned a precipitating injury or illness, and then how it progresses and general course.
SPEAKER_02Sure. So the um people can find the um the diagnostic criteria on uh in on the internet. It's posted um uh uh by the Bahrinese Society and the Journal of Vestibular Research in open access format.
SPEAKER_03Oh, wonderful.
SPEAKER_02Um and um and that's along with other neurotologic criteria for other neurotologic diagnoses like BPPV, Ming Air's disease, and vestibular migraine. Um, but that's a that's a nice place to access it. But the criteria are that um uh patients have um dizziness, unsteadiness, or non-spinning vertigo, so like it's more of a swaying and rocking type of a vertiginous sensation that lasts for at least three months. Um, and it doesn't have to be that they're dizzy every moment, um, but more often than not, so most of the time for most days over that three-month uh period. Um the symptoms uh fluctuate or wax and wane. Um so they're not exactly the same every day. And once it settles in, um, people generally feel worse when they're upright, so sitting upright or up and up and on their feet and moving around. Um uh feel worse with their own motion, so bending, twisting, turning, um, and or uh in in vehicles, so um, riding a car, riding on an elevator, riding on an escalator, those kinds of things. And then lastly, um in places where there's a lot of complex or moving visual stimuli, so crowded malls, sitting in you know, in traffic. Um, some people have difficulty even with the ticker at the bottom of the television screen that goes by and gives sports scores or or you know, stock pickers and those kinds of things. So um and uh so those are the those are the diagnostic criteria. One really important thing that trips people up, but is but is something that we're emphasizing throughout FND, is that a person can meet the diagnosis for triple PD and meet the diagnosis for another uh neurologic, odologic, or or or psychiatric disorder. So it's not a rule-out diagnosis, it's rule in using those diagnostic criteria. And if there's evidence for something else, evidence for veneer's disease, vestibular migraine, something like that, then it's a coexisting problem and not one versus the other.
SPEAKER_03Similar to epilepsy with functional seizures.
SPEAKER_02Correct, absolutely.
SPEAKER_03Wonderful. Okay, great. So you mentioned in in um prior discussion that there's common, maybe triggers precipitating factors or a common trajectory that people might take, not so much in an acute time frame. Like you said, an acute um few days to a few weeks, it's not likely to be triple PD, but it's something that develops after a time period and then seems to settle in. Can you discuss that that trajectory or progression?
SPEAKER_02Yeah, sure. So there the I think the best way to understand what the precipitants are is anything that can cause um an experience of uh dizziness, unsteadiness, vertigo, or spatial disorientation. Um, that's really uh disconcerting to human beings. Um there was a little study done in Germany in an emergency department that asked people, you know, how are you, how are you holding up? How are you faring emotionally with what brought you in? And the most disconcerting, the most anxiety-provoking symptom was vertigo, um, more than other stuff that people go to emergency rooms with. Um and patients say that a lot. I've had lots of other things happen to me, but once my started spinning and I couldn't walk, that was the freakiest thing that I'd ever encountered. Um, especially when it hits out of the blue. So the the things that can um uh the most common triggers for 3PD are acute vestibular events. So vestibular neuritis, recurrent PPPV, you know, though um uh those kinds of uh of problems. Uh the two three um are vestibular migraine, again, episodic attacks of vertigo, and anxiety disorders, but not just any anxiety disorders. Um panic and generalized anxiety can cause um uh dizziness, unsteadiness, lightheadedness, funny-headedness, even subtle turning or or um or motion. Um and it's those patients that have that very that sort of manifestation of anxiety that can go on to develop 3PD. Um go down the list further, and you have um mild traumatic brain injury or concussion. Um, and then um starting to get smaller numbers, people who have dysrhythmias, so like episodic AFib, who get lightheaded or funny-headed, um, and some, and then um uh some other uh metabolic abnormalities. A lot of um uh the evidence for metabolic changes, like with uh glucose abnormalities, um, come in clinics that uh take care of patients who have less access to medical care. So, you know, and um in you know people that are used to having a flow of patients with relatively good access to primary care and don't don't have diabetes that's untreated, don't see as much of that as a trigger, but in other in other places they do. Um, and then the and then um you know side effects of medicines can sometimes do that too, because this is not uncommon with a variety of different medicines. Um, and the the trick to the trajectory is that um as for somebody who's had an acute event like a vestibular neuritis, um, kind of as that acute event begins to resolve, um, that they don't really ever get back