to go and today I really just wanted to go through the assessment of the dizzy patient. So what I'd like to do is go through how our balance system actually works and the clinical assessment of the dizzy patient. Now the special investigations for the dizzy patients and the management of the dizzy patients I think as Reshma quite rightly said we should probably leave to another time but I think today would be a really good foundation in terms of making sure that you understand how to address dizzy patients and some of the pathology that we might see.
So I always start with this slide. It's myths and misconceptions. There's nothing you can do for dizzy patients and they just have to live with it.
That is not true at all and I genuinely believe that you can cure the majority of dizzy patients. who come to you and the ones that you can't cure you can certainly make much much better. Meniere's disease is a common cause of dizziness, no it isn't, it's a very uncommon cause of dizziness and vertigo and I'm sure there are lots of patients out there who have been diagnosed with this condition who never had it and I think we have to be really careful with labelling patients so that not only do we manage them appropriately, but we also make sure that they do not come to harm as a result. My last bullet point, of course, is all patients with dizziness are mad. Now, let's be honest, when a patient comes in in your clinic and sits down, your heart leaps with joy when they tell you that they've got vertigo or dizziness.
Well, mine does, because I find them really interesting. All patients with dizziness are mad. Well, about...
two-thirds of patients who would be referred to a specialist balance clinic will have anxiety, depression, agoraphobia as part of their clinical spectrum and those things will need to be addressed. We did a bit of research a few years ago to look to see if the delay in diagnosis and treatment perhaps made people more likely to be anxious or depressed. And the answer is no.
Actually, it can happen very quickly. But nonetheless, it's important to address depression, anxiety in order to make your patients better. So balance.
Well, a balanced system depends on four sensory inputs and the central nervous system integrating that information. Now, if we went back 20 years, perhaps I would put up a similar slide that said. balance depends on three sensory inputs but we have a much better understanding now of the inputs involved. You might have seen some older slides that would suggest that 70% of our balance is actually our eyesight, 15% is proprioception and 15% is the peripheral vestibular system or a variety of different numbers and what you have to understand is that actually the sensory inputs they're waiting.
changes depending on the situation that the person is in and also what changes have occurred to those sensory inputs and of course the brain. So a better model to start with is this. So there are four inputs. So we have our vision, the peripheral vestibular system, proprioception and our hearing and all that information is relayed to the brain from both sides of that person.
And within the brain, the information is integrated and interpreted. And as I'm sure you understand that, you know, there are three specific outputs for our balance. The first is to stabilize our vision. And that's absolutely essential.
The second is postural control to keep us upright so we don't keep falling over. And the last is spatial awareness. And what I mean by that is a normal person knows if they're standing in the middle of a room with their eyes closed. as opposed to standing next to the wall or standing in the corner. Now, a moment ago, I said the inflation from one's eyes, ears, hearing, our skin and joints was integrated and interpreted in our brain.
And what I really mean by that is that in your head, there are lots and lots of templates that drive your balance system. And what your brain does in the background all the time is it compares the inflation it's received with those templates. If you don't have a template that fits or if the brain can't compare the information Well, that's when you get giddiness, dizziness, vertigo, whatever you want to call it.
This is very difficult because it's not really interactive. And usually at this point when I lecture, I always ask people if they've ever met my wife. And my wife is by far the most aggressive and frightening woman I have ever met.
And she really likes shopping. So she takes me to Blue Water. which is this big shopping centre not far from where I live and she likes going to Marks and Spencer's and I absolutely hate it. So like most of the men who are listening to this I hide in the lingerie section on the ground floor but the reason I hide there is not because I'm a dirty old man it's because it's right next to the escalators and if you hide there and you switch one of the escalators off the escalator that takes people from the ground floor to the first floor and you watch. You see time and time again people will step onto the escalator, they pause for a fraction of a second, they haven't realised it's been turned off and they will always tip forward.
And they, you know, they may hurt themselves, I hope not, but I have a really good giggle. And that's really because we are all hardwired to change our centre of gravity when we step onto an escalator. And that only comes from experience. If you ever watch a toddler... holding a parent's hand when they step onto an escalator, you'll soon realise what I mean by that, because they don't really know quite where to put their feet.
Should they hold the rail? Should they hold their parents? And that comes with experience. Perhaps another good example is the travelator at the airport.
For most people, you step onto the travelator and it will take you forward. You've got all your luggage. I've got two little kids and it's lovely.
If you try walking down a travelator, most people find that peculiar, weird, and that's because everything goes past you much faster than it should. And unless you work at an airport or you walk on a travelator very frequently, you won't have generated a template that fits. If you yourself try running down a travelator, gosh, most of you, well, perhaps you'll manage 20, 30 meters before you fall over and hurt yourselves. And people who run past you on the travelator tend to be very clumsy.
They're more likely to hit you. But again, it's because they just simply don't have a template that fits. So so that's roughly how our balance system really works.
