Dizziness Part 2 with Dr. Anand Bery

Dr. Anand Bery joins us again as we revisit the basics on how to evaluate dizziness by using timing and triggers, and then we look at some of the ways that real life diagnoses, like migraine, chronic functional states, and other disorders overlap. 

We focus on key findings in the history and exam that keep us from overcalling Meniere’s, missing vestibular migraine, or mislabeling chronic dizziness as PPPD without checking for other causes. 

You can find our first conversation with Dr. Bery here.

Further resources recommended by Dr. Bery to further your dizziness knowledge!

Dr. Peter Johns' YouTube channel (Ottawa, Canada) - I recommend novices start with "Popular Videos"

Dr. Dan Gold's entire collection is recommended

• the "Test Your Knowledge" videos (like the one linked here) are particularly helpful for getting comfortable interpreting HINTS. 
  • Putting the following term in the search bar brings a wealth of videos -- creator_t:"gold" hints

Neurology Exam Prep Podcast Episodes

• Acute Vestibulopathy
• Episodic Vertigo

Transcript

Welcome Back To Chief Concern

Michael Kentris 0:05

Hello everybody and welcome back to the neurotransmitters. We are continuing into our part two of our Chief Concern series. Uh I am one of your hosts, Dr. Michael Kentris, and I'm joined as always by Dr. Galena Geikman. Galina, how are you today?

SPEAKER_01 0:22

Hey Michael, you're getting it right, Chief Concern.

Michael Kentris 0:26

I can be taught. It just takes so episode.

SPEAKER_01 0:28

It only took uh eight episodes. Thanks for having me back. I've really loved doing the series, and I'm really excited that we've started part two and we're bringing back some of our fan favorites for a deeper dive.

Michael Kentris 0:42

Yes. So we are joined once again by Dr. Anand Berry, neurootologist extraordinaire, uh, to continue our education on dizziness. So, Anand, how are you doing?

SPEAKER_02 0:53

I'm doing well. I'm feeling good. I'm feeling grounded. Excellent.

Michael Kentris 0:58

Yes, which is especially pertinent uh to the subject matter for today. I love that. So you know, last time you walked us through a lot of the basics, and today we're gonna just uh turn it up a notch, if you will. So for those who have listened to our previous podcast on dividends, because why haven't you? If you haven't, you should go back and listen to that one and then this one. So now that you're back, what uh what should they be building off of uh as far as their next step in assessment amand?

Timing And Triggers Refresher

SPEAKER_02 1:26

Yeah, great question. So I think what I'd love to bring it back to as a bit of a refresher is the new paradigm, right? The new model that we're thinking about in assessing the dizzy patient, which is the timing and triggers model. And so, you know, we spent in the last podcast quite a bit of time talking about how, you know, once you've eliminated red flag symptoms, you're dealing with isolated dizziness and vertigo, one of the first questions we really should be asking is what is the timing of symptoms, right? Is this something acute and continuous? Is this something episodic, or is this something more on the chronic side of things? And we spent a lot of time in the last podcast talking about acute continuous dizziness and vertigo, a really important thing on the wards or in emergency room settings, really that question of trying to differentiate, you know, stroke from an inner ear mimic. So that's acute vestibular syndrome. And then we spent some time last time talking about BPPV. So episodic conditions, but triggered episodic. So an episode comes on after a head movement uh relative to gravity. And so what I think we can do now, what we should do now is go down another branch of that tree, okay, and talk about first episodic disorders that are spontaneous. So where you know you're talking to the patient and you've identified that that these are episodic, but there isn't a specific trigger. They just sort of come on. Excellent.

SPEAKER_01 2:59

Wait, first can we pause and can I report back that I've now done significantly more tests of with a Dick's Hall Pike for BPPV than before? That was something I learned last time.

SPEAKER_02 3:09

Yes, everyone, everyone, do it on every patient.

Michael Kentris 3:13

So when we talk about triggered, we're usually talking about things like movement. I guess if we want to be a little more esoteric, we could say barometric pressure or some something. But uh these these non-triggered episodes, is there no rhyme or reason to it? Any patterns that we should be looking for?

SPEAKER_02 3:32

Yeah, great question. And I'm really glad that you brought that up because really when we're saying triggered, we're really talking about head movement, you know, thinking BPPV or postural change, thinking orthostatic hypotension. And so some of the disorders that we're going to talk about now have other triggers. You know, there are factors that that may provoke them, factors like missing sleep, missing meals, being dehydrated. So that's not to say that spontaneous episodes, you know, don't have any factors, any provoking factors, but it's less discreetly head movement induced or or sort of posturally induced. And so I think now is probably as good a time as any to talk about some of those things. What falls into that that bucket in terms of spontaneous episodic disorders? And so the things that fall into that bucket, you know, one of them is vestibular migraine. Okay. Another one is Meier's disease, a third one that's a little bit less uh uh uh common, but certainly something that you always want to think about would be a TIA, so a transient ischemic attack involving the posterior fossa. So those are kind of the archetypal spontaneous episodic disorders. So migraine, meniers, and and TIA.

Michael Kentris 4:52

You know, a couple of these I feel I feel like you could invert the vestibular migraine and the meniers disease, in as much as you always think about meniers, and it's almost never meniers, and you barely ever think about vestibular migraine, and it really often could be vestibular migraine. But how do we how do we differentiate these in terms of I always feel like me personally, like vestibular migraine is kind of like, well, I don't find anything else. It's episodic, not triggered. What else do I do with this, right?