to their normal baseline, to an asymptomatic baseline, but they stay sensitive to their motion, um, head movements, or or and begin to develop the visual motion sensitivity. Um, and as those settle in, um, they consolidate into the picture of 3PD. For people who have episodic conditions, like attacks of a stev or migraine or attacks of Meniere's disease, some people develop 3PD after the first event. Um, and then they've got sort of two things going on, and their history shows that they have episodic attacks superimposed on a background of daily dizziness. Others will have complete recovery in between attacks. Um, and then as attacks continue, they start they start to have this lingering tail um after the acute attacks, and they don't get all the way better. And eventually that tail sort of lingers to the next attack, um, and then they have that consolidation and again the the dual picture of acute attacks superimposed on the background of chronic dizziness. Um the ones that are probably most difficult to figure out, but but are fortunately the least common are disorders that start insidiously. So um, you know, move movement disorders that affect um that affect gait, so Parkinson's disease or or um um cerebellar uh degenerative disorders, for example. Um and uh or sometimes people who have you know anxiety that just gradually, gradually gets worse because of circumstances that they're under. Um and it it can take a while, um, and sometimes following them prospectively for a few months to really sort out all of what um is going on um with them. So in those cases, it's worthwhile having um 3PD and the differential diagnosis, but it's also um worthwhile making sure making sure that other causes of that sort of slow progression of unsteadiness and dizziness are considered carefully.
SPEAKER_03Wonderful. Um, as you were speaking, two thoughts came to my mind. One, um, any precipitating factor of POTS. I know POTS can be a big trigger for on epileptic seizures, the overlap there. Um, and then comorbidity or overlap with other functional neurologic symptoms. So, what how often and at what point would we start to see other FND symptoms in a triple PD population?
SPEAKER_02Yeah, great. Thanks for reminding me that I left the I left the autonomic disorders off the list. The two most common would be POTS and vasovagal syncopy. Again, people that have recurrent episodes of vasovagal syncopy sometimes will have incomplete, don't don't necessarily pass out completely. They have more episodes of dizziness or lightheadedness. Um, so and that would be you know around the same prevalence as concussion, you know, around 10-15% of people with 3 PD. Um so um overlaps with other FNDs. So the most common one is with functional gait disorders, so functional movement disorders that are gait. Um, and what so the definition of 3PD does not include any overt changes in gait or falls or near falls. So um, but but patients with 3PD can develop caution with their gait. And if it's just a little bit so that they tend to hold on to a handrail um or you know, want to grab a cart in the in the in the grocery store, um, but otherwise they're walking around okay, um, we would just leave that as a 3 PD diagnosis. But if people start to be um have have clearly observable changes in gait, they begin to have a wider stance, um, you know, walk really slowly, place their feet rather than um rather than the natural gait. So adopt a walking on ice kind of strategy um or other alterations in gait. Sometimes we've had people um you know use walkers or confine themselves to wheelchairs because of how uh of how much um they they perceive the risk of of um you know instability is. Uh so if the gait abnormalities are observable and clearly different than normal, and more than just a little bit of caution, then we would say that that's a that's a uh um a second diagnosis, a second F and D diagnosis of a functional move and functional gait disorder. And that's important because that's probab that in treatment, um, starting with normalizing the gait. Is the better strategy than starting with trying to treat the dizziness because it's very hard to get dizziness if somebody's not walking normally. Since we want them to walk normally to get better and better at uh at habituating to the dizzy sensation. So when those two are present, it really is worthwhile calling them both out in the diagnosis and kind of starting with normalizing the gait, which surprisingly people patients don't think that they can do it, but they can. You can treat the gait disorder first, and then you know the physical therapist can, and then move into more of the habituation exercises for 3BD. Um there is uh there are patients who are prone to not just functional neurologic disorders, but other functional disorders, so functional GI disorders or fibromyalgia, chronic chronic fatigue syndrome. Um, and that's a group of patients that um is is also worth being aware of because if you see a lot of functional and chronic somatic symptom burden um in a patient, trying to single out one of those as the point of focus is usually not very successful in treatment, but rather getting them into a more comprehensive rehabilitation program is the better way to go.
