Update in Peripheral Vestibular Disorders

it is not going to be a basic course this is what you need to know because of that but this is what you might like to know this is what might come up in the near future or is already coming up for some of you it's not it's no news at all because you've created it and from some of you it's ridiculous and but for me it's my view its views so they're similar disorders and let's see if this thing works and some trends first of all I asked we didn't have a history lecture I will just give you a short thing I think meet Michael wake up I think you and I have this in the little booklet there quick the quick and dirty the quick the quick and dirty approach of the dissipations four with six quick questions well knowing that most of the patient with dissidence orders will be found among those subjects P P P D standing for for persistent perceptual claustral dizziness or possible phobic vertigo these question might help you quite well first question for how long have you been this it is it acute onset or what have you had for some time generally brain tumors don't longer linger for decades for example is it acute or is it remitted first of all are you dizzy at this very moment this actually tells you that the symptoms you find correlates to what the patient subjectively perceives and that is of importance especially in a recurrent disorder do you have any pain pain and business is generally malignant if there is an ongoing pain together with the dizziness that's a bad sign and you should be more careful at least I should be more careful and then the critical question do you get dizzy when you turn over in bed actually more or less every BPPV patient gets dizzy when they turn over in bed however some other patients do that also a central position of vertigo but they continue in your being dizzy for a longer time do you only get dizzy when you're standing walk if that is the case it's not 100% but its points to the somatoform dissonance so should I so if you ever get this is when you stand a wall that is at least something that points to a somatoform dissonance and I said before and do the patient have migraine before yes well then at least suspect vestibular migraine and if there is some kind of hearing symptoms then you could suspect the same to say hearing associated vestibular disorders that is Meniere's disease vinolas labyrinthitis cholesteatoma so with with these few questions which doesn't take really long time to put to the patients you can get quite much closer and actually you can have your assistant or your your phone nurse asking the question just in advance so then again news and views of some vestibular disorders and it should be pointed out that news are views until proven no but sure so I'm going to linger shortly on these four disorders for a short while because that's what we might be able to do first of all vestibular neuritis we are approaching a definition should Stewart a steroid treatment be done or not and what do we know about a theology not much actually so we will drop the one in because the shortness of time I think well first of all mr. blue neuritis and an acute vestibular syndrome is not the same thing and you heard before Michael Hamada you showed us very neatly and soda might have struck about how disorders with acute onset of establish symptoms could be central as well as there could be peripheral ones so they are not the same thing but we in the very beginning of a vegetable acute system a syndrome we don't know where it will end the definitions of something that would be something like sudden onset of dizziness malaise vomiting spontaneous nystagmus do not tolerate had moments but there should be no obvious neurological or cochlear signs then we could start with you mr. blobbity of some kind corresponding to the hints to the head impulse nystagmus and test q algorithm acute vestibular syndrome patients exposed to head impulses give some information if it is pathological well it could still be a peripheral disorder if it's normal it's generally the PI cap in fortunately cerebellar functions now if nystagmus looks like a peripheral one then it could still be peripheral while against shifting a vertical torsion of spontaneous nystagmus would point to it brainstem and to the interior your cerebral artery again with exceptions except and if we do the tests q variety a vertical shift would again point to the brainstem and while an normal skew would again point to the labyrinth so if if one does the hints test in this order arriving at the peripheral vestibular and organ it's probably a decent an effective way we dropped that one well first of all when we talk about vestibular neuritis or vestibular lovely we should consider that we do have five different kinds of sensors in the inner ear and they are generally and which is now well now supported by two different nerves the superior night nerve will take care of the utricle the anterior lateral canals while the inferior one picks up the posterior and the Sakya so today we know that there are varieties most often we have a superior nerve loss but we could have both down at the same time it should be and we probably have inferior vez develop forces at some kind but they might fly under the radar asset to say because we wouldn't see them we would suspect and I seen a few cases as some other of you have as well and reported on them patient was pertaining his dad was not being present but there might be