I think you're all familiar with this sort of picture. And it refers to the inner ear and the peripheral vestibular organ. Essentially, there are three semicircular canals that pick up.
angular head rotation and you have the utricle and saccule that pick up static head tilt and linear acceleration. Now in the semicircular canals, well there's a dilated segment called the ampulla and within the ampulla is the cupula. It's a fibrogelatinous mass and in the base are embedded these hair cells. So if you turn your head in one direction you can imagine endolymph within the in a year. Moving, it deflects the cupula, the hair cells tilt and they fire, well, either more rapidly or less rapidly, depending on how the cupula has been pushed.
In the uterine and saccule, we have a slightly different arrangement where one has the otoconial membrane, which has a specific gravity approximately 2.7 times greater than the endolymph around it. But essentially, the otoconial membrane is a raft of calcium blocks, and they're all tethered together. Because they're heavy, if you tilt your head in one direction, that raft will slide, and the hair cells embedded in the undersurface will tip over. And that's the mechanism by which one picks up static head tilt.
The linear acceleration, for example, that you might experience in a train. So the train will leave the station. and you feel that well well these are the organs that will pick up that movement. The vestibular reflex is a really important reflex that allows it that our vision to be stabilized and I will come back to it time and time again and it's an incredibly robust and rapid mechanism that allows you to stabilize your vision and in the diagram presented here, you can imagine the subject is turning their head and one side of the cupula is deflected in one horizontal semicircular canal in one direction, while in the opposite direction in the other semicircular canal on the contralateral side.
the firing rate as a result of the ampullary nerve fibres changes and that adjusts the position of the eyes, i.e. it stabilises vision on head turning. I hope that makes sense. So making a diagnosis. So I always tell this story, which I hope makes sense.
And it's a... It's a very old, famous Indian fable, I suppose, or parable. So the story goes that there are three blind men and they happen to stumble across each other in a little village in India. And the three of them start talking. And the first remarks that he had heard that the elephant was a really queer animal.
The second blind man agrees, as does the third. And the first says, well, look, I wish I'd been able to see an elephant. And the third blind man says, well, we wouldn't have to see it necessarily.
We could feel it. And it just so happens that the merchant is passing with a herd of elephants and stops. And he invites each of the blind men to step forward and feel the elephant.
So the first blind man steps forward and takes a hold of the leg. The second takes a hold of the trunk and the third is struck by the tail. And then the three thank the elephant.
merchant and sit down and start squabbling because the first blind man thinks an elephant is like a tree. The last thinks it's like a writhing cobra and the first isn't really quite sure at all. And the point about dizzy patients is that in order to establish an accurate diagnosis and hence actually cure these patients is you need an accurate history.
You need to examine the patient and you need your special investigations. And it's only when you've put all three together that you can be confident that you've made an accurate diagnosis. And we'll perhaps come back to this later. So if we start with the history, taking history from a dizzy patient can be incredibly difficult. And what I tend to do is I sit down.
And I just listen and I don't interrupt them really for the first two or three minutes. And they will often tell me how difficult it's been for them. And they also tell me really how it's impacted on their life.
So it may be the case they can't walk their dog and they really like doing that. And it's the one thing they hope to do. And could I cure them to do that?
And it sounds a bit daft, but now I've got my end point. I know exactly what I need to do. The first episode is the key.
So I always explore that in terms of what symptom did they first experience? Was it lightheadedness, feeling faint, disorientated? Was it vertigo? And with the vertigo, it's really important to make certain that it's an illusion of rotatory movement, either in the horizontal or in the vertical plane.
Was it a spinning sensation? Was it dizziness of some sort? Or was it that every time they move their head, the environment tries to catch up with them? So it's really worth pinning down exactly what they experienced in the first episode, in addition to any additional symptoms, hearing loss, tinnitus.
Was it positional? Did they have a headache with it? Any photophobia, phonophobia? And what was their general mental state?
And what I mean by that is that there are... As I said, many dizzy conditions that will leave a patient anxious and depressed, perhaps even agoraphobic. So it's important to understand that these are common complications and you need to address them to make your patient better.
But in addition to that, there are some dizzy conditions that really just wear patients out. They will often tell you that it's like thinking through fog. and they simply can't understand people. They have to ask people to repeat themselves and it really does wear them out. The frequency and severity of the episodes is important.
You know, does it happen every six weeks? Does it happen every year? How severe are the episodes?
Are they getting better? Are they getting worse? And I also really want to explore the last episode.
You know, is it different from the first? And the reason for that is because there are some dizzy conditions that are actually associated. So, for example.
If one suffers a unilateral peripheral vestibular hypofunction, a vestibular neuritis you might say, then downstream you're more likely to develop posterior canal BPPV. If you have Meniere's disease, well 30% of those patients will also have vestibular migraine. And if you're going to cure these patients then you have to address you know more than one problem and sometimes you have to address them sequentially.
and you can't try and do everything together that just does not work. Also in the history it's about the past medical history that's key so do they have musculoskeletal problems, do they have any visual problems, do they have any other neurological problems, of all the joints that are important with your postural control and and general balance, you know, some people would argue that actually it's your ankles. But actually taking a history in terms of the musculoskeletal system is always really important in these patients.