SPEAKER_03Wonderful, very helpful. I I wouldn't have guessed that um addressing functional gait changes would provide such a useful, useful effect for triple PD, but in some ways it makes sense. And that's actually a good segue into discussing then, in your opinion, the mechanisms, what's happening in the brains of people with triple PD, why the brains are doing this, how that might pull in gate or vision. And as you said, it's it's obviously very distressing for these poor folks who who experience this. Our vision is just so central. Um, and that's connected to movement. But what else do you think is is happening in the brain with these individuals? What do we know so far?
SPEAKER_02Yeah, this is a great question. Um, and it's one of the one of the exciting reasons about continuing to do this work. Um, uh, I mean, I tell some of my um my residents and fellows that you know the the 20th century taught us a lot about structural diseases in the brain, and the 21st century is going to talk teach us a lot about what what the brain does when it changes functioning. Um, and then we'll really know something.
SPEAKER_03Right.
SPEAKER_02Um so initially, because um the precursors um for 3PD that actually go all the way back to you know, writings in in the 1800s in in Europe really focused on anxiety um as a component of it, as a core component of it. A lot of the initial our initial concepts of 3PD centered around uh anxiety-related mechanisms, you know, people becoming too vigilant about their motion, um, fearful about consequences, um, and therefore um uh kind of phobic mechanisms of um uh you know being too aware of an automatic process, which is movement, it's a very automatic process in there, and and um of thinking too catastrophically about the results, therefore, you know, kind of shrinking their world down because they were less and less involved in things. Um I think that the most recent data would suggest that that those kind of fear responses probably play a role in the genesis of 3 PD. So that's so that provocative period in which somebody has experienced a uh an event that triggers the stibular symptoms, um, and they they respond to that in um with with some of those behavioral behavioral factors, becoming more vigilant about their movement, being uneasy, what the physical therapists call balance balanced confidence or losing their balanced confidence. And then rather than kind of getting on a path to recovery, both physiologically and behaviorally, um they they sort of diverge to a path of persistent symptoms. Um, but I don't think that it's anxiety alone that maintains the, you know, over the long run, because there are patients who will say, look, I've been dizzy for a long time. It doesn't make me afraid anymore. Um, you know, yeah, I worry that I'm you know, lose my job and things like that, but I just don't want to be dizzy. So if you can make the dizziness go away, that'd be great. But it's not, it's I've had lots of tests. I know that I've not a brain tumor, know that this isn't gonna kill me. So it just doesn't bother me like it used to in terms of fear. Um, but it's noxious. Um, and so I as there have been um some recent data that suggest a couple of things in terms of a top-down influence. So anxiety would really be a very bottom-up influence. It's really, I mean, anxiety responses are really quite sort of more old, old sort of lower level brainstem to, you know, on on up through the amygdala and so forth. Um but two intriguing pieces of data, one from the UK and one from Japan, both good research groups that have been paying attention to 3PD for a while, um, published in 2023 data to that shows that patients with 3PD overestimate how much they're moving. So one study asked people just to stand on a posture platform, just to stand with their eyes closed, and then um uh demonstrate how much they thought they moved. So, so purposefully sway how much to the to the extent that they felt that they were moving. Um the that was the London group. The group in Japan asked people to tilt their head, roll their head towards their shoulder from side to side, and estimate how much they'd they'd moved from vertical. And in both cases, people with 3 PD estimated that their movement was twice or more what it actually was. Um now that actually may tap a natural mechanism that we had, that we have. Um, we think of motion as pretty fixed, that or our perception of motion is pretty fixed. Namely, if I move, no matter