Spontaneous Episodic Vertigo Differential

SPEAKER_02 5:24

Absolutely. It's the story of my life, the the bane of my existence, you've you really got to it right away, five minutes in. So what I would say is that I always find it helpful to go back to the diagnostic criteria of menieres, because labeling something as definite meniers, it's actually a pretty rigid criteria, right, that you have to go through. And so, you know, if we look at the diagnostic criteria of meniers, you know, the first thing is we're looking at spontaneous episodes of vertigo. And they're really specific about the word vertigo. They really, you know, are again, we spent a lot of time last time talking about how we don't want to uh over-emphasize symptom quality. But the fact that the diagnostic criteria is telling you vertigo, I think is something uh important to at least keep in the back of our mind. Um, so it's spontaneous episodes of vertigo lasting 20 minutes uh to 12 hours. And in order for definite meniers, you have to see two of them. And then the second criteria is that we need to have audiometrically documented low to medium frequency hearing loss. And that hearing loss can be before, during, or after episodes, but it defines the ear that's affected. And so that the symptoms really should be unilateral. And I will say that the classic presentation of menieres really is audiovestibular episodes. It's hearing loss and vertigo at the same time. So if you see that, that's where I'm really thinking menhire is audiometrically documented, a hearing loss. And then we want to see fluctuation. So, you know, fluctuating symptoms in that affected ear. That could be fullness, that could be subjective hearing change, that could be tinnitus. And then, of course, the the main caveat, which is it's not better accounted for by another vestibular diagnosis, right? They they had to put that in. Right. But really, the audiogram is what's gonna help us in many errors, and the strict unilateral hearing features that's gonna help us in many errors. And so I had a mentor at Johns Hopkins, John Kerry, who used to say if the patient can point to what ear is causing the trouble, that's gonna clue us in in terms of of many errors. But really, we want to see those changes on the audiogram. Where things get more complicated is that you know, you heard it here first, but there's a lot of overlap phenotypically between meniers and migraine. Something like 60%. Yeah, yeah, yeah, yeah. Sorry, I couldn't help myself. Yeah, yeah, yeah. I love it. So 60% of patients with meniers have migraine. And so many of my patients really meet the criteria for meniers, but they're migraineers too. And so I really would would never deny someone the opportunity to get migraine treatment if there's anything that looks like migraine. And sometimes even patients in meniers, we want we want to manage them as meniers, but if we're really running into trouble and there are some episodes maybe that don't have audiometric change or hearing change, unilateral hearing change, we will sometimes treat as migraine, and sometimes we have success with that as well.

Michael Kentris 8:28

Aaron Powell That's a great point. And again, I think we might have mentioned it last time, but I saw some meta-analysis looking at like dizziness and vertigo, and it's something like 20 to 30 percent of patients have at least two different etiologies for dizziness concurrently.

SPEAKER_02 8:43

Aaron Powell See that all the time. Yeah.

SPEAKER_01 8:47

I'm so glad you mentioned the overlap with vestibular migraine or migraine in general. And I hope we'll go into some of the details of that. But what was I what I found interesting was the length of the episode because I think that that is something that I often teach to the residents thinking about not just, you know, sort of the pro-droma onset, but then like what's happening once the episode is there. Is it lasting a minute? Is it lasting hours? And it sounds like they can be of a similar time frame. We're talking more hours, maybe up to a day, maybe the vestibular migraine could be a little longer. And so getting that feature that in fact that's not a distinguishing element, um, but it's the hearing loss that's different. So, can you share a little bit more about maybe the kind of shifting to the vestibular migraine is what's the typical length of the episode, and how often do you expect headache to accompany versus not and other associated features?

Meniere’s Criteria And Hearing Clues

SPEAKER_02 9:42

Yeah, that's a great point. So the and great question. The sort of transition that I'm gonna make here is to say that while I tend to be very specific when applying Meniere's criteria, I tend to be less specific about applying vestibular migraine diagnostic criteria. And I think when the when the diagnostic criteria were being developed, you know, we're we were really looking for enrollment into trials, we were looking for commonality. I mean, if you think of where sort of thinking on vestibular migraine has evolved, I mean there was a time where we didn't even think, you know, migraine could could cause vestibular symptoms in the way that it was. So we really wanted to put something out where we were being very sort of the group was very homogenous in terms of the patients that that we called vestibular migraine. But I think my one pearl would be I think migraine, just as we see in terms of aura, you know, thinking about before, during, after migraine, I mean the range of things that migraine can can cause. I mean, migraine's a whole whole brain process. And so I tend to be more inclusive in thinking about migraine. You know, I would say the classic vestibular migraine, you know, who's the classic vestibular migraine patient, right? It's someone who either has a history of migraine headaches themselves or strong migraine features during the episode. So that would be what you would need to make a, you know, a definite diagnosis, history of migraine or other migraine features during the episode. But do we see patients who have recurrent episodes, spontaneous onset of dizziness vertigo, who maybe don't have such a clear history of migraine headaches, and maybe the migraine features during the episode aren't as clear. I would say, you know, all the time. And we don't want to, again, deny someone the opportunity to treat in terms of migraine. So I'm gonna give a few pearls that I think are really helpful when I'm thinking about vestibular migraine. So the first is I often ask my patients about a history of motion sickness. I would say that can be really helpful because many patients with migraine, and particularly vestibular migraine, have a strong history of motion sickness. I would say there are a lot of people out there who do have motion sickness and may not have vestibular migraine, but when and it's like, oh yeah, you know, doctor, like anytime I went in the car, you know, I was the kid on the road trip who got sick, you know, I would never read in the car even from when I was five years old. But that for me is just cluing me in, okay, this is someone who maybe has the gain turned up on processing of visual or head motion. And so maybe I'm thinking they're they're more on the migraine spectrum. Thinking about childhood variants in terms of migraine, did they have sort of unexplained abdominal symptoms, you know, tummy aches, not going to school, all that kind of stuff? Do they have a history of aura? So that's more sort of in their past history. And then with episodes, I really drill in terms of, you know, nausea is nonspecific, you know, that can be there with a lot of vestibular episodes, but you know, is there prominent sensitivity to lighter sound? Like are they really saying, you know, I just shut off all stimuli when I'm having an episode? That's again a soft marker that's going to point you towards migraine. You know, is there sensitivity to head motion and visual motion? Because patients during a vestibular migraine episode, they just don't want to move their head, they're remaining completely still, you know, they don't want to be in a moving vehicle. Again, is it the most specific thing? I think lots of vestibular things might cause that. But if it's really strong, really prominent, that clues me in in terms of migraine. And then I will say that you don't have to see headache, you know, during a vestibular migraine episode to call it vestibular migraine. But if there is headache, and if the headache does have migraine features, or if it's followed by a headache, right, and there's headache with with throbbing, nausea, sensitivity to light, that's gonna increase my pretest probability in terms of vestibular migraine.