Drug history, you know, Prochlorperazine, as I'm sure most of you know, Prochlorperazine should only be prescribed to a patient for seven days and no longer. There was a retired GP who I met a few years ago, and he had self- prescribed Prochlorperazine for 21 years. He shuffled into my clinic, bless him, and he had all the features of Parkinsonism.
So, you know, that's a, that's a complication, unfortunately. Synarazine, beta-histine. Now the importance of the drug history is that it actually helps me understand what other people have tried first. So I'm never really very dismissive of what people have tried.
And in fact... I have the advantage of often meeting patients who've seen other doctors first, and they have quite rightly tried what they thought was appropriate. Anti-epileptic medication, analgesics, are really important here, not only in terms of the potential association with dizziness and unsteadiness, but also in terms of testing patients downstream.
in terms of vestibular function testing, because they can actually affect the tests. And you need to take that into account when you come up with a diagnosis. Sorry. Right.
So the examination. So I very often invite patients into my clinic room. So I'll go out into the waiting area and I will ask them in. And.
I always watch them. I watch their gait. I watch their general demeanour. On occasion, I've seen patients walking down the corridor and then they step into my clinic room and they start holding on to the furniture.
And it's not because they are mad. It's because they are sometimes desperate for somebody to take them seriously. And they really just want to make the point that they are in trouble and they really want your help. So, you know, sometimes people think that the patient's just putting it on. They're not, bless them.
You know, they have come to you because they genuinely want help, because the impact of the dizziness and vertigo has been so dreadful, not only to them, but also their families. Blood pressure. So in a specialist unit, if you're lucky, then what you can also do is have lying and standing blood pressures taken on patients before they come in. So essentially they lie down on a couch for five minutes, a blood pressure is taken then, and then immediately on a rising, you can have these automated blood pressure monitors now, and then after one minute, two minutes and five minutes, you can record their blood pressure.
And the drop in general of greater than 20 millimetres of mercury systolic or greater than 10 millimetres of mercury diastolic would suggest postural hypotension. And certainly in in older patients or patients who've taken antihypertensive medication, then it's just worth recording that and thinking that, you know, could that contribute to a patient's dizziness and unsteadiness? Well, looking in a ear, you know, otoscopy is obviously important. You want to rule out something like this, a cholesteatoma, and some patients can present with either intermittent vertigo associated with a hearing loss. conductive or sensorineural, or you might have had just one single episode of a significant acute peripheral distibular hypofunction which may or may not be associated with a florid infection at all.
It's also worth examining the ear for a previous scar, because of previous surgery rather, and the reason I say that is because, for example, patients who've undergone mastoid surgery are more likely to develop posterior canal benign paroxysmal positional vertigo downstream, perhaps months or even years later, and sometimes, of course, you know, as otologists we think, well look, you know, could it be because of the surgery or because of recurrence? it's quite right to assess and investigate those patients, but actually it may well be BPPV. You have to bear in mind that the posterior canal benign paroxysmal positional vertigo is by far the commonest cause of BPPV and vertigo for that matter, and you have a approximately 2.4% lifetime risk, I suppose, of developing it. So, you know, it's about one in 40 people. But there are certain things that predispose you.
Hemotympanin due to trauma or barotrauma. You know, I'm sure you're all familiar with the potential that a temporal bone fracture might cause significant trauma and a peripheral vestibular hypofunction. That's certainly true.
Barotrauma, again, could potentially cause a peripheral vestibular hypofunction. So it's always worth just having a look. Middle ear effusion.
Now, the reason I included this is because patients who have a middle ear effusion, sometimes people think that those patients aren't suitable for undergoing caloric testing. Now, it's true to say that the thermal response you may get because of a middle ear effusion will certainly affect your results. But there's no reason why you couldn't do it on either that ear or the contralateral ear, because you're going to gain some information about peripheral vestibular function, particularly on the other side if there is no mid-ear effusion. So it's worth just noting that, but it doesn't always mean you can't do the tests. So these aren't my post-op CTs, but I'm sure...
oh, I wonder if my cursor works... But here you can see that this is a patient who's had extensive cholestectomy and unfortunately there's a breach of the lateral semicircular canal. So one might anticipate a degree of dizziness and unsteadiness, particularly with rapid head movements, but also an associated central hearing loss.
So cranial nerve examination, it's really important to check all the cranial nerves, but specifically it's the eye examination that one needs to undertake. And spontaneous nystagmus, well, it's important to document the fast phase. And that usually means that it's a contralateral lesion consistent with hypofunction. The concept of having an irritative lesion is low, actually, for the vast majority of patients by the time they come to see you.
It's most probably a hypo function that you'll be dealing with in one, perhaps both ears, but certainly one ear is in the vast, vast majority of patients. So with spontaneous nystagmus, what's really important is that you stabilize the patient's head and you can put your finger out in front of them and you move it in the horizontal plane, but also in the vertical plane. And what I'd like you to do always is document exactly what you see.