a little upbeat torsional distortion of the mr. Blakely reflex and there would be a loss of a vestibular about myogenic potentials coming to cortical steroid treatments how many may I do in a little a little opinion test how many of you test acute vestibular loss with steroids in your clinic Hansa I guess we are something like 1/4 to 1/3 of the audience that that used to do it that I used to do that still we had the work again by Markus drop and colleagues that's more than 10 years ago I think it had a quite clear results that showed that either methylprednisolone or in combination visit valsa career actually caused a better reoccurrence or going back to normal of the vestibular function and test tested by calorics and we more or less repeated this study with one exception and that is that we used intravenous beta prednisolone or better sorry better medicine at the start with irrational that if patients are vomiting they will perhaps not take up being and and use the steroids for any longer part of time so and we ended up with with similar values like two-thirds of the patients recovering normal vestibular function on there and compared to a one-third in a control or a historic control group so we use steroids but we use them with intravenous administration for the first time with the rationale I gave and there are some better evidence for the use of that because we now know and there will be lectures on that that the stimulus actually causes cognitive impairment as well in the long end so about fistulas third windows well the definition is that well you'd need not only radiology you need radiology and symptoms because it's not always so exactly clear what you see when you see the the labyrinth here is the first report from Lourdes minor in 1998 where you could actually see the the decisions here you can see the anterior canal going up and nothing but it's quite common that you have a thin bone on top of the temporal bone and a certain amount of people are born with that or have it as some kind of well innate malformation or if we should call it like that but one can also speculate that the pulsating brain will over the years even thin lead thin this very thin bone out more and leaving patients with symptoms like this the typical symptoms described by Lloyd was vertigo by loud sound or precious changes and specific dishonest in it is a false conductive hearing loss and bone conduction high for a Costa Cruises and the background physiology is actually that the sound energy when when exposed to the air is not traveling all the way up to the cochlea but a certain amount of the energy picks up the route through the vestibular labyrinth and so to say releasing itself through the the third window and by that causing the vestibular symptoms mainly in the plane of the interior canal together with less energy affecting the inner ear which would show up like it's something that looks like a forced conductive hearing loss yes and what has been well said recently on this is that you should recognize the symptom it's good if you could show that the patient has a Tully or a Henneberg Thein the ankle variable sign is quite good with antal be able we mean that you use a tuning fork and you put the tuning fork on the malleus that is on the feet of the subject and this and you ask the patient not to do you feel this but do you hear this and the patient with a third window will point and say yes I actually hear it in my right ear and some are tests that were done in the lab showed that you can actually evoke auditory evoked potentials by by putting sound to the ankle to the foot of a subject and you could actually reach speech speech discrimination of up to 50% by putting a microphone to the foot of the people no no it doesn't matter which side actually because because because this is probably flu regenerated so if you stimulate the right ankle could be the left ear but they will hear it in the left ear the treatment has been suggested is well now people tend to go two ways either capping that is covering the fistula from the medial fossa side or if that doesn't work you could actually go in but then you need to remove some of the hearing new obstacles and plug the anterior canal on two sides of the fistulas together with that some colleagues have tried a combination of round window wrong window obliteration when an even over window obliteration with fat to reduce a little bit of the over amount of energy making the systems in stable but one should remember it's not only the superior service circular canal the he choses that causes a third window there is actually some other courses that we might run around that are large distillery aqueduct which is an inherited condition as is carefully dysplasia but there might be things like the Haitians to an artery vein and actually even vascular malformations that might cause a third window phenomena and should be looked out for here we have a combination we have a cochlear dysplasia with a very small cochlea here you can see it's not two and a half circles it's just one and a half something and there is a large Vista black products defined as wider than the than the width of the posterior semicircular canal which is there so more than or only the semicircular canal dehiscence can cause the third window system symptoms yeah we'll drop that a short visit to the BPP please the e theology's has been revisited again and and there are some good evidence that the sickle the the the ot Konya