where I'm moving, um, what my vestibular apparatus says or my proprioception says that I've moved, that's what it is. Um, but there was a very cool study done by a uh a wonderful research group in in British Columbia that worked primarily with pay with normal human subjects, so not so much with people with illness. Um, and what they showed is that if you put human beings at height and ask them to move and judge how much they've moved, that they overestimate how much they've moved when they're at height. Makes sense. Yeah, right. So that's a self-protective mechanism. But what it means is that perception isn't fixed, it's not bottom-up deterministic, namely that what the periphery says goes, and all we're doing is basically just processing that, but in fact, we're interpreting it in context. And so if the context is I had something that threw off my balance system, and I have not had great confidence in my balance ever since, because now I'm aware that my emotion isn't normal and my sense of space isn't normal. Um, and if that's the thought that we have, and we get in provocative environments, then an instinct will be to try and be still. Um, and you can't be still and be mobile at the same time, they're fundamentally opposed to one another. And so I think what happens then is in the long run, that initial sort of provocation from various triggers, the hyper-vigilant response in people who are susceptible or who are given false sort of reassurances that, oh, don't worry about it, it'll get better. And then it doesn't, and they say, Oh my goodness, now what? Um, or who have delays in in getting care because people don't seek care right away. And then when they do, we do tests looking for bad stuff that takes a few weeks and makes them a little more anxious that yes, they maybe they do have a brain tumor. Um, and during that period of time, this settles in, this awareness settles in, and then they begin to go about their business being aware of something that we're normally not aware of, which is control of motion.
SPEAKER_01Right.
SPEAKER_02Um, and that then perception of excessive motion creates a vicious circle because now the instinctive top-down drive is to be still when what we really need to be as humans is is is gracefully mobile.
SPEAKER_03Right. And I I wonder, even as you're you're talking about that, that it seems like the situation or perception of risk, such as being in a high building, makes it more important for the brain to prioritize overestimation of movement rather than accuracy. And so if someone's put in a situation where they're suddenly dizzy, even if they're not standing on a building, if the brain interprets that situation as risky enough, right? We shouldn't be dizzy as we're trying to walk through the door, so to speak, and that heightens it and then overestimates and creates risk and vicious cycle. It's oftentimes, and it's it's relieving in certain ways. I just submitted a grant where I where I highlighted that functional cognitive mechanisms have similar mechanisms in terms of catastrophizing and fear responses to normal brain processes that then go awry. So it's very relieving to have you say that it also happens in triple PD this way, not making a liar out of me to the right, right.
SPEAKER_02And fundamentally, the cool thing about this is that um so far, the data on mechanisms um um suggest that what's happening is that people are putting together mechanisms that we use to do things naturally, but they're bringing them together in a way that is um that that sort of gets them stuck. So we do change our our gait when we walk across a slippery floor. We do change our gait when we walk through a crowd and people are bumping us, um, or at night when when you know there's no light. Um, but we don't stay in that shift. We we shift on the fly for different situations and without thinking about it. Um, and in some ways, 3PD can be thought of as settling into a gait pattern and being stuck there as opposed to um as opposed to or gate control, uh posture and gate control scheme and being stuck there um as opposed to um uh you know the fluid um adjustments for circumstances. So it's almost as if people give up the natural range of postural control that we have to move about in all the situations that we that we move about in and stay sort of stuck in this one that is kind of more of a high risk response.
SPEAKER_03Yeah, heightened response and a negative cyclic pattern of symptom formation. Yep.