The peripheral vestibular system, certainly our vision, is optimized for approximately 120 degrees in the horizontal plane and approximately 60 degrees in the vertical plane. Now the reason I mention that is because if one were to take a target beyond, let's say, 60 degrees, it is very common, in fact it's usual, to see... a few flickers of nystagmus that then stop. Now that's not true gaze evoke nystagmus, that's simply end gaze nystagmus. So again, you know, just be wary about how far you move a target from the midline.
If you see direction changing, horizontal, vertical, torsional, pendular nystagmus, Well, those are suggestive of central pathology. And as ENT surgeons, you can't just say, well, look, it's central. It's not vestibular.
That's not my problem. Because actually a lot of these patients do need to be investigated. And again, a lot of them can be managed by us as a specialty. So with gaze nystagmus, you know, your target, as I said, position about, well, it's 20 degrees in the vertical and 30 degrees left to right.
Take your time. If it's a peripheral vestibular hypofunction, then Alexander's law would dictate that the fast phase, well, the nystagmus will intensify to that side and it will be less intense to the contralateral side. But with central pathology, well, that's different.
Actually, it'll be there in the midline. Fixation circades occur, which means that the eyes seem to flicker as they try and find a target. And sometimes you might even find that you have disconjugate movement, i.e. that the two eyes move differently.
And that, again, would make you think, actually, is there a central pathology? And there usually is. And what might be causing it? Smooth pursuit is different. And what you have to understand that smooth pursuit, saccadic movement and opticonetic.
nystagmus are three I suppose phylogenetically different methods by which we have been able to stabilize our vision and they they work on via different neurological pathways. So smooth pursuit is a situation where one would sit opposite to patient and you'd have your finger or I used my pen and that's the target and asks the patient to look at the pen and I move it from side to side and I move it relatively slowly. If you're a young patient, you have no pathology, either central or peripheral, I would expect you to be able to follow that target perfectly.
If you are a bit old like me, then actually a slow movement, well, I would be able to follow that target cleanly. But if the target was moved more rapidly then what you see is something called saccadic intrusion the the eyes will jump from point to point but that's only when the target is moved very rapidly so if you were to see that when the target is moved very slowly well that would suggest central pathology cerebellar brainstem disease you know because what's happening there is that this particular pathway, this neurological pathway for stabilizing vision, is being compensated for by an older, if you like, saccadic eye tracking movement. So it's worth just bearing that in mind.
Saccadic movement is different and what I do with my patients in both the horizontal and the vertical planes is that I would use my finger and for example a pen and I ask the patients to look at my finger, and then I say pin, and they're supposed to look from one point to another. And I would expect a normal subject to be able to look at one, from one object to another, in one clean movement, both in the horizontal and in the vertical plane. If however, they were to overshoot the target, and then there would be an extra saccadic movement back, well, that central pathology.
Okay, so that's peculiar. Or if, for example, they can't, they don't have a single movement from one target to another, and there are small amplitudes, okay, as well, yes, that's myasthenia gravis. If it's inaccurate, and the target, the eyes seem to be moving before they finally fixate on the tie, well, that's cerebellar.
And you can see all sorts of movements when you perform this clinical test. Okay, so going on to different tests, I think you'll all be familiar with the head impulse test. And this was originally described by Halmagi and Courtois in 1988. And the way I do this test is that I take the patient's head and I turn it 30 degrees.
And I ask them to keep looking at a point on my face. It's usually the... the end of my nose. That's a pretty big target. And then what I do is I flick the head back to the midline rapidly.
Now in a normal person, the eyes will flick across in one clean movement. If however, there is a peripheral vestibular hypo function, what you will see is that when you flick the head back into the midline, the eyes will flick across, they'll stop short, and there'll be perhaps one or two extra beats. And you will see this time and time and time again.
And even a patient who has had a peripheral listobular hypofunction, perhaps years or decades ago, it's not unusual to pick this up as a clinical test. And obviously, in a patient who's got a dodgy neck, you know, rheumatoid arthritis, you have to be very careful. But nonetheless, I think it's an incredibly robust test.
And it has a... very good sensitivity and specificity. And we know that because of a number of studies that have been performed over the years.
You know, the original paper would suggest that the sensitivity and specificity of the test was 100%. Now, I don't believe it's quite that high. And there are a variety of papers and publications, which have looked at patients who have come to general ENT clinics, general disease clinics, even specialist clinics.
And it would appear that the sensitivity may not be as good as 100 percent. It might be as low as 30 percent. But the specificity is high. The catch up circades, as we call them, are noted when the head is flipped in the direction of the hypo function. So, again, you know, there have been studies looking at.
the caloric response and comparing that to the head impulse test. You could perhaps argue that, well, look, due to central compensation, a patient who's had a peripheral vestibular hypofunction perhaps months or years previously, well, is less likely to demonstrate this. But I have to say, I think it's a very, very useful test in the vast majority of patients. And it's certainly one of my regular test batteries. And again, lots and lots of data.
