Introduction to Genetics for Meniere’s Sufferers

Sometimes a topic ends up just being too vast for a single article. This is one of those times. I really want to carry you along with me, to help you really understand these ideas, so this first part will be more of a guide to genes and genetics, at least what you might need if you want to follow up on some of the studies yourself. We will then begin looking at why people suspect genes might be involved in Meniere’s. As ever, it will be incomplete as there is always more detail that could be included, but if anything is factually incorrect please let me know so I can correct it.

The term “gene” or “genetic” gets thrown around a lot when it comes to diseases and descriptions of how we appear and behave as humans. You may have even have sent off for some kind of “genetic testing” either to understand what diseases you may be prone to or maybe to give some hints as to your ancestry. You might have some idea that genes are something to do with “inheritance”, the passing of a disease or feature from parents down to children. But before we can understand how genes might be connected to Meniere’s, we are going to need to look at the ideas of genetics a little closer, to see what a gene really is and what it does. Along the way I want to introduce some of the strange terms you might come across if you try to read research on the topic - and hopefully make it a little less scary and a lot more fascinating!

The Basics: Proteins, Amino Acids and Lego

We have covered some of this in previous articles, but to begin at the beginning, you need to know that your body is made of very large complex, tangled up molecules called proteins.

Proteins are hugely varied in their roles in the body. For example, collagen which is part of skin, bones and tendons is a protein. So is haemoglobin that transports oxygen in red blood cells, insulin that tells your body when to use glucose and all the antibodies that make up your immune system. All proteins. They are built using only 20 basic building blocks called “amino acids”. These amino acids clip together into long complex folded up shapes, which are the proteins. From these 20 building blocks, millions of different proteins can be assembled, and there are at least 100,000 different types in the human body. Imagine 20 different types of Lego bricks - the number of different structures you could build is endless. But how are these proteins assembled when a body is growing? If you need some more skin or insulin or antibodies what drives the process of assembling them? That’s where genes come in.

The Protein Recipes - DNA and Genes

A gene is a set of instructions to build one particular protein. That means it needs to contain the information about which amino acids to create, and in what order. Those instructions are held in DNA (DeoxyriboNucleic Acid) - the one bit about genes that most people will have heard of - a long, famously “double-helix” shaped molecule which holds the “code” that details the amino acid sequence.

There are just four key chemicals in the DNA molecule. Those four chemicals are represented by the letters G,A,C and T, the first letters of each of the substances forming the rungs in the helix “ladder” and are grouped in three letter “words” called “codons”. Each of those three letter codons represents the recipe for an amino acid.

Arranging a choice of four letters in threes allows us to have up to 64 different codons (we can spell 64 different three-letter words using the 4 letter alphabet) - and we only have 20 amino acids. So there is some duplication - the same amino acids are made by several different letter sequences - a useful bit of protection against possible errors as we will see. There are also special codons to say where a gene starts and stops in the vast long string of DNA.

(NB - The DNA itself is not actually used to make the proteins - a copy of it is made called RNA and the chemical represented by the “T” becomes a “U” in the RNA but this is less important for what we need to understand)

The Recipe Book - Pairs of Chromosomes

DNA is an extremely long, thin molecule - around 3 billion “letters” in a chain about 2 meters long, containing hundreds or thousands of gene recipes all strung one after the other. So to fit in a cell it has to be wrapped and twisted into packages called chromosomes. There are in fact 46 chromosome packages of DNA in most cells, in 23 pairs with one of each pair coming from each of your parents. This provides some useful redundancy - if there is something wrong with a gene in one pair, maybe the other gene in the pair is OK and will be enough to ensure the right protein gets made. We will come back to this as it is key to what can go wrong.

What Goes Wrong - Spelling Mistakes in the Code

So what can go wrong? Lots of things! For the purposes of understanding gene issues that could be related to Meniere’s we will focus on just a few. We are going to focus on variants of genes that have a single letter wrong in a codon - an A swapped for a T for example. It is possible that one change makes no difference - some amino acids have more than one codon sequence that can make them, so maybe by sheer chance you end up with the same amino acid. That would be called a “silent” gene variant. Nothing different happens. On the other hand, the single letter change could result in a different, incorrect amino acid being placed into the protein. This is called a “missense” variant. The result will be a different protein which might behave very differently and may not perform the intended function properly. Then we have the possibility that the changed letter results in the codon now spelling out the special “stop” word that indicates the end of the gene, which gets called a “nonsense” mutation. In that case the protein creation will terminate early, and the protein will be incomplete and almost certainly won’t function as it was meant to. If the protein can’t work as originally intended, this is called a “loss of function” mutation or variant.

Inheritance: Dominant vs Recessive - What do these mean?

That is just a few ways that genes can contain faults or mutations that might change the way the body works. But we mentioned that genes come in pairs to provide redundancy. So will this gene error have an impact or not? There are two possibilities - you might get one copy of the faulty gene from one parent and a correct copy from the other, or you might get a copy of the faulty gene from both parents should they both have it. Both copies of the gene will be used to manufacture protein, so if only one copy has the variation and the “good” copy can make enough protein for things to work, we have a “recessive” mutation. You would need to inherit the broken gene from both parents before it became a problem. On the other hand if just the poor protein from one copy is enough to upset the working of the related body system, we have a “dominant” mutation and inheriting just one copy is enough.

Meniere’s Clues - Familial and Sporadic Cases

Now we have enough knowledge to begin looking at the discoveries relating to Meniere’s. The hint that maybe there is some genetic component to at least some Meniere’s disease cases came initially from so called “familial” Meniere’s - these are situations where two or more family members have Meniere’s within first or second degree relatives. In Europe familial MD makes up around 9% of MD cases. It seems overall that Meniere’s occurs anywhere from 16-48 times more frequently in siblings and 4-12 times more often in children of sufferers compared to the rates in the general population. Most Meniere’s is actually “sporadic” meaning it just seems to crop up at random in the population with no obvious links to family, but these statistics do suggest at least some aspect of it is capable of being “inherited”.

The Myth of a “Meniere’s Gene”

At this point though we have to say something about inheritance of disease. The way genetics is usually presented in the media is in terms of “the gene for” certain diseases or conditions. But this is very rarely the case. It is rather like the possible causes of a car crash. Sometimes it might be failure of a single part of the car, but it is much more commonly several things acting together such as a tired driver, poor lighting, slippery road surface and worn tyres. Similarly, there are diseases that are down to a single variation in a single gene, such as Huntington’s disease, cystic fibrosis or sickle cell anaemia, but most diseases if they have a genetic component are the result of the interactions of many different gene variants and environmental factors. In some rare familial cases of Meniere’s it may be that a single gene or pair of genes are the root of the problem, and changes in genes responsible for the structure of the inner ear hair cells and their connection to the surrounding membranes have been suggested. However in the majority of cases we are not going to find a magic “Meniere’s gene”.

Also just because the condition gets labelled as sporadic because you don’t have an obvious familial connection does not mean that genes are not responsible in some way. A lot of the genetic changes that might occur are of a form where the resulting protein change does not always result in a damaging or noticeable change in the body. They might also be recessive, as we saw, meaning you have to get the change from both parents which makes it much less likely. Genetic variations can also occur as brand new mutations in the sperm or egg or even during early stages of embryo development. So you might be the very first in your family with such a change.

Looking Ahead to Part 2

In the next part of this look at genes and Meniere’s, we will see what genes might be implicated and what roles they have in the body. The Meniere’s parts of this article and the next are based on an excellent recent review paper which I recommend reading in full here. In the meantime, a good demonstration of just how much activity there currently is in Meniere’s gene research, as I was writing this, a significant new paper was scheduled for publication in November 2026 from Professor Lopez-Escamez’s team about using machine learning to identify gene variations that can distinguish between familial and sporadic types of Meniere’s - you can already read it here.

References

Cytokines and Inflammation in Meniere’s Disease https://www.e-ceo.org/journal/view.php?doi=10.21053/ceo.2021.00920

Types of Inheritance and Genes associated with Familial Meniere’s https://pmc.ncbi.nlm.nih.gov/articles/PMC10335989/

The Impact of Genetic Factor in Meniere’s Disease (2026 review) https://www.mdpi.com/1422-0067/27/6/2788

Nov 2026 Detecting genetic differences between Familial and Sporadic Meniere’s https://www.cell.com/iscience/fulltext/S2589-0042%2826%2903219-0

YouTube Channel

Reminder that Meniere’s Without the Spin also has a YouTube channel where you can find summaries of the articles, and interviews with doctors and researchers. https://www.youtube.com/@MenieresWithouttheSpin

AI Statement

No AI was used to produce the text in this article. AI was used to assist with the research as it is embedded in search and hard to avoid. All information obtained by AI research was followed to the source and checked for veracity where possible. AI was used to help clean up some diagrams

So we know that Meniere’s symptoms fluctuate in the short term - the vertigo, tinnitus, fullness and hearing loss can change from hour to hour, day to day, week to week. It can come in flares or waves lasting weeks or months. But what about the overall progression over years? What does Meniere’s have in store for you?