is actually aged as everything else does in the body but their age of being more rough on the surfaces and less or more and probably more easy to get loose from the macula but also probably they get more easily adhering to each other and that is suggested by some authors to be an explanation of the increasing amount creasing frequency of EBV in older subjects and I think we will hear more about that in this meeting there was a long discussion about traumatic vs. spontaneous nystagmus but most of this ends up that they have about the same kind of history and same kind of prognosis actually has been some arguing for that traumatic BPPV should be more more difficult to cure but but the last the lay the discussion goes back and forth and it seems to land that there are about the similar well BPPV is as you all know the most the bread and butter as my calamari put it the most common disorder that we see as a genealogist some data is on it here there is a little bit of a female predisposition for it there is an age dependencies older ages have more BPPV kids pre adults and kids more or less never have EPP visa most of the cases are idiopathic though well what you do need and what could be good to know is that we actually just need two tests and again these are two tests that can easily be done in clinical work up you know in a any kind of room but preferably with video Francis or with Francis of some kind but in any kind of room and that is the Dix wall plaque test and the lateral positioning tests let's look upon it like this if you do the Dix wall pie test and that creates a nystagmus well that talks for BPPV especially if it fades out now if the nystagmus is torsional or towards the upper eyelid it's a posterior canal of the same side of the air which is down easy if it is towards the upper eyelid it suggests the interior canal of the opposite side so that is what you need to know do Dix walk like you test actually the lateral the the all the vertical canals now if the nystagmus fades out within a minute or less yes then it talks for it canal devices and it's easily treated with the all the different kinds of of movements and maneuvers that we you heard of if it is not it talks for cube Lilith Isis was something that adheres to the cupola and then you have another and bigger problem same thing goes for the lateral canal with a little twist if you position the subject side to side as was trailing before and you have a nystagmus that beats toward the center of earth then it's gee you drop it will fade out and coal agency that talks to it canal Olaf ices the side with the most missed Atmos is the affected side if instead you get an a Padilla tropic nystagmus nystagmus beating away from the center of the earth towards the sky then it talks for and it suggests acutely elias's that has ethyl it's a draconian adhering to the cupola and it shouldn't fade out as as quickly again it's it's it's it there is a side difference but now it is the lesser side that is when the lesser side is down that is when you have the need the lower level of nystagmus in both ways the strongest nystagmus pointed to the lesion side so you only need actually those two tests the big small pike and the lateral canal test for diagnosing the BP praveen patients there is a little caveat though and that is that sometimes plastic only it hasn't you can see this in the literature that sometimes the posterior canal Elias is on the wrong side and the wrong limb may be mistaken for an anterior canal that is when you do the dig swirled Pike man over you expect Ethel it's to move away from the cupola sucking it away from the Utrecht coercing and that is from the posterior canal an excitation which means that you will have nystagmus towards the in the plane of the canal but two or two words they affect it here that is when you do this whole fight like this you would have at or she'll know what windshield wiper nystagmus to the side or towards the upper eyelid now if the earth a–let's is residing on something course in the other part of the posterior canal and you do dig small pike they will fall back to the low Mosport part of the cab and by doing that pressing the the cupola towards the utricle causing a downbeat or in stag was towards the lower eyelid it will fade out again but this may then be diagnosed as an interior canal and wrongly treated or not treated as easily as it could have been treated now the simple way to find out if you get something like this is actually to repeat the test we have come quite a bit of wear away and and deciding on what canal is what and again as mike i say you are welcome to take a photo of this of this slide which is a table for what kind of stagnancy you would expect from different courses yep otherwise you could download that from from Hamish MacDougall and others from the a vor app where you can actually simulate the different kinds of BPPV everything goes I said well there are a number of tricks to treat the posterior canal but doing this Aman doing the Epley maneuver seems to be rather having rather the same outcome more or less it seems like if you use to do in one way you probably will be more successful with continuing using that but don't forget the prolonged positioning it can be quite useful in some times however more and more data shows that if you have a cure canal only fastest one in one canal then you might end up with having it in more than one canal for example the the majority in in this series of about 