But in summary, with the head impulse test, you know, you're looking at a sensitivity of somewhere between 34 and 100 percent. I would I would say it's very high and a good specificity as well. And obviously, the greater the level of the peripheral vestibular hypo function, the more likely that you're going to see these catch up circades. And this is just a table that simply puts together at the top, table 7.3, some of the patients involved and the sensitivity and specificity. So that takes us on to the head shape test and I'm not sure how many of you are familiar with this test and Reshma might say that I only do this on patients when I'm feeling particularly cruel and I think that'd be dreadfully unfair I have to say.
The head shake test has become increasingly popular, actually, certainly in South Korea. And I've had to review several articles where it's being used. But in a nutshell, the patient sits forward, the head's tilted about 30 degrees, and then you take the patient's head and you turn the head rapidly from side to side. Really, it's for about 30 seconds.
The patient has their eyes closed throughout. And then... what you say is open your eyes and the patient opens their eyes and if you witness horizontal nystagmus then it would suggest that there is a peripheral hypofunction away from the side so in terms of the fast phase as we call it you know the nystagmus the fast was a wave of that nystagmus will be on the opposite side of the hypo function Is it a very good test? Well, I'm not entirely convinced. The nystagmus that it provokes can be transient and certainly from a clinical setting it can sometimes be quite difficult to see it and record it.
It is nonetheless gaining popularity both for peripheral and central pathology and we might see this more as part of our test battery. in the future. So in general with this particular test you know of picking up a peripheral list of the hyperfunction well yeah The sensitivity varies again enormously and the specificity again is relatively high.
Persisting nystagmus, vertical nystagmus, disconjured nystagmus can all be demonstrated with this test. And again, that's why it's become of such interest to so many units. Dynamic visual acuity, we don't very often do this actually in ENT clinics, but it's still a useful test. And essentially it depends on having a Snellen eye chart and you ask a patient to read the letters and find out how low essentially they can read a line to, and then you turn their head from side to side, approximately two hertz, and what should happen.
is that most patients would still be able to read the lines. But if that drops to less than two lines from their original, well, that would suggest either a poorly compensated peripheral vestibular hypofunction, or perhaps even a bilateral vestibular hypofunction. So it's a good test.
And perhaps we ought to be using this more often. You know, the data out there, again would suggest that it is useful. It can be difficult to turn the head appropriately when you're doing this.
Some people use a metronome to make sure that they are turning the head at two kilohertz, but it's a good test and I think part of a useful test battery for us. So cerebellar signs. So I think like most of you, I look for, I ask a patient to, you know, put one hand over their watch and turn their hand over rapidly and then do it on the other side.
And DDK, well, you know, that's quite good at looking at lateral zone and basal ganglia pathology because it's usually central. Finger to nose. Again, that's more lateral lobe with a cerebellum. Heel to shin, gait starts, heel to toe, I think is more midline pathology, actually. So all the patients.
you know, undergo that test. Romberg's test, I've put this in brackets because we'll talk about this in a moment. It was considered to be a useful test to elicit cerebellar pathology.
And I'm not entirely convinced for most patients, but it will come back to that. So we've done most of these things. And so we get to the Romberg's test.
So Romberg's test was originally described in 1846. And it was actually for Tades dorsalis, i.e. tertiary syphilis. And it's a test of proprioception. So what we're really talking about is the posterior colon being affected by syphilis. So gracilis cuneitis. So it.
In that situation, you lose your somatosensory and distal proprioception in your lower limbs. The way the test is actually performed is you get your subject to stand up with their feet together, their arms by their side, and they close their eyes. A normal subject, well, I would expect that normal subject to be able to stand in that position for 30 seconds. There are lots of different ways of measuring. a subject sway during a Romberg's test and measuring the sway is of value, it really is.
You can make the test more difficult, a sharpened Romberg's, and what you can do is if you stand up and you put one foot in front of the other, so heel to toe, put your hands by your side and close your eyes, you will notice. that you sway much more, you wobble much more. You can sharpen Romberg's test even further and what you can do is you can get a piece of foam, in fact there's a standardized density piece of foam that we use for this, and you can stand on it again with your feet together, hands by your sides, you close your eyes and again you should notice because you've lost some of your proprioception that you sway more.
You can sharpen it even further and you get your subject to stand up with one foot in front of the other on that piece of foam. and hands by your, you know, your side, and you will wobble much, much more. So this simply makes the test more and more difficult. If you haven't got a piece of foam, and you're at home and you want to try this, you can actually just, you know, get your pillow and stand on that.
And I think you'll understand what I mean very quickly. So Romberg's test, interesting, I think, you can tell how boring I am and sad. In 19... 10, I think it was, that Barani suggested that actually the Romberg's test could be used to assess peripheral vestibular function. And he suggested that if you had a peripheral vestibular hypofunction on one side, then you would lean over towards that side.
So quite a lot of work has been done actually to see if that... is true and actually it varies enormously and the Romberg's test as a test of peripheral vestibular hypofunction is not really that great. You know you can see time and time again that patients don't necessarily sway over to one side but they might sway more you know we have seen that.