Stages of Meniere’s

You may have come across graphics like this describing “stages of Meniere’s” which lay out the changing nature of the disease over time, and divide it up into somewhat arbitrary phases. Some people also label the “end stage” of Meniere’s as “burn out”, based on the suggestion that after years of symptoms, the balance sensors are damaged to the point where vertigo no longer gets triggered. There are many estimates offered about how long these stages take and when “burn out” might arrive. Seven to ten years is a range I have heard repeated. But how much truth is there to these ideas? Let’s look at both the anecdotal reports and the research to see what we can uncover.

My Experience

I do not intend in any way that my personal experience should be taken as authoritative - no one anecdote can establish a pattern in science or medicine. Indeed even lots of anecdotes, which we will come to, are no more than a hint at what might be happening. On the other hand I do have Meniere’s and have spent a lot of time, maybe too much time, thinking about it.

I’m currently approaching 20 years since my first attacks, and to some extent I would say that the progression fits those classic “stages”. In the early years there was a very clear separation of attacks, with an obvious build up where hearing loss, tinnitus and fullness in the “bad” ear would increase, usually for a few days, then hours of intense room-spinning vertigo and vomiting, and afterwards tiredness and a dramatic improvement in the hearing symptoms. Between attacks I would pretty much have no symptoms.

I went through some long periods of remission, but then a few years later, incredibly bad vertigo episodes, several per week for months at a time, and the hearing trending downward with some constant tinnitus and hearing loss beginning. At present I am in a phase where although I get quite a few vertigo attacks, they are generally significantly less intense, and less well defined, my overall balance is less good and hearing issues are continuous, requiring hearing aids, with tinnitus as a constant loud companion.

I think for me what the “stages” narrative does not capture though is the fluctuation layered on top, which I have written about before. For example there can be months of terrible hearing, which then significantly resolves. But the overall direction and symptom progression of the “stages” fits me reasonably well so far. I have also seen this reported from others in the many Facebook support groups.

Anecdotal Experiences of Burn Out

So after 20 years I am still having periods of vertigo that put me out of action - my Meniere’s has not “burnt out”. But what do other people report?

The first issue is that there is quite a lot of disagreement over what is meant by “burn out”. Some people seem to feel it means that the balance system has become more unpredictable and there is more rather than less vertigo. For example:

“My ENT says I’m in the burnout phase as well, vertigo is much more unpredictable.”

“…Having both more vertigo and off balance feelings then I’ve had in several years. I got diagnosed over 20 years ago.”

“I’ve had Meniere’s for decades and have reached burn out phase and vertigo/labyrinthitis episodes have become unpredictable where before the Meniere’s was more manageable”

So rather than refer to “burn out” let’s forget the label and focus on the idea that the vertigo reduces or stops at some point. What is the anecdotal evidence for that? Again from the forums:

“I am in late stages but my symptoms are… more hearing issues and fewer vertigo episodes, thankfully.”

“Mine has burnt out too but so did the dizziness and vertigo. I have no balance from my ears and have 2 cochlear implants”

“I think I’m in the burnt out stage! I’ve gone 6 years without an attack. But the trip to get here was filled with attacks non stop!”

“I've had this illness for 61-years. Lots of injuries. No consistent relief.”

“If you mean come through it at the end, yes I have. I suffered with Meniere’s Disease for about 20 years…The good news is that I haven't had an attack for 2 years.”

“I thought l was at burnout at about 16 years in. Hadn’t had a major vertigo attack in a few years and my hearing loss has been stable for as long. Then bam, went bilateral and it seemed to start all over in my ‘bad’ side.”

“We thought my husbands had burnt out, but he is getting spells again. Luckily he can sleep it off most times. He was diagnosed at 38, he’s now 78.”

Pretty varied experiences for sure, but for many things seem to reach a stage where vertigo was less or stopped. The length of time is clearly very variable, and many people have suffered decades of symptoms and still have vertigo.

Research Studies

The idea of stages is not entirely anecdotal. There have been attempts to formalise them - either through symptom progression (hearing, tinnitus, vertigo etc), or just focussing on the level of hearing loss - but these guidelines are rarely adopted in clinical practice to my knowledge.

However, you will be happy to know that the progression of Meniere’s has been studied. This research from Professor Ilmari Pyykkö in Finland asked 365 people with Meniere’s about their symptom progression with a focus on vertigo, drop attacks and hearing loss. The average age of people studied was 63 and they had Meniere’s anywhere from under a year to 48 years. Below is, I think, the most interesting chart from the report. It might take a little explanation but it is very revealing.

Each dot is a person in the study. The further to the right the dot, the longer they have had Meniere’s - you can see 3 years, 10 years and 30 years marked. The higher the dot is the longer the time since their last vertigo attack, ranging from a couple of months to over 500 months. Two things are immediately obvious - first the upward trend - there is a tendency for the time between attacks to get longer as the disease progresses. But not for everyone. There are still many dots in the lower part even after 30 years. So some people are experiencing something like “burn out” or a very long period since their last attack, but others are not. The authors conclude:

There is a lot of fascinating detail in the paper and I recommend giving it a look.

One reason to try to understand how Meniere’s progresses is that it can help inform decisions we have to take over treatment options. If right now you are suffering daily hours-long room-spinning vomit-hell vertigo episodes, and that might continue repeatedly for years then you may consider a more drastic form of treatment than if you know that those episodes could lessen in future. This is the perspective that was investigated in this research from the Netherlands. The authors specifically set out to find out if there was any truth to the idea that “attacks diminish over time”.

They looked at 35 patients who were considering participating in a trial of a surgical approach called “endolymphatic duct blockage” to deal with vertigo. This is a procedure to place a clip on the tiny tube connecting the endolymphatic sac to the rest of the inner ear. Twenty-five of them eventually chose not to go ahead, whilst ten did. The reason for this huge drop out rate was thought to be that their symptoms improved dramatically whilst waiting for the trial to begin, a wait of around 1.2 years on average. Over 60% of the participants ended up free of vertigo some years later. The conclusion of the study was that “most patients will experience relief of symptoms over time” and whilst surgical treatments may speed up relief from symptoms the evidence for these approaches is not clear and side effects could be serious.

So a very different research strategy but again we see symptoms trending downward over time. This knowledge is increasingly used to steer people away from destructive surgical approaches. The one exception to this might be for regular, serious drop attacks, which can be highly dangerous. At least one prominent doctor considers drop attacks the only reason to adopt treatments like gentamicin injection, which kills off the balance sensors in the impacted ear, or labyrinthectomy that removes the whole balance portion of the ear.

Hearing Loss Progression

If you spend a lot of time in support groups, you can easily come away with the impression that profound deafness or a cochlear implant is the guaranteed endpoint for all Meniere’s sufferers. Many clinicians also seem to adopt the view that a decline to a “dead” ear is likely, and the view is well summed up in this chart that shows a gradual decline, with attacks that cause temporary short term worsening - a chart I have used before in other articles:

But is there good evidence to support this? Tracking hearing loss over the course of the disease has not been done in many studies I can find, but there are a few, and they conclude that most of the hearing loss tends to occur in the early years, and that it slows later. Over 5-10 years, an average loss of 50-60dB (around 40%) overall has been found. When it comes to ending up “deaf” in the impacted ear, estimates vary wildly from 5% to 50% of cases. But this is just for one ear - the most disabling and life-impacting problem would be bilateral deafness, which is estimated at a low 1-6% .

Balance Issues Over Time

So hearing loss is likely, but for most people maybe not as bad as sometimes portrayed. What about balance? Certainly anecdotal reports seem to suggest that over time the balance of many people with Meniere’s may get worse, and the thought was that rather like the hearing decline, repeated attacks cause damage to the balance sensors in the inner ear.

The damage can actually be seen in samples from Meniere’s patient’s ears. When people opt for “labyrinthectomy”, complete removal of the part of the ear that senses balance, the removed parts have sometimes been examined and clear evidence has been seen. This has also been done after patients have died. All the balance sensors of Meniere’s patients show degradation to some degree. Again however, modern studies tracking the actual decline in function over time seem to be hard to find.

Some researchers have suggested that deterioration in responses to a battery of vestibular tests could be a good way to measure the progress of Meniere’s - using the results of the tests to track the spread of hydrops, the excess endolymph fluid, from the cochlea (the hearing section of the inner ear) into the vestibule and semi-circular canals (the balance sensing part).

On the bright side, if attacks of vertigo have lessened or stopped, vestibular therapy stands a good chance of helping compensate for the damage, which is a topic we will definitely revisit.

Summary

• Hearing loss frequently stabilises at some point, deafness is not inevitable

• Vertigo can persist for years but attacks often get less intense and less frequent and may stop altogether

• The “stages” of Meniere’s are very variable and there are large fluctuations.

It certainly seems the case that Meniere’s changes as the years progress. Maybe it helps some people to split this up into stages, but there are no clear boundaries - it seems to be a gradual change in the severity and nature of symptoms, with massive fluctuations layered on top. It is hard to come up with solid timescales - figures that are thrown around are averages with huge variation either side.

The positive things I’ve taken away from looking into this topic are that it is not uncommon for hearing loss to stabilise at some point, deafness or cochlear implants are not inevitable, and that whilst vertigo attacks seem to continue for decades for some unlucky people, over time the chances of vertigo lessening and stopping increase.