SPEAKER_02One one really curious mechanism um that I think we're is is gonna need us to look into a little bit more, um, but uh from data um from a group in Santiago, uh Chile, um, that have been very interested in cognitive processes in people with 3PD. And so they've used um uh virtual versions of uh different laboratory tests that have been used in in rodents for years around spatial orientation tasks. Um, and people with 3PD perform worse than people with peripheral vestibular disorders, um, and obviously worse than normal people. In fact, they really perform quite badly, um, as if they really just lose all spatial, lose, lose the ability to use spatial orientation cues to sort of guide them to targets. Um and you know, the question is why is that? There's not, I mean, what there's not anything that has been um structurally injured in you know spatial orientation systems. Um there's one interesting functional uh uh MRI study that suggests um a possible brain correlate to that, and that is that um um the hippocampi have a lower connectivity with all of the main areas that they would typically connect with throughout the brain in patients with 3PD at rest and in fMRI. So the question is, why would that be? You know, why would the natural um uh pathways that work together um to process information through the through the hippocampus, you know, which is our sort of space uh and and you know, place place and and and and positioning in conjunction with andorhinal cortex, why would that go awry? Um here's what I think I think about that, and I said that on purpose because I'm not 100% sure. Um, but if if the uh top-down mechanism is be still, then the only thing in the world that you need to be aware of is what you're immediately in contact with. So I only need to know what's under my feet or what's under the seat of my pants if I'm sitting to be still. I don't need to know what's even five feet from me. Um, unlike if I really am focusing on smooth mobility, in which I need to know what is in the wider world, not only where I am, but where I'm going. And that's really what spatial orientation and locomotion are about, is where we're going, where we're heading, where we are, what the map is, about where our the space is and where we're going. So if I'm prioritizing being still, that's much less relevant than if I'm prioritizing being mobile. And so why would I waste brain power and processing power on um on trying to trying to sort through a task that is lower in the priority list?
SPEAKER_03Yeah, it's not relevant at that moment.
SPEAKER_02Right, at that moment. And so, and so we'll I think we'll see and as we continue to look um and try to delve into both the phenotype um of 3PD and its influence on mobility and the correlates um in the brain. But but that seems to be how to put uh some of these pieces of information that have you know been coming around from laboratories all over the world.
SPEAKER_03Wonderful. That's a great segue into treatment. So now that we have some idea of mechanisms and hopefully increasing recognition of this condition and wonderful people like yourself who actually want to treat patients who are presenting in this way, what are the gold standard treatments? What's the best tree best treatment pathways for these folks?
SPEAKER_02Yeah, so I think the first thing to recognize is that all of the three um treatment modalities that we use for 3PD were adopted from something else. We right now do not have a purpose-built um intervention for 3PD. So um if we start first with vestibular rehabilitation or therapies, um they were really developed in the 1980s for people with chronic dizziness. Um and that's the first group of people that vestibular that physical therapists um uh tried to help. And many of those would um, you know, would have been called chronic vestibulopathy or psychogenic dizziness or what sort of whatever, just sort of chronic dizziness and no acute illness or or or ongoing illness. Um, I suspect these days we would have diagnosed um many of them with 3PD. Um, but they showed that you could habituate people by having them do what made them feel uncomfortable, um, having them do what made them feel symptomatic, even if it wasn't fear-related, even if it was noxious related, um, over and over again until they built up tolerance for it. So sort of classic habituation. Um, and that has continued to be sort of the heart and soul of um uh vestibular rehabilitation, building up tolerance to the person's own motion and to movement of objects in the environment. Um the second treatment that um that really was quite um surreptitiously found um by my group when I was at the University of Pennsylvania and simultaneously by a group in Japan that we didn't know at the time, but but we do now, um, was that SSRIs um could make a difference. And how did we find that? Uh frankly, because we said to patients, we don't exactly know why you're dizzy, but you are really anxious or depressed. So let's at least treat that part. Um, and they came back and said, and now I'm not dizzy either.
SPEAKER_03Wonderful.