And certainly in post-chirography studies, you know, that's certainly been demonstrated. The other thing to remember is that even without sharpening the Romberg's test, if you have a patient who has peripheral proprioception problems or somebody who has, in fact, cerebellar pathology, then you might well find that the subject cannot stand with their feet together with their eyes closed, but they can stand with their feet. further apart. And again, you can see patients who have bilateral vestibular hypofunction, who are unable to stand with their feet together, but may well be able to stand with their feet apart with their eyes closed.
So again, you know, it's a useful test, although not necessarily specifically for the peripheral vestibular system. Unterbergers or Fakuda. So the Fukuda or Unterberger's test, Unterberger originally described this test. And what he suggested was that you take a subject and you have them, their hands are really, their arms are actually by the side, but they march on the spot for a few seconds, a few minutes.
And if there's a peripheral vestibular hypofunction, they will rotate round to the side of the hypofunction. Fukuda quite rightly looked at this test and suggested in fact if the arms were outstretched and you standardize the number of steps you could actually assess the degree of rotation the extent of displacement much better and I think most of us are now used to using the Fakuda step test. But is it a very good test for peripheral vestibular hypofunction? Well you know there again there are a number of studies that have been published which would suggest that this is not a particularly sensitive or specific test you know sensitive 50 percent specificity of 61 percent i you know 61 out of 100 patients with a significant peripheral list of the hypofunction will rotate round to the affected side um you know it perhaps isn't quite as um as accurate as we would hope and in some units the the Fakuda test test has been dismissed really.
From a personal perspective I still think it is useful especially in a young patient in terms of assessing their extent of their rotation and their peripheral list of a hypo function. We actually had a problem when I worked at Medway and both our force plate and our dynamic post-choreography machine broke down. So what we actually did was we developed our own iPhone app. So you attach an iPhone to a subject.
And what the app did was not only measure extent of sway on a Romberg's test and sharpened Romberg's test, but it also, when you attach the phone to the subject and they perform the Unterberger or Fukuda step test, It actually simply exploited the compass function and measured the extent of rotation. From my perspective, I think it's important that it's not the number of seconds that are used, but it's number of steps, because you can clearly measure and count the number of steps undertaken by your individual. So I take 50 steps and I take 30 degrees of rotation to be significant. And if it's significant, it would suggest in the majority of cases a peripheral listoblohypofunction. to the side that the patient has rotated to.
Now one has to remember that there are lots of things that can affect the Winterberger test and we've published a series of papers to explain this. For example, if you have a ticking clock in your examination room, in your clinic room, Well, the patients will fixate on that and they are unlikely to rotate. If something as simple as, you know, if one if the patient has musculoskeletal problems, there's a problem with one ankle, one knee or one hip.
And again, that's going to affect the test. But but I'm hoping that by standardizing the test, being able to actually accurately measure the extent of rotation that I think we can make this test more useful. as part of our test battery and I would not dismiss it, I really wouldn't. And as I said in a young patient it is still of significant value.
So the Dix-Hallpike test. Now the Dix-Hallpike test is a positional test to induce nystagmus and what I need you to all understand is that a positive response does not necessarily mean that the patient has benign paroxysmal positional vertigo, BPPV. It is absolutely essential that you accurately document the nystagmus that's provoked by this clinical test. It is absolutely essential. So how do we perform it?
Well, if you take pictures one and two, so you sit the patient on the... on a couch um i always say to the patient look you know pop up here um i'm going to hold your head and on the count of three i want you to lie down and they lie down at their own pace it doesn't have to be very quick um and i say to them look i'm going to hold your head i just want you to lie down no matter what happens you must keep your eyes open and you must keep it looking at me um and so I'll take the head, drop the head down, it's turned 45 degrees in the horizontal plane, and when you tip it down it should be about 30 degrees off the end of the bed. And what's important is you then wait, and you need to wait about 30 seconds to see if any nystagmus is provoked and to accurately document what sort of nystagmus you see. If I were to perform a Dix-Hall Pike test on this case in the right ear, I get no response. Then I will go to the other side, the left ear, which is depicted on the right side of this slide.
Oh, it worked. I'm so pleased. So this is a patient, a really nice lady, and I've dropped her head down and you can see that her eyes are now rotating.
and it's just starting okay and you can see that eyes are twisting really well and that torsional movement is getting stronger and stronger and stronger and will eventually abate so it stops completely so if i were to record this in my notes i would say that there was a latency perhaps in two seconds there'll be geotropic torsional astagmas that abated after 15 20 seconds um and that it completely abated. That's really important. And that's what you're likely to see when you form a Dix-Hall-Pike test on a patient presenting with vertigo in your clinic. But the reason why it's so important to document exactly what you see is because, as I said before, the Dix-Hall-Pike test is a positional test to induce nystagmus, and there are different forms of nystagmus that you might see.
and they mean very different things. Okay, so the Dix-Hall pipe test for posterior canal benign paracosmolar positional vertigo, which is what we basically seen in that video just now. OK, you know, the sensitivity and specificity are in the 70s. OK, there is some suggestion that actually for posterior canal BPPV, you're more likely to get an accurate to provoke nystagmus and increase your sensitivity and specificity in the morning, as opposed to seeing a patient later on in the day.