Maybe change is good after all.

Links

Classification of Menière’s disease https://pubmed.ncbi.nlm.nih.gov/8372918/

Committee on Hearing and Equilibrium Guidelines for the Diagnosis and Evaluation of Therapy in Meniere’s Disease https://aao-hnsfjournals.onlinelibrary.wiley.com/doi/10.1016/S0194-5998%2895%2970102-8

Changes in symptom pattern in Meniere’s disease by duration: the need for comprehensive management https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2024.1496384/full

The evolution of intractable Ménière’s disease: attacks resolve over time https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2024.1469276/full

Dr Steven Rauch discussing drop attacks and destructive treatment (whole video is well worth a watch):

Long term follow up of 610 cases of Meniere’s https://journals.sagepub.com/doi/epdf/10.1177/003591577106400823

Long-term vertigo control after cochlear implantation in patients with end-stage Menière’s disease https://pmc.ncbi.nlm.nih.gov/articles/PMC7518986/

Long-term hearing progression of Menière’s disease https://www.researchgate.net/publication/359463954_Long-term_hearing_progression_of_Meniere’s_disease

Pathogenesis and pathophysiology of Meniere’s disease https://cdn.istanbul.edu.tr/file/JTA6CLJ8T5/65754AAE01C04D79891B3340E723F14C

Towards a new staging of Ménière’s disease: a vestibular approach https://pmc.ncbi.nlm.nih.gov/articles/PMC6966777/

YouTube Channel

Reminder that Meniere’s Without the Spin also has a YouTube channel where you can find summaries of the articles, and interviews with doctors and researchers. https://www.youtube.com/@MenieresWithouttheSpin

AI Statement

No AI was used to produce the text in this article. AI was used to assist with the research as it is embedded in search. All information obtained by AI research was followed to the source and checked for veracity where possible.

There are many reasons you may end up needing some kind of balance testing and if you suffer from Meniere’s some doctors include this kind of test in the process of diagnosis - a topic we will cover in a future article. Whatever the reason, there is a wide range of possible tests, each of which can tell us different things about what may be going on or going wrong.

To begin, let’s briefly review how your balance system works to keep you stable. Your brain is going to try to use your muscles to stop you falling, tipping or moving in ways that you don’t want to. But how does it know what is currently happening? The starting point is knowing which way up you are right now, and if you are moving at all in any particular direction or if there are things pushing or pulling on you. There are three main ways your brain gets this information. First your eyes - you look at the world and see objects that you think should be horizontal and vertical which gives you a very strong sense of which way is up and which way you might be moving. Layered on that is information from your ears which contain incredible sensors that can tell which way gravity is pulling, and which way your head is oriented as well as what movements your head might be making. The various sensors are in and around a part of the inner ear called the “vestibule” as it is an open area like a foyer, so this part of your balance mechanism is called the “vestibular system”.

There is a third system sending signals - your muscles and tendons themselves. They actually have sensors in them that can tell the angle or position of joints and if the muscle or tendon has some force acting on it. This sense is called “proprioception”. Should you begin to topple sideways for example, even if your eyes and ears were not to notice, the muscles and tendons around your ankles and legs would tell your brain what’s happening.

Sometimes you can end up in situations where these systems are getting conflicting signals - for example, inside a ship in a big swell where your eyes see the cabin and surroundings stationary but your ears and muscles tell your brain you are moving. This difference can make you feel odd or nauseous. The opposite happens in virtual reality where the eyes can be given a very convincing sense that you are moving around in a 3D world but both your ears and muscles say you aren’t. Again this can make some people feel uncomfortable or sick.

Alongside all these signals about what is happening we have evolved some useful little feedback loops that use this information to make life easier, to prevent us consciously having to think about making adjustments as we move. One is the “vestibulo-spinal” reflex that automatically drives leg, torso and arm muscles to react and keep us upright. This is the one that can go haywire when given faulty signals and give rise to drop attacks. The other is the “vestibulo-ocular” reflex. Here information from the inner ear is used to move our eyes so we can stay easily fixed on a target even as our head moves around. Again it can be misled when the ear sends false signals, leading to the involuntary eye motion called “nystagmus”.

These various systems and the feedback loops are the basis of the many different tests for balance issues. We will go over a few examples but there are many other approaches you might come across and I’d love to hear from you in the comments if you’ve experienced a novel or interesting balance test of some kind.

Standing on one leg

First up we have something you can easily do yourself. Standing on one leg is a great way to check your balance, and can also be used as a way to improve. Always make sure you are beside a wall or table for support if you need it. With eyes open you should be able to manage between 10-45 seconds depending on age. You can then compare how you do with your eyes closed. This will be much harder and shorter - but if you find it especially hard it might indicate underlying balance issues as it depends much more on the inner ear.

Tests like standing on one leg put the entire balance system - vision, proprioception and vestibular system - to the test all at once. However, the vestibular system itself is the source of many balance issues, and the sensors are locked away inside the rock hard bone of the inner ear. So how do we find out what is going on in there?

Videonystagmography (VNG) and Caloric Test

Some strong clues are available from the vestibulo-ocular reflex we mentioned already. When things are working well, signals from the inner ear sensors drive the eyes to move in the opposite direction to the head so that we can keep looking at the same object. Now the problem is how to trigger the movement sensors in the inner ear without also giving the brain signals from the eyes or muscles. The sensor that most strongly drives side to side eye motion is the horizontal semi-circular canal - which senses turning of the head from side to side. So if we can somehow make the fluid in that canal move without turning the head, we should get eye movement if that system is working properly.

A way to do this was discovered by Robert Bárány who won the Nobel prize in 1914 for his work on understanding the vestibular system. (The organisation that outlined the diagnostic criteria for Meniere’s is named after him). What he discovered was that by flooding the outer ear canal with warm or cold water you could trigger the eye movement reflex and see involuntary eye motion. The temperature change travels across the eardrum and into the inner ear where it changes the temperature of the fluid in the nearest semi-circular canal. This causes the fluid to rise (if heated) or fall (if cooled) creating a small flow. This moves the sensing hairs at the canal entrance and drives the eyes to move in the opposite direction to the movement that the body thinks is happening.

The procedure is that you lie with your head propped up at an angle of about 30 degrees, which arranges the so-called “horizontal” canal vertically, allowing the thermal currents to work properly. You wear goggles that prevent you seeing anything, but they contain an infra-red camera that can track your eye motion in the dark. First warm and then cold water (or sometimes air) floods your ear canal and the movement of your eyes (nystagmus) is recorded. Warm water should result in one direction of nystagmus, and cold the opposite.

The rate of eye movement from the two ears are compared. In people with damage to the sensors in the semi-circular canals, the response on that ear might be less or not happen at all, an issue called “canal paresis” or “reduced vestibular response”. People with at least one healthy ear are likely to feel a spinning sensation of vertigo that will pass quickly when the test is over.

You may also be asked to stare at a target spot in the goggles. Healthy people normally manage this as their brain should be able to override the gentle false signals and redirect the eyes. This is called “visual fixation suppression”. Not being able to do it suggests there might be some problems with the brain areas involved. So if you can’t stay focused on the spot it may suggest a central nervous system problem rather than or in addition to inner ear issues.

Vestibular Evoked Myogenic Potentials (VEMP)

So we have a test for the rotation sensors of the semi-circular canals. What about the other two - the utricle and saccule which sense gravity and acceleration? This is where the “Vestibular Evoked Myogenic Potentials” or VEMP test comes in.

Again the idea is to somehow stimulate the sensors, and then monitor how the body reacts. If your body senses you suddenly falling or lurching forward, you have reflexes that try to compensate, driving the eye and neck muscles. Properly placed electrodes can sense these small muscle activations - “myogenic potentials” means electricity coming from the muscles. But how do we fool these sensing organs in the inner ear that we are really moving?

It was discovered that playing clicking sounds into the ear can actually disturb the Utricle and Saccule because they are quite close to where sound enters the inner ear. So the procedure is to use electrodes to measure automatic tensing of muscles (neck or eyes) caused when special sequences of clicks are played into the ear.

Two different sets of electrode placements are needed to test the two sensors, giving us two slightly differently named tests. The “cVEMP” or Cervical VEMP measures saccule function. The saccule is the up/down and gravity sensor so triggering it should cause automatic compensatory movements of the neck muscles. The “oVEMP” or Ocular VEMP checks the utricle, which senses horizontal jerks and accelerations - when this is activated it should cause muscles around the eyes to react.