SPEAKER_02Um, and so we pushed the envelope and said, let's try to treat more and more patients who are don't have overt anxiety and depression and see what happens. Um, and um showed that we could um, you know, reduce the symptoms um reasonably um with medications, even in people who did not have overt anxiety or depression. Um so that's been continued. And then third is that psychologists um uh basically looked at this and said if there are anxious and phobic elements to this, um catastrophic thinking, hypervigilance, well, we know how to treat those kinds of things with cognitive behavioral approaches. And so there have been a number of nice studies looking at that. So there are right now no level one or level A, um there's no level one or level A evidence for any of these. Um, but the accumulation of the public liter the published literature from again uh groups and laboratories around the world um you know has you know eight to eight hundred to a thousand patients reported for treatment for each of those modalities. Um they're roughly equal if used by themselves. There's some evidence that when combining them, it helps a little bit, more than a single uh single treatment alone. And the overall outcome is that if you take all comers and begin treatment, you'll reduce their dizziness handicap from um a moderate to severe level, and that means interfering with activities, to a mild to moderate level, which means sort of nagging in the background. Um, so that's cutting symptoms and cutting handicap more than in half. Uh and no um patients and we aren't satisfied with incomplete responses, but I do emphasize to people that there really is a big difference between dizziness holding you back from who you want to be with and what you're doing, um, and the dizziness sort of being there, you know, from you know, and and kind of sneaking to the forefront from time to time, but not, but but still allowing you to be able to focus on on your valued activities and the people that you want to be with. Um, there are people who do who we can treat 3PD into full remission and keep them there. I don't want to say that that doesn't happen. Um, but I think treatment-wise, we have more work to do to to um ensure that we can get more people from better to well. Um and we may, you know, if we think about mechanisms, we may be up against um uh up against a a tough mechanism. Um, and that is that if 3PD has been going on for a while, I suspect that the brain, the brain's plastic, and so I suspect that it's probably settling into the new strategies, and that if it's been too long, we can undo them only to a to a to a part. Um and so that really suggests that we understand 3PD better, that we diagnose it earlier and we get more effective treatments as early as possible. Um, but I think it also requires us to think a little bit differently. You ask at the beginning, what would I like to see going forward? Um, and I think that understanding mechanisms more so that we can actually either develop de novo treatments specifically built for 3PD, or probably better adapt the treatments that we just talked about in ways that that that um are more specific for for the disorder. So let me just give you one example of that. So one of the things that happens with 3PD is that people rely on vision more than their sense of touch or their vestibular input. Um, and when we do this uh the the visual habituation exercises for 3PD ask people to do more and more visual tasks, um, we can habituate them, people can tolerate those tasks more, but we're also at the same time asking them to pay more attention to visual tasks. And in reality, what we want is people to be processing all those visual spatial cues automatically without paying attention to them. So I wondered if the very process of habituation exercises is a plus-minus, um, that it's working to a point, um, but not undoing that over-emphasis on vision. So, do we have to adjust it so that we are um uh you know decreasing that over-reliance? And sort of how would we do that? Um, would we be have to people do exercises with um vision obstructed or partially obstructed or you know, other ways? Uh and you know, lots of ways that we can speculate around that. Um, you know, what about this spatial orientation problem? You know, how do we rehabilitate that and have people focus back out on where are you going rather than where you're standing? I think those and and a question I think that we have potentially about all functional disorders is if we can map the pathways of functional change in the brain, can we use either and can we use uh intervention strategies, you know, electrical, magnetic, or even deep brain stimulation. To correct those. I mean, that would seem, you know, to be like, um, you know, if we were in the conversion world, it's like, why would you even think to do that? Um, because this is psychological. But if we say, you know, it's it's all brain processing and changes in processing and we can and we can nail it down, um, then why not try to intervene in those ways? And there have been a few small studies looking at those with some promising but inconsistent results so far for 3PD.
SPEAKER_03Yeah, I just um the guest right before you was Beatrix Garcin um in France with transcranial magnetic stimulation. And that was just such an interesting discussion. Um and just very promising. I and I I agree it's it's a real problem to think that psychological processes don't happen in the brain.
SPEAKER_02I mean, it's just where do they happen? I don't know.
SPEAKER_03Like, is there some black cloud outside the head that like revolves around these things? But yes, it's it's it's a big problem with that assumption in in mind um that is that is a big limitation. Um, and I it's enjoyable or somewhat validating also to hear you say about the the problem with with retraining a system, you have to attend to the system, but then there is a problem with overattention because that's that's to an automatic system. And that's one thing that I commonly talk to my patients with functional movements about, you know, how how to approach physical therapy and say, or their symptoms. Like, well, there's a glitch in a system that you shouldn't have access to, you know, kind of like down in the server room behind the glass. We don't know the wires of it. You're gonna have to go in and rewire that a little bit. But at some point you need to put the glass back down and let that system just run after it gets retrained. But at what point is it, okay, attend to retrain, but now disengage again? Right, put that glass back down, walk away, and and the mechanisms to make that happen, you know, dual attention tasks, specific instructions about split attention or um sort of uh not half attention to it, to the process versus you know, fully attending to it to correct it, so to speak.