And there are some American units, for example, that will open their doors at 6.30, 7 o'clock in the morning as a result. But, you know, it is still a very useful test in patients with vertigo. And I would ask you all to perform this test, unless, of course, the patient has got a fragile neck, an unstable neck. So going back to what I mentioned earlier, so if you perform a Dick's Hall pipe test and there's a short latency, there's geotropic torsional astagmus that completely abates and both orbits will twist, then that's... canalolithiasis, so that's debris within the posterior canal, the lower posterior canal, and that's benign paroxysmal positional vertigo.
If you have no latency, geotropic torsional astagmas that completely abate, well that's cupular lithiasis of the posterior canal, BPPV. So what that really means is the debris is adherent to the cupula. If you have a short latency, high frequency horizontal astagmas that again completely abate, that's horizontal canal BPPV.
And that's important because for my patients, I will form a Dix-Hall pike, I'll perform an ectoly manoeuvre if they've got posterior canal BPPV, but then I'll repeat my Dix-Hall pike because in approximately 5% of cases, there is some phenomenon called canal switch occurs, where the debris moves from the posterior canal to the horizontal canal. And you need to treat those patients, not with an Epley manoeuvre, but with something else, something called a barbecue roll. And we'll talk about that later on. If, however, there's short latency, a geotropic torsional astagloss, well, that's suggestive of a contralateral anterior canal BPPV. I have to say to you, if you see that, that is rare and you're better off still thinking about a central pathology.
In actual fact, I would treat those patients with something called a Jans maneuver, which if you've ever seen any videos is quite bizarre, but it works. But again, I will still arrange an MRI scan for those patients. Horizontal nystagmus, if it's persistent, i.e. does not stop, well that's central. And in my experience, if it happens in a young woman, then my greatest concern is that actually that represents multiple sclerosis. and that's usually the case.
Downbeat nystagmus on a Dix-Hall-Pike test, if it's persistent, well that's central. It can be associated with some drugs including the anti-epileptic medication that I mentioned earlier. Gabapentin, for example, again can be associated with it. Upbeat nystagmus, if that's persistent, that's central. So when you're looking for nystagmus at the very beginning in both the horizontal and the vertical plane, Always document if you notice any downbeat or upbeat nystagmus.
Upbeat nystagmus, in my limited experience of these things, is a disaster. And it would suggest a brainstem lesion. And that patient probably has weeks or months to live. So be very careful.
So the Dix-Hallpike test is an incredibly useful clinical test. But there's no such thing as a positive Dix-Hallpike. point test. That doesn't mean anything really to me.
I need to know exactly what's been witnessed in order to establish a diagnosis. Gait assessment, you know, so as I said to you, I will go and call the patients in and I watch them and I watch how they walk. And that's a really useful thing to do. And you can pick up lots of pathology, both, you know, in terms of peripheral, but also central sometimes. in terms of their gait.
There are specialist gait assessments that we use, for example, a dynamic gait index that's used by the physiotherapist to assess their patients before and after a spell of vestibular rehabilitation and if you look through that there are eight specific tasks and that's useful. it is useful to see how patients have progressed. And there's lots of data.
If you're sad and boring like me and you're prepared to go through all the papers, you'll see how useful some of these tests really are. Some of the clinical tests, so I've included, you know, some of the things that I've mentioned and what they mean on this slide, and I hope that's useful to you. But what I'd also just like you to bear in mind, so there's the other test, the Von Berg smooth pursuit and circades, is this slide.
which essentially summarizes the sensitivity and specificity of the commonest vestibular clinical tests that we perform. And what you have to understand is no one single test will give you all the answers. You have to take everything in combination and often, as I said earlier, supported by any special investigations that you might undertake.
I think I will stop there. So I will start the questions and this is a really obviously all my questions are I've proven I'm not always very intelligent but when you're doing the Dick's hall pipe maneuver and the patient feels that they are dizzy but there is no nystagmus how do you interpret that? Okay so okay that's actually a brilliant question so you If you perform a Dick's Hall pipe test and the patient has suffered spells of posterior canal BPPV, they will be incredibly apprehensive and in my experience you drop their head down and they will grab hold of any appendage that you might present them with, so just be careful.
What you have to understand as well though is the utricle in that affected ear is different. It works differently. So it's not unusual to drop the patient's head down, not to see any nystagmus at all. They will be fearful, they'll be apprehensive, but they will tell you they feel giddy.
Okay. And that's, as I said, it's because if you like, the thing I told you about, about the different, the different inputs and the templates that drive the balance system. Well, those templates work slightly differently now. So so that's what you will see, you know, in a patient who's who's had previously posterior canal BPP, but that is settled.
OK, brilliant. Thank you. OK, I think this might actually be the last question.