Both utricle and saccule may be damaged in Meniere’s ears so for these patients there may be little or no VEMP responses. Interestingly vestibular migraine seems to cause a poor response to the oVEMP test but not cVEMP and this may be a way to tell the difference between VM and Meniere’s.

vHIT Head Impulse Test

The caloric test outlined has some drawbacks. First, the movement of fluid generated by the temperature changes is very slow. So it simulates very slow movement of the head, demanding high sensitivity from the movement sensor. In fact, you have two types of hair cells in the semi-circular canals, one of which detects rapid high-speed movement and the other handles slower drifts of head position. So caloric testing can’t tell you the whole story. Also it is only testing rotation horizontally, and won’t tell you anything about the other semi-circular canals. To overcome this, another really rather simple and slightly brutal-sounding test is done - the “Head Impulse Test”

Here again we are using the feedback loop that tries to keep the eyes focussed on one spot. You look at a fixed target in a well lit room. Typically you will wear some goggles with a camera to again record your eye movements. It might also contain motion sensors to record the head movements that are going to occur. The test administrator stands behind you and uses their hands on either side of your head to quickly rotate your head some 10-15 degrees to one side or up and down. The camera records how your eyes react.

In healthy people, the eyes typically remain more or less tracking the target, so the eye movement perfectly balances out the head movement. When there are issues with the vestibular sensors, the eyes might turn with the head and catch up later, even overshooting, or twitching during the rotation. These “saccades” might be so subtle and rapid that only the high-speed camera can notice them.

It can be useful to have both vHIT and caloric testing done. If there is an issue with the vestibular nerve that sends signals about balance to the brain from the inner ear, both of these tests will show problems. However in Meniere’s patients, something odd may happen - the caloric test may show problems whilst the vHIT indicates no issue. It is thought that maybe the excess endolymph fluid and swelling in the inner ear that accompany Meniere’s might make it harder for the gentle thermal currents in caloric testing to get established.

In addition, studies have shown that doing both caloric and vHIT testing may be a way to tell the difference between Meniere’s and Vestibular Migraine - people with Vestibular Migraine tend to show no issue on either test.

Other Tests

You may come across other balance and vestibular tests. For example:

Rotary Chair Test - This is another test of the vestibulo-ocular reflex where the patient sits in a rotating chair in the dark whilst a camera records eye movements. It is not common due to the expensive equipment, space and darkness requirements. It is also not good for pinpointing which ear may have issues.

Computerized Dynamic Posturography (CDP) - The basis of this test is VR goggles plus a motorised sensor platform that can both change orientation and sense forces from your feet. It tests how well your entire balance system is working and integrating everything plus how well you react to changes.

Dynamic Visual Acuity (DVA) - A very simple test where you read a chart with a fixed head position then read again while the doctor turns your head back and forth forcing your eyes to track - again checking how well the vestibulo-ocular reflex is working.

Romberg Test - You stand with your feet tight together and arms crossed. First, you hold this position with your eyes open for around 30 seconds, then you close your eyes. If you balance perfectly with eyes open but sway heavily or fall when your eyes close, it reveals that your proprioceptive pathway or vestibular system is failing to compensate when vision is removed.

Modified Clinical Test of Sensory Interaction in Balance (mCTSIB) - You first stand on solid ground, then on a soft foam surface, both with eyes open and closed. The idea is that on solid ground with eyes open, you have feedback from all your balance systems. Closing your eyes removes one source of input - the visual. Standing on foam then removes or degrades the feedback from your feet and ankles so you have to rely more heavily on your inner ear vestibular system.

Fukuda Stepping Test (Unterberger Test): In this very old test from the 1940s and 50s, you close your eyes, extend your arms straight out in front of you, and march in place for 50 to 100 steps. Healthy people should remain relatively centered. Drifting a lot to one side might indicate a vestibular issue. This test may be helpful in spotting problems with people who had treatment for BPPV and still have some unsteadiness. However in general it is not considered at all sensitive or reliable as healthy people often drift quite a lot too during the test.

That is just a little overview of some of the ways that doctors can get some insight into what might be going wrong with your balance. It is important to separate this from identifying vertigo - you would not want to do any of these tests whilst suffering a vertigo attack and the main way vertigo is assessed is simply by describing what you have experienced (although if you can record your “nystagmus”, the flicking of your eyes side to side using your phone camera, this can also be useful to show the doctor. But the tests described here are frequently not used as part of an initial Meniere’s diagnosis - what is required for a diagnosis is something we will look into in more detail soon!

YouTube Channel

Reminder that Meniere’s Without the Spin also has a YouTube channel where you can find summaries of the articles, and interviews with doctors and researchers. https://www.youtube.com/@MenieresWithouttheSpin

References

BBC Article on “Standing on one leg” https://www.sciencefocus.com/the-human-body/dr-michael-mosley-standing-on-one-leg

Robert Barany Work on Caloric Testing https://www.sciencedirect.com/science/article/pii/S0960982214012305

The Barany Society https://www.thebaranysociety.org/

Clinical Assessment of the Nystagmus Fixation Suppression Test: An Experimental Study https://pmc.ncbi.nlm.nih.gov/articles/PMC11232042/

Evidence-based diagnostic use of VEMPs https://link.springer.com/article/10.1007/s00106-019-00767-2

Predictive Value of Vestibular Evoked Myogenic Potentials in the Diagnosis of Menière’s Disease and Vestibular Migraine https://pubmed.ncbi.nlm.nih.gov/32271263/

The dissociation between pathological caloric testing and a normal video head impulse test helps differentiate between Menière’s disease, vestibular migraine, and other vestibular disorders: a confirmatory study in a large cohort of 2,101 patients https://pmc.ncbi.nlm.nih.gov/articles/PMC11350975

Computerized Dynamic Posturography https://www.interacoustics.com/academy/balance-testing-training/vestibular-rehabilitation/computerized-dynamic-posturography

Modified Clinical Test of Sensory Interaction in Balance https://www.interacoustics.com/academy/balance-testing-training/vestibular-rehabilitation/modified-clinical-test-of-sensory-interaction-on-balance-mctsib

The assessment of fukuda stepping test results in prognosis of benign paroxysmal postural vertigo https://pmc.ncbi.nlm.nih.gov/articles/PMC9734258/

Utility of Stepping, Walking and Head Impulses for Screening Patients for Vestibular Impairments https://pmc.ncbi.nlm.nih.gov/articles/PMC4175306/

AI Statement

No AI was used to produce the text in this article. AI was used to assist with the research, and helped to generate or clean up some of the images. All information obtained by AI research was followed to the source and checked for veracity where possible.

“Meniere’s sufferers are the safest drivers out there!”

“Driving with Meniere’s is one of the most dangerous things you could do!”

Both of these things are potentially true. How is that possible? What are the rules and responsibilities around driving with a condition like Meniere’s? Let’s have a closer look!

First, the obvious bit - why would driving with Meniere’s be unsafe? Meniere’s disease for most people involves unpredictable attacks of intense world-spinning vertigo, with a loss of control of eye movement resulting in the eyes unable to stay fixed on one spot. Sometimes Meniere’s can give rise to drop attacks - sudden involuntary complete loss of muscle tone in the legs and torso, or a feeling of being violently thrown to one side. Some people have reported that whilst driving the visual horizon is suddenly tilted, or even up to 180 degrees rotated. All of these different visual and spatial disturbances make it impossible to drive safely during an attack. However most Meniere’s sufferers are well aware of this and choose to avoid driving if likely to suffer an attack. This leads to the paradoxical statistic that Meniere’s sufferers may be safer drivers, having less accidents overall.

The question that often gets asked though is “Am I allowed to drive if I have Meniere’s?”, and “When it comes to driving, who do I need to inform about my Meniere’s diagnosis?”.

As with so many things in life, a lot comes down to personal responsibility. In theory, of course you could drive a car or motorbike without even having a license or insurance. You clearly shouldn’t do that - in most places to do so would be illegal and irresponsible. To some extent the situation with Meniere’s or vestibular migraine (VM) is similar. You could drive whilst suffering with these conditions, but should you? What are your legal responsibilities?

The answers to these questions are going to depend on where you live and the exact nature of your condition. At the outset I have to say none of what follows is legal or medical advice. It is simply a collection of the best available information I could find about how some example countries and states deal with the problem. I am also only going to discuss rules for non-commercial driving of cars and motorbikes - commercial vehicles often have different regulations. You absolutely must check the rules for your own situation yourself and not just rely upon what you read here. You may also have received different advice - there seems a lot of conflicting information out there. I have tried to provide links to the sources of the information I am basing this article on where appropriate. I have looked at the UK (as I used to live there), Germany (as I now live there) and the USA and Australia as I know a lot of readers come from these places.

Whichever country we focus on, there are two important areas to consider. First is the right to drive the vehicle, to hold a driving license for the specific class of vehicle you want to drive. The second is insurance. The driving license is issued and renewed on the basis that you have the ability to safely drive the vehicle without endangering yourself or others, whilst insurance is a business interested in minimising their losses through accidents. These two things are not necessarily aligned, but they are to a degree - if you are more likely to endanger others, both driving licensing authorities and insurer may need to know, might even have a right to know. Many insurance policies contain a clause saying you must inform them of any “material change in circumstances” that might impact your ability to drive, and there are lists of “notifiable” medical conditions. Meniere’s is on that list in many countries, but there are nuances which we will come to.

There is one aspects of your Meniere’s or VM that is most important in all the rules I came across. Do you have sudden attacks of vertigo or drop attacks without any warning, or do you first get a build up of additional symptoms like increased tinnitus, hearing loss or fullness, called a prodrome, that would alert you to the possibility of vertigo and allow you to pull over or choose not to drive? This distinction is crucial and leads to different rules in most places.