Michael Kentris 13:44

Do you find there's a lot of overlap? I know you mentioned kind of the abdominal pain, abdominal aura, if you will. Um because I do find that a lot of, again, with with the few patients I've managed to diagnose over the years, uh, a lot of times they kind of go through the whole GI rigamerole where they've had scopes and been tried on like antispasmodics and so on and so forth. How often do you see those coexisting in your experience?

SPEAKER_02 14:11

No, it's a really good question. I don't see it as often as I think I might. And I think it has to do with the setting that I practice in, where kind of the filter to get into a vestibular clinic is much more so the dizziness vertigo, that kind of thing. But I would say in in someone who you know has had a complete GI workup whose symptoms are quite episodic, you know, and maybe the other thing that we haven't talked about yet are triggers, right? Migraine triggers. If if the symptoms seem to come on in in the presence of what are otherwise more conventional migraine triggers, and that's someone whom may benefit from from a treatment where it's both diagnostic and therapeutic. But it's kind of funny how we're all looking at a different part of the same elephant, if you will, that certainly that you know there's there's abdominal migraine out there, maybe more in more in in sort of children and adolescents, but I I haven't seen it as much, as much as I would think.

SPEAKER_01 15:09

I know we're mostly focusing on that diagnostic algorithm, but I can't help but jump in a little bit with management. And I'm curious for these vestibular migraine diagnoses, do you approach the treatment in a very similar way? Do you use the frontline migraine medications and counsel similarly, like use the abortive, you know, as soon as possible, use the preventative daily based on a frequency of symptom management. I'm just curious if you, once you kind of lay it in this category, approach it exactly the same or if there's nuances that you consider for management of vestibular migraine.

SPEAKER_02 15:44

Yeah, 100%. It's a really, really good question. The one caveat I should probably make is that almost all of the medications that we use for vestibular migraine are off-label. And of course, this is not medical advice, but for for education. So, you know, when I sit down and I'm having a you know a conversation with a vestibular migraine patient, I think, you know, the first step really is to explain to them, you know, what I'm thinking when I use the word migraine, because the way I'm using migraine differs from how we use the word migraine in in our everyday life. I mean, I really kind of explain to them, go through a handout with them that that really I'm I'm talking about migraine as a sensory gain issue, where the gain is just turned up on all kinds of sensory information and sort of explain to them. I once had a mentor in the UK who actually wouldn't use the word migraine because it just caused too much confusion. He he would stay away from from using the term migraine, but really, really explaining what I'm talking about, really big emphasis on the conservative things, uh, you know, sleep, really number one, stress reduction, regular meals, hydration. It's amazing sometimes what the conservative stuff can do. Where I would contrast things a little bit from migraine headaches without vestibular features is I gravitate a little bit less towards abortives. I think that's more a personal style. You know, there are some patients who may benefit from a tryptan, for example. I have had some success with that, but I tend in these patients to move a little bit more towards a daily preventive. And I will say that in the vestibular community, a lot of us tend to gravitate towards tricyclics, amatryptaline, nortriptaline. And the reason for that is they help with sleep, which is often often a big trigger. They're good anti-migraine medications, and they seem to have some nice secondary effect on dizziness because they have a little bit of serotonin action. And these are patients who are at high risk of developing chronic dizziness. Uh, we'll talk a little bit about triple PD in a minute. And and you know, treatment for triple PD would be would be a serotonin-acting medication. So TCAs tend to be, tend to be used sort of a little bit more so than in in migraine headaches. We have had good success with CGRP medications. Uh, there was one trial out of Jeff Sharon's group at UCSF and that showed benefit. And so that's a new new frontier uh worth worth trying as well. So we approach it very similarly to to migraine headaches, just trying to increase that that threshold, that patient's migraine threshold.