86 page 85 patients had a posterior canal BPPV but not a few of them also had signs from other canals lateral canal even more which me might be a problem from for treaty and for treating we've seen we seen some kind of a revival of the of the automatic chairs to be able to treat the patient the Omni axis this is the Sydney Omni acts with myself inside which I don't think is easily available anymore but this is the trv chair emanating from France that is not machine but or a man operated and this is the same guy who got the little cane here and survived this one too and that can that that can actually be quite helpful especially when it comes to barbecue maneuvers like this and you can do the power of barbecue in case of other other cube Lilith Isis which actually can be quite effective and especially when you have more than one canal and whether other options failed and impatient with cervical lesions a mobile patient so I think we would see more of this coming around and we can act we can actually now using high-power x-ray show we can actually see Ethel it's for the first time I think in a living in their living being of some kind this is a high-powered x-ray that we did in in the European synchrotron research facility where you can actually see the mark electrically and the marketer secondly the calcium is picking up is picked up by the x-ray here yes the base of turn of cochlea and the Pula and they actually looked like they're pretty much angular as they are in the histology that we get so well we drop that and then we move over over to the last one to make many R disease there are some trends in many years disease there is a lot of papers the last two years there are more than 300 papers on mainly at many years disease some of the things I would like to mention is the MRI of hydrops coming up and the caloric video hate despise parity and some new insight on inner ear metabolism and and and treatment well first of all talking about history and meeting the patients one of the most important thing where the treating many as patients was already formulated by Phillip young K as many many years 50 years ago when he said that you should always you should always be try to use cycle supportive therapy and for many years we told our patient that we cannot promise anything about your hearing or tinnitus but we can surely and always help you with a distance problem and I think we can do that we can always surely help you with the business problem and as you will see in the end we can actually there is actually a little help even in the most dire cases for hearing but the Menier disease is not only vertically attacks it's not only the hearing it's not only the tinnitus it's also the effect it has on so to say the turkic well-being of the individual this was known already by madam dicks in the and she wrote a number of papers in the sixties on this subject but we should not forget it we shouldn't forget the type of attacks the patient has if the patient had few attacks or can easily foresee the attacks that's one thing but the few patients with apoplectic attacks that just fall to the ground that just get extremely dizzy without really a warning they are in a really dire position where they might end up with suicide or something like this and we shouldn't we shouldn't sir to say mr. day's the last years has also seen yuka terrors from for diagnosing many years disease headed by the international classification of a stable disorder group with with Alex bestows supervision with with antonio nobis s coming as first writer and what it and now for the first time we have some kind of unity in the definition between the american academy the european academy the japanese and korean black balance societies so we someway approach some kind of a unifying diagnosis this paper can be read in journal vestibular research it is shortly defined like definite many as disease is defined like two more spontaneous episodes of vertical of at least moderate to severe severity that last foot between 20 minutes and 12 hours it should be there should be documented lomi to medium frequency sense for hearing loss there should be fluctuating oral symptoms of some kind and it shouldn't be better explained by some other stabler disorders and make a little break when we've through the slide for photos but you connect but i could recommend the reference here the probable ammonia's disease include the same thing as the above but exclude the documented low medium load medium frequency hearing loss but now for the first time we do have a kind of unity in definition of many years disease and I would urge all the participant here to use this definition in further studies and further writing what also happened is that we started to be able to see or visualize the possible high drops in Meniere's disease this has been headed by Nakashima an iguana which gear called my pick and others who've been working on this for several years the Japanese a group has been on it since the 90s and where we can actually see that as the peer lymph is gathering they're gathering gadda lynnium the endolymph is not which makes it possible to see difference Saade between the two different partitions of a labyrinth and by doing that we could get at least a kind of view there is a high drops or not now a high drops isn't the same as the disease but we are approaching something here we can see on the cochlea with the the black little thing here is the the endolymphatic space