A final consideration is the role and responsibility of doctors. This varies - in some places they are consulted by the vehicle licensing department for a formal statement after you personally inform the authorities of your situation. In other places they can advise you directly based on a knowledge of your symptoms. There are also places where they have a duty to inform the relevant authority.

Let’s get specific and look at the rules in various countries and states.

United Kingdom

Having grown up in the UK and originally been diagnosed with Meniere’s there, I’ve got direct experience with the rules. The relevant authority for driver licensing in the UK is the “Driver and Vehicle Licensing Authority” or DVLA. For dizziness and vertigo the government website has a specific page where you can either download and fill in the hilariously named form “DIZ1” or answer the questions online. Meniere’s is explicitly listed as one of the conditions. Depending on the answers you give, they might allow you to continue driving, contact your doctor for more information or suspend your licence.

A doctor can advise you to stop driving, but it is up to you to report this fact to the DVLA via the above forms, and it is an offence not to. If you always get warning signs and your doctor confirms this to the DVLA typically you will be OK to continue driving and the DVLA will write to you to confirm this. This was my situation. On the other hand if you suffer sudden, unpredictable attacks you should stop driving immediately until you can demonstrate via your doctor that symptoms are under control. There appears to be no mandatory period for this

When it comes to insurance, the situation in the UK is less clear cut. Some insurers like Aviva explicitly say “our standard motor insurance policy only requires you to tell the DVLA of a medical condition and have a licence on that basis.” - in other words if the DVLA say it is OK, they don’t need to know. But other insurers may have different policies, and some sources suggest that not informing your insurer could invalidate your policy. So the safest thing is always to check with your insurer as soon as you receive a diagnosis.

Germany

Germany has some of the strictest laws relating to driving and Meniere’s I have come across. There is no EU-wide regulation - each country can adopt its own approach. The rules (as of 2026) are contained in the 137 page “Guidelines for the Assessment of Fitness to Drive” - here is the section on Meniere’s in full:

“Drivers (of cars and light vehicles) with Ménière’s disease are considered fit to drive if attacks are consistently preceded by prodromal symptoms; an observation period of 6 months following diagnosis and a specialist examination are required. In cases where the diagnosis is confirmed but prodromal symptoms are absent, fitness to drive is established after a one-year attack-free observation period, subject to a specialist examination. Depending on the symptoms, the observation period may exceed one year in individual cases. Fitness to drive single-track vehicles is generally not recognized.

Following an initial spontaneous attack of vertigo (consistent with the first manifestation of Ménière’s disease or vestibular migraine) where the diagnosis has not yet been confirmed, fitness to drive is established after a 6-month attack-free observation period; a specialist examination is required.”

The rules are also available here.

First thing to note - motorbikes are explicitly singled out and can not be ridden under any circumstances with a Meniere’s diagnosis. For other vehicles, in all cases, a period of observation by a doctor is required before driving is allowed. With warning signs, that period is 6 months, without warning signs, it is at least a year.

So which authority or department in Germany do you have to inform? No one! The system is entirely down to personal responsibility. Once diagnosed, you must stop driving. It is then your responsibility to talk to your doctor and begin the relevant period of observation. The doctor will not inform anyone of your condition. At the end of that period, you could simply start driving again, but it is recommended to get a letter from the doctor saying that you have had this period symptom-free, which you can keep on file in case of any future questions.

Ignoring these rules is likely to invalidate your insurance and could lead to fines or prosecution in the event of an accident. You do not have an obligation to immediately inform the insurer upon diagnosis - because you have an obligation to immediately stop driving until a doctor explicitly says otherwise.

Australia

In Australia, the basics are the same - the key distinction is whether there are warning signs prior to disabling vertigo. The details however are again different. The rules are contained in the national Assessing Fitness to Drive (AFTD) standards, published jointly by Austroads and the National Transport Commission (NTC) - and Meniere’s is listed under “Other neurological and neurodevelopmental conditions”. The process is that upon diagnosis you must inform the driver licensing authority (DLA) in your state. In two states (Northern Territories and South Australia), the doctor themselves has a mandatory duty to inform the DLA. The doctor will then need to supply information on your “Medical Fitness to Drive” - how this is done will vary by state. The key aspect there yet again is whether you get warning signs or not. The DLA will then use this information to either suspend your license, or issue a conditional license, valid for say 12 months, after which another assessment would be required.

When it comes to insurance in Australia, you must inform the insurer immediately when something like Meniere’s crops up, either a diagnosis or change in your license status from the DLA. You also have to state it at renewal or when taking out a new policy.

USA

For private, non-commercial vehicle driving, there is no national country-level regulation in the USA. Everything is managed by the individual states. Each state department of motor vehicles (DMV) will evaluate sufferers on a case-by-case basis and typically again the essential criteria is whether there is enough of an “aura” ahead of any vertigo.

There are a variety of ways that the DMV could discover that you have Meniere’s. In some states, it is mandatory to report serious medical conditions, although Meniere’s falls into a bit of a grey area. When renewing your license you are likely to have to mention it. The DMV could find also out if you are involved in an accident or traffic stop, or if your doctor feels that you have gone against their advice not to drive. It seems you can even be reported by family or friends if they feel you are unsafe to drive. If you do not get warning signs for vertigo, you would be unsafe to continue to drive. The likelihood is also that even with an aura before vertigo the DMV may suspend your license temporarily until your doctor can confirm to them that your symptoms are controlled or you do indeed have enough time to pull over and are safe to drive. Doctors themselves can not, as far as I know, on their own authorise you to drive. As an example, here is the medical review process from the Virginia DMV.

In the USA, it seems you do not have a duty to tell your insurer about a Meniere’s diagnosis immediately upon receiving it. As far as the insurer is concerned, if the DMV says you can drive that is all they worry about. You do need to inform them the moment your license is suspended but generally not when your insurance renews or you apply for a new policy. One thing to bear in mind though is that in the USA choosing to drive against medical advice could easily lead to huge financial costs should you be involved in an accident and sued.

Summary

So the good news is that a diagnosis of Meniere’s does not automatically mean no more driving ever (unless you are a motorbike driver in Germany that is), and if you have good warning signs prior to vertigo, or your symptoms are well under control and you have not had attacks for a long time, in many places you may be ok to drive. But it is vital that you go through the correct process where you live, otherwise you may be in for a nasty shock if you are involved in an accident.

Stay safe and spin free!

References

Links to relevant supporting information are in the article - follow the links in the text

YouTube Channel

Don’t forget Meniere’s Without the Spin has a YouTube channel too! Researcher interviews, summaries of the Substack articles and more here https://www.youtube.com/@MenieresWithouttheSpin

AI Statement

No AI was used to produce the text in this article. AI was used to assist with the research, and helped to generate or clean up some of the images. All information obtained by AI research was followed to the source and checked for veracity where possible.

Before we look closely at BPPV, we need to be clear exactly what we mean by vertigo. The terms “vertigo”, “dizziness”, “unsteadiness”, “disoriented” and more are often used fairly interchangeably, but they refer to different kinds of experiences and usually hint at different types of underlying causes. Let’s start with the big one - vertigo, which will be familiar to most people with Meniere’s. This is quite specifically a false sense that the world is moving around you or that you are rotating or spinning when in fact you are not. It can often be accompanied by nausea or even vomiting due to the extreme sensations. Dizziness on the other hand is most commonly a catch-all that encompasses a broad range of experiences including light-headedness, feeling woozy or faint, out of balance or unsteady. Sometimes people include vertigo in the category of “dizziness” but it is a very distinct and separate sensation.

BPPV - Benign Paroxysmal Positional Vertigo is by far the most common cause of genuine vertigo in people. We can learn a lot just by looking at the name itself - “Benign” because as we will see it is not due to any serious underlying health issue and is often easily fixable. “Paroxysmal” means coming in short, sharp bursts. “Positional” because the symptoms are triggered by having the head in certain positions. Tipping the head back, to the side or lying down are the most common triggers, but rotation of the head in other directions can be the issue for some people.

To understand the cause of BPPV we need to revisit the structures in the inner ear that help us with balance that we looked at previously when discussing drop attacks. If you aren’t familiar with how the inner ear is structured, this and previous articles go into more detail.

There are two sets of movement sensors - the three semi-circular canals each sense rotation of your head in different directions, and then two special sensors in the utricle and saccule that between them sense movement horizontally and which way is “up”. These last two sensors include a sheet of jelly with a bunch of little pebbles called “otoconia” attached to the top. This is the source of the problem in BPPV. These tiny stones can become detached and drift off into the surrounding liquid that fills the inner ear. They might just sink down into the bottom of the vestibule and cause no harm, but they might also end up in the semi-circular canals. To understand why this could be an issue, we have to take a look at how these weird-looking hoops themselves work.