Vestibular Migraine Clues Beyond Headache

SPEAKER_01 18:12

Yeah, well, admit um a mistake I made was that I do think about them so similarly once I've made the diagnosis. In terms of my counseling, it's like basically the same. And I have a patient who I could follow for a long time. And every time they would come in, I'd be like, okay, so tell me about your headaches. They'd be like, Doc, I don't have headaches, I have dizziness. And I was like, right, right, you're in dizziness syndrome. We talked about this, but sometimes that was a faux pas on my part. But I do think of them so similarly in terms of the counseling, about the episodes, trying to figure out what the triggers are for them, trying to do prevention and educating them as well about potential unexpected triggers. So this particular patient was very sensitive with flying and sort of this idea of like with the jet lag and with the transitions to just anticipate that those might be one or two bad days. And that really reassured them, just knowing that it wasn't, you know, some unexpected thing, um, but something that they could plan for and deal with.

SPEAKER_02 19:05

Absolutely. And along those same lines, barometric pressure is often a really strong migraine trigger. Uh, Galina, you'll appreciate this story. So when I was uh landing where I was gonna land or finding where I wanted to land for residency, I spent about two weeks out in Calgary and it was in the summer. Sorry, in the winter. I'm sorry, it was in the winter. And what happens in Calgary is they have the warm wind, they have the Chinook that comes through, and it's a major change because it's basically a high pressure system that comes in. And every day I was there, I got a migraine, you know, with the change in pressure. And apparently this is a thing with the Chinook that that folks get migraine. So I deeply empathize with my patients. You know, it's like our heads and our ears are like little weather veins, and just like when the weather changes, you know, we're we're at high risk. So that's another big one barometric pressure. Uh, you know, hormone changes, obviously. Yeah.

SPEAKER_01 19:56

Well, if we're gonna if we're gonna share personal migraine stories, and I'll quickly throw mine in. And mine is uh every night call, I would get visual aura, and at some point I couldn't take my type my notes, and I was like, I gotta go lie down.

SPEAKER_02 20:09

Yeah. Medical residency has a way of of bringing out migraine. That's why like 80% of neurologists have migraine, because we we drive ourselves there.

Michael Kentris 20:20

No, I don't have migraines. I just have plain old tension headaches, unfortunately.

SPEAKER_01 20:25

Well, there's a there's a type for everyone.

SPEAKER_02 20:28

Right, right. Great. So I think we've uh we've gone down the spontaneous episodic branch of the tree. Maybe now we can change gears a little bit and talk about more chronic disorders, chronic vestibular disorders, talk a little bit about the situation that we see a little bit more commonly in the clinic setting, in the outpatient setting, patients who maybe have entered into an everyday dizziness, or or patients who have more issues with balance, maybe, maybe dizziness is kind of a smaller, a smaller symptom for them. And so the first thing that might be helpful to talk about is probably the most common uh disorder causing kind of a chronic dizziness, not not episodic, but but more days than not. And that's uh another mouthful. Uh PP And so PPPD is is an acronym. It sounds for it stands for persistent postural perceptual dizziness. And when I'm explaining to patients what that is, I find it helpful to go through each uh of the letters in the acronym to explain exactly what we're thinking about. And unlike the other disorders, the other conditions that we've talked about so far, PPPD or triple PD is more a situation, a state that patients can find themselves in as opposed to an etiologic diagnosis. And so uh PPPD, again, it's a mouthful. The first P stands for persistent. And persistent, we normally take to mean present for more days than not for about three months. So it doesn't have to be every day, doesn't have to be all day, but present for for more days than not. To get a sense for what patients are experiencing, sometimes I'll ask them to tell me what percent of an average day they have dizziness. So to take their waking hours and just tell me like, are you feeling dizzy 10% of your day, 50% of your day, 80% of your day? And uh many, but not all patients with with triple PD will say 50, 70, 80% of the day, I'll be having some dizziness. So it's persistent. The second P is postural. So it tends to be worse upright. And it's not postural like orthostatic hypotension in the sense of, you know, when they stand up, but they tend to experience it more when they're standing than when they're sitting or lying down. Tends to be worse often when when patients are walking around. So when they're self-motion when upright. The third P is perceptual. So there tend to be certain environments that that make the dizziness worse. So that could be going through the aisles in the supermarket. That's a classic one. Um, you know, motion on a screen, self-motion, you know, vehicular motion, so passive motion. Sometimes even uh a static busy environment or a static, you know, busy scene affects them. So if one goes and looks at the original description paper by Staub and colleagues of Triple PD, they actually show uh a carpet, a hotel carpet that's really busy with a lot of jagged lines and colors. Um and that's the kind of thing that would really affect uh patients with triple PD, you know, being out on a street in Tokyo or New York City. And so there's a there's a perceptual quality to it. And then the last D is dizziness. So it's not a room spinning, but a dizziness, an unsteadiness, perhaps lightheadedness, not feeling connected to the ground. So that that's kind of what triple PD is. Triple PD, I feel, is a state that, you know, a lot of patients who who are in a vestibular disorder, having vestibular disorders that are coming on a lot could could easily get into. And the way I describe it sometimes to patients is it's a little bit like that feeling that you get if you went out on the ice, like if you were walking on the ice, what would you do? You would kind of take on a high-risk posture, you'd be a little bit more vigilant, you'd be much more careful and apprehensive. And that's kind of the state a lot of our patients with triple PD are in a month, three months, five months, a year after their initial vestibular insult. And so while helpful in the first couple of hours, that that that state is kind of working against them. And so our goal is to try to get them out of that fight or flight state and that they might be in months or or years later.