being enlarged and actually giving honor to korea late phone Sangli and others published this paper in 2012 where the decrement documented and the lymphatic hydrops and correlation with order vestibular function testing in patients with definites many years disease where one could see the hydraulic cochlea here in correlation with symptoms and lately we've been ourselves been able to to do this by in an animal model where we can actually and I will talk about that later in the meeting where we can actually cause the hydrops compare this here the scala vestibuli and here the scala vestibuli and the this is the same mouse at two different occasions with vasopressin or without and it is a beauty to see you'll be able to see the the the how well you can visualize the structures here this is a mouse in rear with the scala media vestibular and timpani and the saccule and the utricle visualized so we are heading there now one should say a few things more about many years to see some therapeutic stuff many or has a problem with diagnosis it is criteria and diagnosis although that we are now approaching unity of some kind but there is an extremely variability when it comes to symptoms in course because we have spontaneous remissions and they differ from one patient to another we have a strong placebo effect and what I would like to suggest to be called the two third problem of menus disease that is whatever you do two thirds of the patient seems to better and if you just wait enough 2/3 of a patient's stop having symptoms and this poses an enormous problem when it comes to studying in many years disease for example Alan Kerr published a paper on the effect of threatening with surgery he would tell patient that he would operate on them within a week or something over two or three weeks and that cure the symptoms and he would find that at least 2/3 of his patients would stop having symptoms make a call by and myself did the same with gentamicin it's just as effective as surgery well when it comes to threatening the patient's yes Betty a Steen has been the problem and I think Michael will we'll talk more about that later but there are some evidence now that better his team which has been a workhorse in the treatment of BPPV does not really have that heating or is hard to discern at least in the dough dudes doses tried from any from placebo so we have to perhaps rethink this now that there will be always be discussions on this subject but I leave that to Michael later on another thing coming up has been the suggestion of using the anti secretory factor and the secretary factor is some kind of a proto hormone used in the that we have in our intestines which control the water leakage over over membranes and there are some pilot studies that have suggested that this has an effect but there are no RCTs yet that demonstrate this but it might be something to look out for again as as placebo it's not really harmful it's just expensive so again decreased calorics is another is another thing in many patients with many years disease we found find that they might have decreased calorics but lee mcGarvie and others observed that even if they had decreased calorics they had normal the video hits and i think the idea is something like that when you have a distended in lymphatic hydrops in the in the canals you can actually or might actually have a reflux flow doing a mod caloric stimulation while you that is not what you happen in the normal normal ear but i think my lee will talk more about that later in this meeting and i strongly recommend you to listen to it but it actually gives us an idea that that actually gives us an idea that perhaps one of the new approach is to decide on many years see or not is to have a patient whether typical symptoms where the calorics is down but the video head is not that the combination might actually be something that we could use for diagnostics in the future will you talk about that li7 so a bit yeah okay yeah to end last but not least after everything failed in treatments for many years patients we have had the labyrinth actually but the problem was always that with labyrinth ectomy there is a loss of hearing now some years ago independently a number of colleagues started to think well wait a minute labyrinth EXA mean if I do a labyrinth ectomy I could actually do a cochlear implant in the same time in the same procedure and if I do a cochlear implant there will be at least better hearing than if I do not do one and if I do a cochlear implant well the nerve is still there so there would be a fair chance that that ear would actually be to set to a certain level hearing again and there I know that that Bruce Gans and his colleagues has done a number of procedures more than ten of them and there are two reports the first one was by Machiavelli and Ramstein from Manchester in 2014 where they described two cases with a simultaneous cochlear implant and libraries ectomy where they had really good hearing results on the patients afterwards on the ears and there's another one just coming out now so if we end up where there is nothing else that helped the patient then we might go for elaborate ectomy but doing that today we should at least consider the possibility of doing it together with a cochlear implant and I Hammond I think I've kept the time and thank thank you and I think one for the organizers is really beautiful thank you very much [Applause]

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