Each of the loops has at its heart a tube filled with fluid, the same “endolymph” that bathes our cochlea and which Meniere’s sufferers tend to have too much of. As you tip your head in certain directions, that fluid will tend to stay put and then slosh around to catch up. This fluid flow is what tells your brain about the head movement. But how is the movement detected? If you have been following along from the drop attacks article, this is the final piece of the puzzle and the final set of sensors in the inner ear - the grandly named “crista ampullaris”. There is one at the entrance to each of the three loops. They are sensors that have evolved to tell when the fluid in the inner ear canal moves or changes direction. Like all our inner ear senses, this one relies on bending of little hairs. In this case the hairs are embedded in a lump of jelly called the “cupula” that sticks out into the way of the fluid. So the fluid pushes against it, bends the cupula over and in so doing bends the hairs to fire off signals to the brain.

It is a very sensitive system. Normally this would be a good thing. But for BPPV sufferers, there are one or more rogue chunks of calcium carbonate, the “otoconia”, that may have found their way into the loops of fluid, and as we sit still, settled to the bottom. The most likely location for the pebbles to collect is at the lowest point of the lowest of the loops, which is the one that senses nodding the head up and down and also tilting it toward your shoulder. Then when we move our head, the fluid moves as it should, and the little stones now roll around causing additional currents and disturbances in the fluid just after we stop moving. The sensitive jelly lumps feel these extra currents and the hairs send false signals to your brain as if you were moving, leading to the brief spell of vertigo until the stones settle again and the fluid stops moving.

Diagnosing BPPV is usually a simple process of trying to trigger the movement of the otoconia using a series of movements called the Dix-Hallpike test. Since more than 85% of cases tend to occur in the “posterior” canal, this test is focussed on creating motion in the fluid in that loop. If other canals are suspected due to the way the patient normally triggers vertigo, other sequences of movement are possible to lead to diagnosis.

BPPV episodes typically only last a minute or so, but are still very unpleasant and can leave sufferers anxious, and also feeling unwell for a while after. Fortunately it can usually be treated. This involves first working out which canal contains the mischievous pebbles, then using a series of careful movements to tip them back into the utricle area where they can no longer trigger the balance system. The most well known of these is the “Epley Manoeuvre“ - the sequence needed to get the little grains to fall out of the posterior canal. It is possible to do this yourself at home but it is probably better to get guidance from a qualified medical practitioner, especially if you have neck issues or are unsure of your diagnosis. Of course in the process of carrying out these various head movements, you may experience brief spells of vertigo. There are other movement sequences if it turns out that a different canal is the issue.

It is not fully understood why the otoconia might detach in the first place, but several factors seem to make it more likely. One is simply wear and tear through age - the vast majority of BPPV occurs in people over 50. Blows to the head can make such detachment more likely and even activities involving lots of jolting of the head like mountain biking or acrobatics have been implicated. Inner ear infections and spending long periods with the head motionless can also increase the risk. And vitamin D also seems to play a role. It has been found that reduced levels of vitamin D significantly increase the risk of BPPV. This is thought to be because vitamin D is required for the body to properly process and use calcium, the mineral that the otoconia are made of. Hormonal changes, osteoporosis and vitamin D deficiency all contribute to women being two or three times more likely to suffer from BPPV than men.

What about our friend Meniere’s? Estimates vary but BPPV seems around seven times more common in Meniere’s sufferers than in the general population, and the ear impacted is usually the same one, suggesting a real link. It is thought that Meniere’s may cause damage to the utricle and saccule, as we discussed in the article on drop attacks, increasing the risk that the otoconia will fall off.

So if amongst your usual Meniere’s symptoms you start noticing sudden short bursts of vertigo when you turn your head, don’t ignore it or blame Meniere’s - it could be BPPV and may be easily treatable. But until then, Don’t Look Up!

YouTube Channel

Don’t forget Meniere’s Without the Spin has a YouTube channel too! Researcher interviews, summaries of the Substack articles and more here https://www.youtube.com/@MenieresWithouttheSpin

References

Dix-Hallpike Test https://my.clevelandclinic.org/health/treatments/24859-dix-hallpike-maneuver

Johns Hopkins Epley Manoeuvre https://www.hopkinsmedicine.org/health/treatment-tests-and-therapies/home-epley-maneuver

Johns Hopkins BPPV and Causes https://www.hopkinsmedicine.org/health/conditions-and-diseases/benign-paroxysmal-positional-vertigo-bppv

Vitamin D Deficiency and BPPV https://www.nature.com/articles/s41598-021-96445-x

BPPV Risk Factors Unique to Perimenopausal Women https://pmc.ncbi.nlm.nih.gov/articles/PMC7596253/

BPPVin Meniere’s disease: systematic review and meta-analysis of frequency and clinical characteristics https://pubmed.ncbi.nlm.nih.gov/31410549/

AI Statement

No AI was used to produce the text in this article. AI was used to assist with the research, and helped to generate or clean up some of the images. All information obtained by AI research was followed to the source and checked for veracity where possible.

This is a drop attack. One of the nastiest, weirdest symptoms of Meniere’s disease. Fortunately many patients can go through their entire Meniere’s life without experiencing one but for those who do, estimated at between 3% and 20% of sufferers, it is utterly terrifying and often ends up with some form of injury. This is not vertigo. Vertigo is the sense that the world is spinning around you, or that you are spinning within it, a very powerful sensation that often comes with nausea and vomiting and can last hours for Meniere’s sufferers. Drop attacks are something else entirely.

Descriptions of the experience vary, some people saying that one minute they are standing and the next they are on the floor with no idea why, but without losing consciousness. This is not like fainting or “passing out” either. The most common phrase people use is “being pushed hard or violently” by some unseen force, and some people report feeling thrown across the room. Very often, these episodes happen entirely out of the blue, with no warning symptoms before and no vertigo after.

Drop attacks tend to happen in the mid to later stages of Meniere’s, after maybe 5 years or more, and although they usually have no warning at all and no symptoms after, can occasionally occur during or at the start of an episode of vertigo. That was my experience. I was suffering the onset of what I could tell would be a bad spell - tinnitus had ratcheted up to 11, I could hardly hear anything, and that weird sweaty out-of-body feeling was creeping over me. So I had grabbed my rescue medication, put a pill in my mouth and tipped my head back to swallow it with some water... and I was shoved, as if rugby-tackled by an invisible 100kg guy. I went down, and in my case, the vertigo started full on and I remained motionless for the next three hours other than throwing up periodically.

So what is going on? Since there are no invisible 100kg rugby players, what is causing people to forcefully throw themselves onto the ground, or into nearby furniture? The official name for it is the “Otolithic Crisis of Tumarkin”, named after the early 20th Century ENT doctor Alexis Tumarkin from Liverpool, UK who was the first to document these episodes in patients, and also the first to suggest that the cause was something going wrong in the balance system. The “Otoliths” are the tiny crystals that we have in our inner ears, that ones that cause all the trouble if you happen to suffer from BPPV (Benign paroxysmal positional vertigo) - more about them in a moment as they are crucial in our story.

The cause is indeed a catastrophic failure of the balance system, a huge false signal coming from the inner ear which tells the body, wrongly, that it is either suddenly falling or suddenly moving sideways. Emergency recovery systems go haywire. These systems are designed to protect you, to react super fast, bypassing the brain and conscious decision making to keep you upright. But now they trigger big muscles in the legs and torso to recover from something that isn’t happening, resulting in those muscles dumping you on the ground or into a nearby object.

The next obvious question then is where are these faulty balance signals coming from? You probably know already that your ears do a lot more than hear, and your inner ear contains some incredibly intricate sensors to tell which way is up and to detect position and movement in all directions. We’ve previously talked about the cochlea, the snail-shaped part of the inner ear that does the hearing. To understand balance, we have to look at the other half - the alien-looking vestibular system

This has two main bits - the semicircular canals that many people are familiar with, which use fluid sloshing around in them to detect when you turn and tip your head, and then the vestibule, the area between the semicircular canals and the cochlea, which often gets overlooked.

The vestibule contains two sensors, called the utricle and saccule, both of which detect changes in straight line movement - up and down in the case of the saccule, horizontal in the case of the utricle. For example, if you are in a car, the utricle will be telling your brain when it speeds up and slows down. If you are in an elevator, the saccule will detect the force of gravity downwards, and give you the weird sensation at the start and end of the ride. The way they do this sensing is an absolutely fabulous bit of evolution, although as with all bits of the body, it can also go wrong.

At the heart of the utricle and saccule there are a bunch of cells with tiny fibres or hairs called stereocilia at the ends, looking a lot like the hair cells that sense sound in the cochlea. In a similar way to the cochlea hair cells, it is bending of these hairs that triggers a signal to the brain. The cells are embedded in a sheet of jelly-like substance, the otolithic membrane, on top of which is attached a layer of tiny pebbles - the otoconia. Now imagine the head jerks forward. The little pebbles in the utricle, being a bit heavier than the jelly around them will try to stay put through inertia, so the base of the hair cells moves first, bending the hairs in the jelly. This tells the brain that some acceleration has happened. The same happens if your head is tipped forward - gravity will pull on the little stones and bend the hairs.

Then when the acceleration stops, the weighty otoconia catch up and restore the hairs to straight again. The saccule works exactly the same way, but is positioned so that the sheet of jelly is vertical and movements up and down cause the bending.