Michael Kentris 24:46

So it's kind of I remember reading an article about PPPD a few years back. And this was the again, I my own ignorance, this was the first time I had come across it. Uh I was in a continuum review for the neuroontology article like four or five years ago. It was interesting. So it sounds like some people kind of are putting it in the same family as of other functional neurologic disorders. And kind of like what you were saying, you have like all of these maladaptive behaviors, both in like the hypervigilance and the kind of like, as you said, they they hold their gait in an unnatural fashion, so there's increased energy expenditure and all of these negative things that uh that tend to come along with it, in addition to perhaps whatever their original dizziness was that may or may not be treated. And anecdotally, I find a lot of these people have been on chronic, either like uh meclosine or you know, diazepam for you know years and years, and then they finally come to you as the neurologist, and you're like, oh, this is a this is a big ball of wax I gotta take apart here.

Vestibular Migraine Treatment Approach

SPEAKER_02 25:52

100%. I'm really glad that you you brought up uh vestibular suppressants and suppressant overuse. I think vestibular suppressants can, you know, they have their role, they can be helpful in the acute setting. You know, in in some cases, if someone has really, really strong symptoms from BPPV and we need to do a Dix Hallpike, or they need to go to PT and and have multiple sessions, then we'll have them pre-medicate. I mean, they they have their role in in limited situations, but over the long term, they can really work against patients who have chronic dizziness. So exactly as you're saying, you know, part of what I'm doing is just slowly tapering off those those medications, explaining to the patient why we're doing that. But absolutely, yeah, I think uh I think triple PD is maybe a little bit different from some of the other functional neurology that that we see in the sense that uh I think um it's just so common among patients with not that F and D isn't common, but it's just, you know, it's like the number one uh cause of chronic dizziness, because I think it's a final state that a lot of patients with with vestibular disorders, you know, and and end up in.

Michael Kentris 27:02

It was interesting. I I think there was uh a motion capture study from a gate lab, if I remember correctly, right, the little ping-pong poles all over them. And they were comparing the patients with 3 PD to people with like bilateral vestibular neuritis, uh like like chronic, and they had like worse gait stability and worse self-reported dizziness markers than these people who had no vestibular nerve function bilaterally, which I just thought was just wild.

SPEAKER_02 27:31

Absolutely. Yeah, the functional limitation can be quite profound. And again, that discrepancy in terms of certain environments, right? Certain kinds of environments can be very tough for for patients with triple P D. So I would expect patients with bilateral loss to have a lot of trouble in the dark where you're taking vision away, whereas triple PD patients are going to have a lot of trouble in a busy environment where there's a lot of motion. So if you you put them in a scenario where you're asking them to walk or demonstrate balance when when there's a lot of commotion, they would they would have more trouble there. But it can be very, very functionally limiting.

SPEAKER_01 28:07

Anon, you mentioned that it's sort of like the end stage of any vestibular syndrome. So do you typically hear that part of the story that it starts with, say, an acute vestibular syndrome or some other kind of vestibular insult um and then ends in this way? Or is there ever someone for whom like they're they can't pinpoint a kind of an acute episode? I've sort of seen a similar situation, and of course, it can be hard to separate or parse it out like into post-concussive syndrome, because obviously then there's been like a you know a head injury and there's dizziness as part of that, and then at one point is it and being stop being post-concussive and start being 3 PD. Um, but can you talk to us a little bit about that sort of let's say like the natural history and is there always an initial insult that you can point to and and then a follow-through?

SPEAKER_02 28:57

Excellent question. So I would say there are probably a f a few groups, and I'm really glad that you brought that up. So I would say the first group is, as you've described very well. You have a patient who had BPPV or they had a vestibular neuritis, or they had some other, they might have had Meniers disease, and they have frequent episodes, and they've they've they've sort of entered the state where where they have chronic daily symptoms and they would meet the criteria for triple P D. So that's you know one subset. Another subset is sort of this more vague overlap between migraine, chronic migraine, triple P D. And with those patients, you know, the the symptoms are are are daily or close to daily. But the way that I'll sort of try to tease it out is I'll try to ask a patient to describe what a bad day looks like to see, you know, do you have bad days? Like do you have days where you just wake up or something changes and you feel worse? And often we'll we'll be able to pick up that there might be worsening, kind of spontaneous worsening. And that worsening might have migraine triggers, it might have some migraine features with it, they might have a headache on those days. And I think there you've got this overlap between chronic migraine and and triple PD or episodic migraine, you know, triple PD. And then I would say there's a third group where there may not as cleanly be a vestibular insult, but they're more in the triple PD category. And so, you know, sometimes a stress event can provoke uh triple PD. Sometimes we we just don't know what exactly triggered it, but their phenotype you know matches with the with the triple PD, and so we treat the same. So I would say they're they're different different groups that that end up with 3PD.

Michael Kentris 30:42

So I know you skirted around and we've talked about a few different etiologies, but how do we approach the treatment? You know, I I assume it's not just, as we said, put everyone on meclasine and diazepam and call it a day, everyone goes home happy. It's probably more complicated than that. So how do you approach the treatment for some of these specific syndromes? I know some have very specific treatments, others are a little, let's say, more nebulous.