SPEAKER_02And I I think there's I think that's spot on. I think that we're all of in in all of the uh the the functional disorders, but particularly with movements and 3PD, um, I think even to seizures, because many people do have a leal of a premonition in which these when they have the full full spell. Um, and that is that if we really think about our attentional systems, the only time that we appear that that we're consciously aware of movements or space is when it's temporarily goofed up, you know, when we've slipped or when um, you know, when um another movement that we planned didn't go quite right, and then we temporarily are pay attention to it to help to sort of redirect. And um, so I've started to, and this is just purely anecdotal so far, um, um, in addition to the dual tasks, which which we oftentimes use to help patients understand this. So having them say, stay in a rot, say, say in the Romberg position, a lot of people with 3 BD will be very stiff. Um, and then I will have them do sort of cerebellar testing with their arms, um, and and then ask them afterwards or ask their their person who's with them, did you see what happened? And most of the time they will see what happened is that they relax. So helping them understand that um that when their attention's on a valued activity, that their brain will do just fine with controlling stance and movement. But I've also begun telling patients when they do vestibular rehabilitation that we want you to do these exercises until they're boring. Because if you because anything new, any new task you have to pay attention to to get it right. So you're going to be paying attention and we're going to build up your tolerance for it. But I really would like you to keep doing them until you can do them without paying attention. You can think about what you're going to do at work or go to the grocery store to buy or what your kids are doing or something else while you're standing there and doing your movement and gates and gate stances. Because if you can do that, then you're letting your brain take over.
SPEAKER_03Isn't it a wonderful facet of the brain to do that, to just eventually habituate to something enough that it goes onto your laundry list? You know, like, well, what am I gonna have for dinner tonight? It's it's a beautiful facet of it. And I think it's great advice to potentially suggest that, yeah, do it to that level till your brain gets bored. I often tell my psychotherapy patients with emotions too. I'm like, focus in on your emotion, feel it. Like, and at some point your brain's gonna wander to, well, what TV show am I gonna watch? Or, you know, and it's just just wait long enough and the brain will eventually get bored and move on, which is thank goodness.
SPEAKER_02Cause yeah, yeah. So I I think I think that um, as you mentioned, some of split split attention, uh, dual tasking, some of those kind of things. I think we have to find ways to um adapt those concepts to rehabilitation um and to psychotherapy both, because the nice thing is with 3PD is the vestibular exercises and the psychotherapy techniques dovetail so wonderfully. Um and uh and some physical therapists are starting to uh to do psychologically informed physical therapy, which is a very, very beautiful blend um of the two disciplines. Uh so um I think more attention to understanding the behavioral processes. So not just the psych, you know, I use the term behavioral because it not just justice is a nicer word, but as a more natural word. It it's it's you know, the just the move, what we we we as humans are mobile, and that's a natural behavior for us. Um and uh and so just understanding all of what goes into that behavior, um, I think will help to lead the way a little bit.
SPEAKER_03Wonderful. Well, I want to be mindful of our time. This has been an absolutely excellent discussion. I have enjoyed it so much, as I'm sure our listeners will. And we will link to um the Barony Society and a few of the key open access publications um when we post this podcast.
SPEAKER_02Terrific. Thanks so much. I appreciate you doing that.
SPEAKER_03Thank you. One final announcement for our listeners: please consider attending the upcoming FNDS summer course, Functional Seizures and Epilepsy, Cutting Edge Diagnostic, Biology and Management, which will be both virtual and in-person in Boston from June 13th to the 14th. The course organizers are Dr. Barbara Dwaritzky and Dr. Mahinda Yogaraja.