Your brain makes you aware of these signals, but there are also things going on that you are not conscious of. As you read this, turn your head slightly left and right (unless you are feeling dizzy right now, in which case give this experiment a miss!) You should notice that your eyes stay focussed on the word you were reading, even as you move your head. You don’t have to actively move your eyes, they just move in the opposite direction to your head automatically. Even if you try to override this, and turn your head you will find your eyes tending to fix on objects and jump from one to the next. This eye-movement compensation is deeply automatic and although it does go via the brain, it bypasses conscious awareness in order to happen fast. It also goes wrong in Meniere’s when we have vertigo. Faulty signals from the inner ear lead to uncontrollable eye movement called nystagmus that gives us a strong visual spinning sensation.

There is another important automatic system hooked up to your balance sensors - called the “vestibulospinal reflex” - this is a high-speed pathway from the balance centres in the brain down your spine to your trunk, arms and legs, which works to keep you upright. Again, reactions here happen before you know it - for example a train you are standing in brakes and you tense your body to stop from falling. Maybe an arm goes out to balance you or a leg moves your foot across to stop you toppling. Fast feedback from the balance sensors through special circuits in the brain to the spine and main limbs. All wonderful and essential.

This system relies on getting signals from both ears, and integrating them to produce the right muscle responses. Meniere’s messes this up in several ways. First the signal that the damaged ear produces is not caused by a real movement that needs responding to. Second, the size of the signal can be huge, much bigger than anything the ear would normally send. And finally the signal is coming from only one ear. This sends the reflex system into panic and shutdown. The brain thinks it is possible we’ve suddenly started flying sideways, or turned upside down, or that something else is badly wrong. The most common response is that it cuts muscle tone totally in the big muscles, collapsing you to the ground, and the processing of the signals leads to the impression of having been violently pushed.

So why then do the motion sensors send these faulty signals? It seems that in some Meniere’s sufferers, over time, changes in the composition and pressure of the endolymph fluid that bathes the sensors may degrade the jelly membrane surrounding the sensing hairs. When the inner ears of meniere’s patients are examined postmortem, this membrane is very often damaged or detached. There is also a potential genetic fault that could potentially lead to the membrane not being well attached. The result may be that the hairs are able to waggle around much more freely and give rise to spurious signals. This damage may also result in some of the otoconia pebbles detaching which could be the cause of BPPV in some Meniere’s patients, and there is even a theory that these small stones can block some fluid pathways causing more fluid buildup and making Meniere’s worse, or even triggering it in the first place.

The impact of drop attacks on sufferers can be huge, and not just from the physical injury that can result. Meniere’s is renowned for leading to a poor quality of life for many due to the fluctuating, unpredictable nature of the illness. Drop attacks are the most extreme manifestation of Meniere’s and once you have experienced one, the knowledge that another could come anytime without warning is psychologically corrosive, mentally wearing and hugely anxiety inducing. A small study found 7 out of 8 patients suffering drop attacks also had depression.

Drop attacks can lead to increased social isolation, through social anxiety, fear of embarrassing oneself, and transport challenges. Normally Meniere’s patients in many countries are allowed to continue to drive, as long as their symptoms include a “warning” phase before any vertigo attacks. Studies in fact show that Meniere’s sufferers have fewer car accidents than the general public - almost certainly due to them being careful not to drive if they feel unable to, or choosing not to drive at all. Drop attacks change that picture entirely. If you could, without warning, feel like your passenger has tried to push you through the window, driving is no longer safe.

The only real treatment for frequent drop attacks is to remove or destroy the balance sensors or signals from the damaged ear, through gentamicin injection, complete removal of the semicircular canals and vestibule, called labyrinthectomy, or cutting of the vestibular nerve that is transmitting the faulty signals to the brain. Increasingly, for most Meniere’s patients, these approaches are less and less used, but in the case of drop attacks, the potential for injury is so severe that they are often the only option.

There is still much that is not known about drop attacks, and more research is required. It is a difficult subject to study - Meniere’s itself is already comparatively rare, and drop attacks rarer still, and seem to occur only within certain periods of the Meniere’s lifecycle. For example, the exact mechanism that is causing the faulty signals has not to my knowledge been demonstrated, and it is far from clear whether drop attacks “burn out” as Meniere’s progresses, as the vertigo is reported to in some patients. We can speculate that it should - if the burnout is due to the balance system being destroyed by years of Meniere’s. But like so much with Meniere’s and drop attacks in particular, it is far from settled. If you have suffered drop attacks I’d love to hear from you - what has your experience been? Have they continued for years or stopped? How do you cope?

If I come across any new research into drop attacks, I’ll be sure to let you know!

References

Dizziness and Balance Overview of Drop Attacks https://dizziness-and-balance.com/disorders/central/drop.html

Vestibulospinal tract (Wikipedia) https://en.wikipedia.org/wiki/Vestibulospinal_tract

Otolithic Membrane Damage in Patients with Endolymphatic Hydrops and Drop Attacks https://pmc.ncbi.nlm.nih.gov/articles/PMC5358090/

Managing Drop Attacks In Patients With Meniere’s https://pubmed.ncbi.nlm.nih.gov/41909990/

Vestibular Drop Attacks and Meniere’s Disease as Results of Otolithic Membrane Damage -- A Numerical Model https://pmc.ncbi.nlm.nih.gov/articles/PMC9971529/

Driving and Meniere’s https://pmc.ncbi.nlm.nih.gov/articles/PMC6750787/

AI Statement

No AI was used to produce the text in this article. AI was used to assist with the research, and helped to generate or clean up some of the images. All information obtained by AI research was followed to the source and checked for veracity where possible.

Dapagliflozin, a name you will immediately forget so we will call it Dapa, is a well established drug for helping those with heart failure, type 2 diabetes or chronic kidney disease. It was patented more than 20 years ago and is has been sold under the brands Farxiga or Forxiga for the past 12 years or so. The existing benefits of the drug mainly come from the way it influences the kidneys, and understanding this might also help to see why it could benefit Meniere’s.

The kidneys have the job of filtering the blood. They divert unwanted substances into the urine and keep hold of the stuff we need - electrolytes like salt and potassium, red blood cells, proteins, and glucose. Normally, dumping these things out as waste would be .. well, a waste. Dapa is one of a class of drugs that stop the kidneys from keeping hold of glucose, so more of it ends up in the urine. One side effect of this is that additional water and salt leave the body along with the glucose.

This makes Dapa sound rather like a classic “water pill” or diuretic, which are sometimes prescribed for Meniere’s. However Dapa and other drugs of the same class (called SLGT-2 inhibitors) have some benefits over more traditional diuretics. They tend to leave levels of essential minerals like potassium and magnesium intact, they encourage removal of fluid from the body’s tissues rather than direct from the bloodstream and are overall felt to be gentler.

Dapa has two other effects which could be relevant to Meniere’s. It has been shown to damp down the immune response by reducing the number of immune signalling molecules called cytokines circulating in the blood, which can help reduce immune-related inflammation. And it may help to improve the health of the smallest blood vessels in the body, by keeping the walls of the blood vessels flexible and working well.

So we have fluid reduction, inflammation control through reduced cytokines and small blood vessel improvement. For those who know a lot about Meniere’s this may already sound good. Here’s why. Meniere’s disease is associated with excess fluid in the inner ear - so called “endolymphatic hydrops”, which is why salt control and diuretics are sometimes proposed. In addition, Meniere’s patients often have higher levels of cytokines, the immune signalling, pro-inflammatory molecules, in their blood, and finally poor circulation in the all-important layer of inner ear cells called the Stria Vascularis has long been thought to be a possible contributor to Meniere’s. So there are good reasons to think that Dapa should at the very least be tried in Meniere’s patients.

In fact it already has been. A very small trial of a similar drug to Dapa given to 6 patients was published in 2025. This was a very simple study, just looking at how the Meniere’s patients fared on the drug. There was no comparison with a placebo, and the participants knew they were getting the drug, which means it is not possible to draw firm conclusions, but both vertigo and hearing seemed to improve significantly over 3 months on the drug. Additionally, a large study of nearly 400000 people with type 2 diabetes noted that those on Dapa were 16% less likely to develop hearing loss than those not taking it, so it may have a protective effect against the hearing loss that often accompanies diabetes.

Inevitably, given all the recent interest in SPI-1005, which I have contributed to with my article and video a couple of weeks ago, there will be comparisons. SPI-1005 is further along in terms of testing specifically for Meniere’s but still isn’t approved and has been in trials for over 10 years. Does this mean we have at least a ten year wait for Dapa? No - there are two big advantages to repurposing an existing drug. Firstly, the drug is already approved for use as a medicine in humans, so the safety profile is known. What is missing is an adequate demonstration that it helps for Meniere’s, which would be required for it to be routinely prescribed to patients. It could right now be prescribed “off-label” in both the USA, UK and EU but doing so is not trivial - insurance is unlikely to pay for it, and the doctor shoulders the responsibility for any adverse effects. The precise details depends on the country and state - if you are interested you need to ask your doctor and be prepared for it not to be easy. I’m not aware of anyone who has tried this drug for Meniere’s - let me know if you have.