What PPPD Feels Like

SPEAKER_02 31:08

Yeah, it's a great question. So the first thing I always try to do is to identify anything that's addressable, treatable, sort of a perpetuating factor, if you will. And so if there's any BPPV, you know, keep checking for it. Even on the first visit, if you don't see it, you'll be surprised how many times it's been a part of the story and we don't get that clear positional flavor. And we test them the first time, and they actually didn't have it at the time that I first met them. But one day I test them and wow, you know, they've got a BPPV. So addressing that, certainly if there's any part that's migraine, at a minimum you want to address it conservatively, but but certainly medically as well, perhaps trying to find a medication that might address um, you know, migraine and triple PD. And then what I would say is I kind of think about the different, you know, sides of things. So, you know, the things that are helpful in triple PD, uh, you know, certainly CBT and psychotherapy and counseling can be really, really helpful again, because of that secondary, you know, fight or flight state. You know, movement. We really want to expand what a patient with triple PD is able to do slowly. Um, you know, some patients are really apprehensive about head motion, really apprehensive about visual motion. And we want to, you know, instead of having them avoid those things, which is a natural thing to do, slowly sort of move more and do a little bit more. So the movement piece, I think, is really important. I think the sleep piece is really important. We don't know if that's through a migraine mechanism. I mean, it makes intuitive sense that a lot of the connections and rewiring that that's going on around vestibular input is happening when we sleep. We showed a couple years ago that patients with a triple PD tend to have sleep apnea at a much higher rate than the average population. Even in patients who don't have clear risk factors in terms of neck circumference and BMI. So making sure we optimize sleep. And then from a from a medication standpoint, we really tend to see benefit from antidepressants. So SSRIs, SNRIs tend to help as well. Uh and I really explain to patients that I'm not primarily using it for mood. If it helps with mood, that's that's a nice benefit, but I'm really using it to address the daily dizziness. So those are kind of the things in in sequence that that I look for. I think we've said in different ways vestibular suppressants would try to pair for those back as much as possible. Benzodiazepines try to clean things up from that perspective. Um, because again, what happens with those is when they're on board, they suppress the vestibular input. So they make things more manageable. But then as soon as they're off, you know, the symptoms go way up because the gain, the problem with a lot of these disorders is that the gain on vestibular and head motion are just turned way up.

SPEAKER_01 33:54

I have so many questions. I'm gonna like try to only do one at a time. But I guess my first one has to do with thinking about vestibular therapy for these patients. Um, you mentioned that you want to be conservative and you know, that there is definitely a role for the SSRIs or another antidepressant. How do you think about vestibular therapy in the chronic setting? Is that something that's still worth a shot? Um worth like once in a while? Um is it a different approach or is it less helpful when it's actually been kind of set, kind of when things are more stable?

SPEAKER_02 34:26

Yeah, it's a really good question. As far as vestibular physical therapy for APD, I think there is a role, and I I have seen pen patients benefit a lot. I think what I really like is to make sure that the physical therapists that I'm working with and I are kind of on the same page in terms of, you know, what are we seeing on exam? What are we trying to address? Because, you know, there's different kinds of vestibular PT. And so, you know, we wouldn't want to put a 3 PD patient through, you know, multiple Eply maneuvers, right? If we were really sure that they didn't have crystal. Sure, we want to check, you know, once every other visit to make sure. You know, similarly, you know, just doing pure gaze stability that we would do for someone with unilateral loss, you know, looking at an X and moving their head side to side, I mean, I think not necessarily the exact thing that we would want to do, but understanding where the patient's at, identifying what would, you know, what are they avoiding? What are they not able to do? And how could we get them there? You know, if there are specific things that really bother them, visual things, could we in a gradual way, with the support of someone working one-on-one with them, gradually increase their tolerance? I've seen that be really helpful. So I think it really depends on the situation and you know, making sure that you're aligned with PT on what you think the diagnosis are. You know, how how are we going to help the patient from a from a function standpoint? A related question that comes up a lot is what about migraine? What about patients who have vestibular migraine? Is PT helpful? And I think the principles are the same. Where migraine is a little bit more tricky is that, you know, as we do PT and as we try to do habituation or try to help the patient, because again, migrainers, again, it's a similar phenotype. Sometimes they can be very sensitive to head motion and visual motion. We just want to make sure that we're not every time they go to PT pushing them over their threshold. And so sometimes what I'll do is I'll try to increase their migraine threshold, do some conservative things, maybe get them moving a little bit more on their own, and then maybe bring up the idea of PT if they're still having a lot of difficulties with function. Sorry about that.

Michael Kentris 36:37

For the folks we mentioned a little bit in passing, but the folks who have bilateral vestibular nerve dysfunction, whether that's because of like recurrent uh vestibular neuritis or some other event that have kind of a persistent dizziness, how how do we manage them as far as the symptoms? Because it's like probably not something that's going to improve on its own, I would assume, at that point in time.

SPEAKER_02 37:02

Yeah, great question. I think this is a great moment to kind of talk about how in a patient with chronic dizziness or imbalance, there are certain things on the exam that we, you know, we want to make sure that we check carefully before we call something uh triple PD. Because again, patients with other disorders can have persistent, you know, dizziness and it can have some features of triple PD. And so I think a great one to talk about now, I'm really glad you brought it up, is the case of bilateral vestibular loss. So those are patients who have loss of vestibular function from both ears effectively. And so the things on the history that make me think about bilateral vestibular loss, well, definitely loss of balance in the dark, right? Because when we close our eyes or we're in a dark environment, we're taking vision away. So then we're dependent just on proprioception and vestibular function. And I know in other uh other podcast episodes, for example, the gate one, you you've talked a lot about you know the Romberg test and the self-Romberg or the Romberg machine, aka the shower.