So you've been let off easy and is an introduction to your next talk, whenever that may be, which is what are your indications for vestibular function testing? Oh, okay. So I'm, I suppose I'm a little bit of a purist in so far as there are some pathologies that concern me.
And for example, Meniere's disease. So any patient who I think has Meniere's disease, I am unusual in so far as I consider those patients to... I treat Meniere's disease as a surgical emergency. So if you were to come and see me, and quite a few doctors do with Meniere's, then within four to six weeks, you'll have had your MRI scan, all your vestibular function testing. I'll have seen you at least twice, and we will have planned our intervention at that stage.
Vestibular migraine is the third commonest cause of Dyspnea and Vertigo. And those patients, I prefer to have vestibular function testing performed. Because from my perspective, vestibular migraine is a diagnosis of exclusion. So an MRI is the minimum that's required to exclude any central pathology. And that's important because some of these patients will actually have multiple sclerosis.
If you look through the data. and five percent of patients with S will present with dizziness and vertigo and at the time of diagnosis 40 percent of patients will have dizziness and vertigo as one of their symptoms. I think patients who present who you think have a unilateral bilateral vestibular hypofunction again they ought to actually be formally assessed.
I think it's useful from a vestibular physiotherapy point of view, especially if you're looking at a patient who's got bilateral vestibular hypofunction in terms of, you know, telling the patient what sort of level of improvement they're likely to get. and also guiding the vestibular physiotherapist as well. So the answer in a nutshell to your question is, the majority of the patients who I see, I think benefit from formal vestibular testing. But there are some groups where testing is absolutely essential.
Okay, great. Thank you. Actually, we've got one more question.
It invites a suggestion for, again, another talk about... specific diagnoses in um in dizziness um so you can keep this one brief because it's a huge topic which is how would you diagnose vestibular migraine sorry i i you're breaking up okay how would you diagnose vestibular migraine but keeping it brief because i feel like this suggests another talk on specific uh dizzy diagnoses you Okay, so vestibular migraine is the third commonest cause of dizziness and vertigo. And to put it into context, between 10 and 16% of the adult population in this country suffer from some form of migraine. And of those, 30% will have dizziness and vertigo as part of their migraine package.
And what's slightly weird is that I have vestibular migraine. So I honestly know what it's like. The diagnosis can be quite difficult. In my experience, the majority of patients in their history, the episode will come on after a period of intense stress or anxiety.
That's by far the commonest trigger. They will describe not true vertigo, but what they classically describe is that when they move their head quickly, it takes a while for the environment to catch up with them. And sometimes actually you have to put it to them. you know, is that what you're experiencing? And they'll say, do you know what, that's exactly what's happening to me.
They get a low frequency sensual hearing loss. And so they often describe their hearing to be muffled or their ear to be full and blocked. And that is a problem for us because that then mimics to a degree Meniere's disease, early Meniere's disease. I've got the data actually on another presentation, but you know, is headache very common?
The answer is no. You know, do they always get an aura? Actually, the majority do, the minority don't, insofar as they know that something's going to happen to them, they feel it creeping up on them.
Photophobia, phonophobia are really common symptoms. But again, you have to ask them directly. But interestingly enough, the commonest symptom, but you have to prize it out of them, is that is that during spells it's like thinking through fog.
Mentally everything is much harder work. The duration of the spells vary enormously. It could be 30 minutes, an hour. Sometimes patients come to see me and they say look I just haven't been myself for three weeks. It's gone on and on and on.
There are dietary triggers of course. Caffeine and MSG in Chinese food are my triggers. Certain smells, so lush at blue water. sets me off um and working with you is quite stressful that sets me off as well and there are certain hormonal triggers so in a woman who has very regular periods the attacks tend to happen a certain time in her cycle um in a woman who's just delivered it's not unusual actually um two three weeks perhaps after she's delivered then the attacks really come on bless in a podgy middle-aged asian bloke like me it's slightly different so my vestibular migraine it simmers in the background and then I can get discrete attacks but so for that reason you see it has to be a diagnosis of exclusion and vestibular function testing is so important because it will you will pick up with that sensitive testing central pathology but you'd expect a peripheral vestibular function to remain intact.
And that would then take out, for example, Meniere's disease. So that's a different opinion to Mr. Waring, who told me that every dizzy patient that walks through your clinic has vestibular migraine and less proven otherwise. Well, the funny thing is, is that when you start in a new place, you tend to mop up all the vestibular migraine patients.
The other thing, the other problem with... dizziness and vertigo and it happens to us quite a lot actually I suppose in medicine is that we tend to try and squeeze everything into one diagnosis. and with vestibular pathology you can't do that yeah as I said before you know there are different vestibular pathologies that are actually associated um and um I think you know there was one patient last week who'd undergone surgery quite rightly for his vestibular problem but he also had vestibular migraine but it was only by sitting down and going through the rest of his symptoms you know once you've taken one pathology out of the equation you then you can identify another. But it's only by actually addressing both that you're going to cure him.
Okay. Well, thank you very much for spending your Monday evening talking to us. And thank you everyone for joining.