SPEAKER_01 38:04

So that you know, that's like to do some space learning here.

PPPD Management And Avoiding Suppressants

SPEAKER_02 38:07

So we're taking vision away and we can bring out you know a vestibular problem. The other thing that patients with bilateral loss will often describe is a movement of the visual world when they're they're walking around. So it's kind of like the the Blair Witch project, if you will, that the scene is just moving. If they're in a car on a bumpy road, they have a lot of trouble reading road signs because they've lost that inner ear input that stabilizes our gaze, that keeps our eyes steady, the you know, the vestibular ocular reflex. And so when I'm hearing that, I'm already thinking, you know, I've got to, I've got to check, you know, vestibular function. And so on exam, what we would look for was we would do a head impulse test, as we talked about last time. And if we see catchup saccades on both sides, that's gonna point us towards bilateral vestibular loss. And obviously that's something we would think a little bit differently, think about a little bit different differently from triple PD. So if we have a patient with bilateral vestibular loss, I think it's really important to think about why and how did they get to develop bilateral loss. I think it's worth thinking about a sequential neuritis if they have a history of that. Did they have an acute vestibular syndrome and then a few months or years later have another one? You know, it's certainly possible, more rare, but certainly possible that you can have, you know, vestibular neuritis on both sides. I would say the more common situation is more an idiopathic bilateral vestibular loss or a genetic uh bilateral vestibular loss. So there are now genetic conditions like canvas syndrome, cerebellar ataxia, neuropathy, and vestibular a reflexia that can cause bilateral vestibular loss. And I predict that in the next decade we're going to identify even more genetic causes of bilateral vestibular loss. So identifying it, making sure if there's anything on the story that makes you worried about, for example, a past um subarachnoid hemorrhage, uh, cos hemociderin deposition can kind of trace down, you know, and cause a bilateral vestibulopathy. Again, that's that's rare. It's usually ediopathic. Thinking about thiamine deficiency, which can sometimes cause bilateral loss, but provided you've excluded those things, often it is idiopathic. So, how do we manage the patient? These are patients who really can benefit from PT, particularly if they have decent proprioception, you know, and their vision's good. We really want to work with them in PT to use those other modalities, to use those other senses to compensate. I always think about safety, right? So making sure that they've got night lights at home, that they're avoiding situations where they're in the dark, you know, not taking risks from that perspective. Always want to work with PT and get you know, get PT's input in terms of gate aids. But in some of these patients, having something like a walker can be really helpful because you're adding more proprio more stronger proprioception, you know, something to support them. But yeah, bilateral loss can be difficult.

SPEAKER_01 40:58

It's really helpful to hear you talk about the role of proprioception and vision and how that's something that our brain is using to stay balanced and then something that we can use on our history as a clue that there may be an issue. And I'm I know we're circling back a little bit, but can you contrast that a little bit with 3PD? Do we know why those patients have such a challenge with like visual input and stimuli? Is it something about that disruption between the the role of vision input for balance? Or am I thinking, like mechanistically, do we have any understanding?

SPEAKER_02 41:32

Yeah, it's a great question. In in a archetypal patient with triple PD, vestibular function is normal. Although I will say that there are a lot of patients who have a unilateral loss, maybe even bilateral loss, and they they end up with a phenotype that's a lot like like triple PD. So I think kind of a good way to answer your question is, you know, what's going on in a patient who has normal bilateral vestibular function and is still experiencing triple PD? And so what we think is going on there is, you know, it's a simplistic high-level thinking about it, but whatever happened to cause the bilateral, sorry, whatever happened to cause that initial insult, whether it was migraine, might have been meniers, might have been triple PD, you know, force the patient to be much more visually dependent. Because that's one of the common things that we do, you know, when we're having a BPPV. I see this all the time. You know, patients with BPPV are maybe having some visual motion sensitivity even in between episodes. And that's because their brain has become more visually dependent. The input that was coming in from the inner ear couldn't be trusted, if you will, and they were more visually dependent. And so for a period of time, you know, they're more visually dependent. I think patients with triple PD have become, in a maladaptive way, much more visually dependent. And so that's why when they're in a situation where there's a lot of visual stimuli, it just overwhelms their system, right? The gain is just turned up on that visual information and they have more difficulties with balance. Their underlying vestibular function, most of them is normal. So it's more about calibrating the gain, it's more about habituation, it's more about preventing that secondary fight or flight response from happening. So the exam can really help you out there. You know, if they're looking like a bilateral loss patient, um, then that the treatment is a little bit different. We want them to do a little bit more gaze stability, a little bit more sensory substitution, although there are similarities. You know, we want both patients to kind of use what else there is beside vision as well.

Michael Kentris 43:33

You know, there's there's one entity, I'm gonna go a little off script here, that we didn't talk about, but I see it thrown around, and that's uh cervicogenic vertigo, which I know is a little controversial of an entity. So I was wondering: do people ever come to you with that diagnosis? And what is your opinion on it as an entity?

How To Use Vestibular PT Well

Bilateral Vestibular Loss Red Flags

SPEAKER_02 43:53

It's a great question. Wow, you guys know how to pick the hot topics in in vestibular. I'll tell you something. Funny, I have to, because I submitted a paper recently and we had two reviewers. One reviewer said, Why haven't you talked about cervicogenic dizziness? And the other reviewer said, What is this? I thought we decided as a field that, you know, we shouldn't be talking about cervicogenic dizziness. So what I can say, and I'll try to be diplomatic, um, you know, what I can say is that there is a lot of interconnectivity between all of the afferents, you know, that go to the neck and drive cervical proprioception and the vestibular nuclei. Like we know that the trigeminal system and the vestibular system in the brainstem are closely wired. And you can you can see why that would be important, right? They're both inputs in terms of balance. You know, we do we see a lot of patients with neck tension and and complaining of dizziness? Absolutely. What is the direction of that causality, right? Is it patients who are dizzy who are holding their neck tense all the time? Is it the opposite? Is it the neck tension is directly impinging on the vestibular nuclei? Or is it sort of the thing that we've been that we keep coming back to, which is could it be that migraine is a is a common thread? Because we know migraine turns up the gain on vestibular and sensory information. We also know that migraine can cause neck tension, right? It's part of the prodrome and the and the sort of ictus of of migraine. And so when when I have a patient who sort of has a lot of neck tension, I want to address it, right? I want to address the neck tension. I think they should be doing PT to strengthen their neck. They should be doing massage. If they find acupuncture helpful, I think that can be good. We talk about ergonomics. We're all hunched over on our screens and and uh and phones. Certainly that's not helping dizziness or or migraine. So so I'm I'm very kind of practical in that regard. But if someone has, you know, anything, any whiff of migraine, I'm not going to uh sort of deny the opportunity to try to treat them for that because they have a lot of neck tension, actually, quite the opposite. You know, I would I would try to think of migraine as being an underlying cause. So, you know, cervicogenic is, I mean, it's really a description, right? It's dizziness from the neck. And so I just say, sure, like they probably do have dizziness from the neck. But what what does that actually mean? And what do we actually do about that? You know, there's a lot of active interest in this area. Perhaps we may find something, we may find specific treatments, but yeah, a lot of interconnection between cervical afferents and and the trigeminal system and the vestibular system at the level of the brain stem. You know, a lot of patients who have who have both and we try to manage for both, but don't forget migraine and and certainly wouldn't deny the opportunity to treat someone as migraine. I don't find cervical imaging helpful, but of course, if there's another indication for it, that that's something that you could could think about. But I don't see what you would find on neck imaging that would answer this question. I think it's more a function problem than than a structural problem.

Michael Kentris 47:00

I think that's that's beautifully said. Thank you.

SPEAKER_02 47:03

So maybe now we can add one more entity that we really should be looking closely for in a patient with chronic dizziness, right? We don't we don't want to call this a triple PD. And that's downbeat uh nystagmus, downbeat nystagmus. And so, you know, we want to look carefully when we examine our patients. We want to uh sort of have them look in the distance, we want to add light, all the tips that we talked about last time, really advantage ourselves to pick up subtle nystagmus. And what do we see with downbeat? Well, we see a spontaneous nystagmus with a slow drift up, and then the fast phase is down. So the eyes look like they're beating down. And the things that we can do to bring out downbeat nystagmus are to bring the patient to lateral gaze. So downbeat nystagmus usually worsens in lateral gaze. So you can bring the patient to the right and to the left, and then you're looking carefully. Is there a little bit of downbeat? Uh, we can remove fixation. So if we have frenzyl goggles, we can do that. Uh, or simple trick at the bedside, cover up one eye and shine a pen light in the other eye. Credit for that to Dr. uh David Newman-Toker. Um, they call that the penlight cover test. So that's a way to remove fixation. Um, and you know, look carefully. Does the patient have a little bit of downbeat uh nystagmus? Because downbeat nystagmus localizes to the vestibulo cerebellum, and that is a central, I mean, it's a cerebellar problem, and it's going to take us down a completely different path from triple PD. So we want to look carefully for downbeat nystagmus. No, that's excellent.

SPEAKER_01 48:35

Well, Anand, as proven at the start, you are an extraordinary otoneurologist who just gave us a whirlwind dizzying tour of dizziness, all the way from acute vestibular syndrome through to episodic momentary dizziness and uh through to chronic weather PPD or else. So thank you so much for this summary and tour. And uh it's been a exciting wild ride. Learned a lot. Is your head spinning yet? Oh yeah.

Cervicogenic Dizziness And Downbeat Nystagmus

Michael Kentris 49:05

From the terminology of nothing. So if people want to find you, find more of your work, just to remind them, uh, where should they look for you?

SPEAKER_02 49:17

Yeah, so so I work at Mass INER and Mass General Hospital here in Boston, and I'm on faculty at at Harvard Medical School. So what we'll do maybe again in the show notes is we'll we'll share some of the other resources that I recommend in terms of starting with for all all manner of dizziness and vertigo, and that that'll be my calling card. Excellent. Perfect.

Michael Kentris 49:44

Galina, anything to plug for you today?

SPEAKER_01 49:47

No, I think just check out the podcast episodes with Anand. Um they're like really good summary kind of board review. And yeah, we'll see you next time.

Michael Kentris 49:57

Yeah. No, I think everyone should continuously listen to teaching materials about dizziness. Uh, it would save me a lot of consults in the hospital. So thank you so much, as always, uh, Dr. Nan Berry. Very much appreciated. And thank you everyone for listening. You can, of course, find our past work at the neurotransmitters.com, and you can find us at our various social media handles. Share the episode with a friend who you think needs to learn more about dizziness. Thanks, everybody.