In addition to already being approved as a medicine, Dapa has the advantage that the original patents on it have expired, meaning that other companies can make generic versions of it more cheaply. The price has dropped significantly in recent years for that reason. A brand new, patented drug like SPI-1005 is likely to be much more expensive for the first few years after is it approved. These are the advantages. The disadvantage is that with a new drug like SPI-1005 the company holding the patent is willing to invest the vast sums that can reach into the billions of dollars, needed to bring a drug to market. The trials needed to repurpose a drug that is out of patent must come from state organisations like the NIH in the US or charities such as Meniere’s and Vestibular UK or VeDA in the US.

All of which brings us to the proposed new trial, called DAPA-MD. It is being designed by the Liverpool Clinical Trials Centre and will run across 12 hospitals in the UK.

It will be a “randomised double-blind placebo controlled” study. In other words, the 200 participants will be randomly given either the real drug or a dummy “placebo” drug, and neither the patient nor the people giving the drug and measuring the results will know which the patient received. This is the best way that we know of to test new treatments. There are other good features of the trial. Firstly it runs over a whole year, hopefully long enough to allow the notorious fluctuations of Meniere’s to be accounted for, to some extent at least. It is measuring both vertigo and hearing loss. And, very significantly, blood tests will allow the potential identification of Meniere’s subtypes. There is also an outside chance that MRI scans might be OK’d to enable monitoring of the level of hydrops in some participants. All in all a very comprehensive Meniere’s trial. What is also impressive is that at this early stage where the trial proposal is just being drawn up, the team are inviting feedback from the Meniere’s patient community into the trial design - the presentation from Matt was part of that. Whilst I was writing this article, I received an email invitation to join the group applying for the grant and help contribute to shaping the trial - which I gladly accepted. It will be so interesting to see this trial develop and be able to bring the thoughts of the community to the rest of the trial team!

To be accepted into the trial, patients must have a definite diagnosis of Meniere’s according to the Barany Society International Criteria, as well as having had at least 2 episodes of vertigo per month for the past three months. They must not have had any destructive treatments such as gentamicin injection or invasive surgeries. I do see one potential issue with the criteria of lots of vertigo - this could mean that there is more chance people go into remission during the trial as most people will be in a major flare at the time of joining. But on the other hand, accepting people into a trial for a vertigo-reducing treatment that don’t have much vertigo also doesn’t seem right - these are the challenges of testing Meniere’s treatments!

What will probably come as a disappointment to some of you is that the application process, the trial itself, analysis and publication of results is expected to take about 5 years in total. Drug testing has to be done carefully which I know is hugely frustrating for those suffering now. You do though have an opportunity to at least feel like you might be helping a little - you can help to shape this trial by providing feedback at this early stage. The team want to hear from you about what they are planning to measure, and how they will share the results.

Here are some of the things that they would love to hear from you about:

• Do you think that the 50/50 chance of receiving a placebo drug is ok? (Note that participants can continue taking whatever usual medication they take to control their Meniere’s)

• Do you think a timescale of visits at 6 weeks, then 3,6,9 and 12 months sound doable?

• Is a blood test at start, 6 and 12 months enough? Too much?

• Is an MRI for some participants at the start and at 12 months reasonable?

• Vertigo is considered the most important thing being measured, with hearing loss as a secondary measure - do you feel this is right? Is there anything else you would like to see measured?

• How would you like to hear about the way the trial is progressing and the final results?

• Is there anything that would put you off being involved, assuming you could be?

So we have a potential new treatment, and a chance for you to influence how the trial goes forward. There is hope, and I am personally very happy to be able to get involved. I hope some of you will too - I look forward to hearing your thoughts.

YouTube Channel

Meniere’s Without The Spin has an associated YouTube channel - a summary of this article will appear there. https://www.youtube.com/@MenieresWithouttheSpin

References

How kidneys work https://www.niddk.nih.gov/health-information/kidney-disease/kidneys-how-they-work

What are SLGT-2 inhibitors? https://my.clevelandclinic.org/health/treatments/sglt2-inhibitors

Repurposing SGLT-2 Inhibitors as a Novel Therapeutic Strategy for Treatment-Resistant Meniere’s Disease https://pmc.ncbi.nlm.nih.gov/articles/PMC12470965/

Barany Society Criteria for Meniere’s https://www.otoscape.com/eponyms/barany-criteria-for-meniere-s-disease.html

The relationship between SGLT2 inhibitors and hearing loss https://pmc.ncbi.nlm.nih.gov/articles/PMC12751864/

AI Statement

No AI was used in writing the text of this article. AI tools may have have been used to support some of the background research.

The medicine is code-named SPI-1005 by Sound Pharmaceuticals who make it. It is based on the active ingredient Ebselen, and in this article I want to take a closer look at this drug - what is it, why is it thought to be helpful for Meniere’s, what do the results of the trials so far say and, if it comes to market, is it likely to match people’s expectations?

A word of caution as always - I am not an expert in these topics. I am not a doctor, medical researcher or biochemist. I am simply someone with enough science background to gather the information that real experts have put together, and present it to you. Nothing I write should be taken as any form of medical advice.

Ebselen is an antioxidant, like vitamin C, vitamin E, glutathione, CoQ10 and others. Some of these like glutathione can be produced by the body itself, and others like vitamin C have to come from the diet. So what is an antioxidant, and what is special about Ebselen? When cells in the body convert food from the blood into energy, the waste products of the process include harmful substances called “reactive oxygen species”. The main culprit, called “superoxide” is highly toxic to many cells, potentially killing them. The body uses natural defences to mop them up and neutralise them. The first phase of this clean up is to convert this highly reactive “superoxide” into something you may be familiar with - hydrogen peroxide. The problem is that in itself hydrogen peroxide is also damaging to cells, and further clean up is needed.

One of the body’s most powerful neutralisers of hydrogen peroxide is a substance called “glutathione peroxidase 1 (GPx1)” - you make it using selenium from your food. When GPx1 interacts with hydrogen peroxide, it gets used up - you have to keep making more. Ebselen is a substance that looks to the body a lot like GPx1 - it does the same job of neutralising hydrogen peroxide, but in a clever way that results in the Ebselen not being used up! It can go on and on working. There are other ways in which Ebselen can interact potentially helpfully in the body but this neutralising of hydrogen peroxide is mainly what we are interested in.

So cells work hard, sweat out superoxide, an enzyme quickly converts this to hydrogen peroxide and then in theory Ebselen could help mop that up before it does damage. One thing to note - there is a first step that produces superoxide which Ebselen is not expected to help with, and could still result in damage. It is not a “universal” antioxidant in that sense.

Ebselen is being tested as a potential treatment for all kinds of conditions. For example, research is underway to see if it helps in: hearing loss due to loud noise, tinnitus, protection from brain damage after a stroke, reduction of brain damage after head injury, bipolar disorder, depression, prevention of hearing loss due to chemotherapy… and of course Meniere’s disease.

You will have noticed there are quite a few hearing-related conditions in that list. Why is that? It turns out that parts of the inner ear require a rich blood supply to support the intensity of their processes, and have a high metabolism. For example, the hair cells and the “spiral ganglia” that carry hearing signals away from the ear to the brain work very hard due to their high rates of firing, and during very loud noise can become overwhelmed by waste products.

The Stria Vascularis, which we have mentioned many times before, that lines the inside of the cochlea, the hearing part of the inner ear, is another highly active area. It has a tough job keeping the balance of sodium and potassium correct in the inner ear fluid and produces a lot of these waste products, especially in Meniere’s ears where there is an excess of fluid (endolymph) meaning more work for the cells to do managing levels of chemicals.

There have previously been some successful trials of Ebselen to protect hearing against damage from loud noise, in animals at least. In those experiments, the drug had to be administered both before and after the damaging noise in order to be effective. This does though suggest that Ebselen may have some benefit when it comes to hearing damage from reactive oxygen species. But what about Meniere’s?One of the potential ways that Meniere’s symptoms could arise is inflammation, and the membranes that manage exchange of chemicals becoming overwhelmed with waste products, so it is natural to wonder if Ebselen might be able to help there too. Bear in mind that Meniere's is still not at all well understood, there are many potential ways in which the symptoms may be being caused. So it is hard to give a definite rationale for why Ebselen could be expected to help, but its role as an antioxidant and its success in protecting hearing in some experiments was enough to make it worth trialing for Meniere’s.

The expectation therefore was that maybe Ebselen can help protect the hearing from oxidative damage which might be happening with Meniere’s. Given that tinnitus may be caused by dead or damaged hair cells, an improvement in tinnitus was also possibly expected. Beyond that there was nothing to go on - we don’t know if the vertigo or fullness in Meniere’s are caused by the same kinds of damage. It also isn’t clear how Ebselen would improve hearing if cells are already damaged. Given that it seems to have a “protective” effect in previous experiments, it would seem most likely that it might reduce further future damage from Meniere’s. But the way to tell if a drug “works” is to trial it in a structured way, which Sound Pharmaceuticals has done.

Drugs have to go through several phases of trials. Phase one for SPI-1005 began in December 2015, a small trial to demonstrate that the drug was safe for further investigation. Phase 2 began in September 2017, to further demonstrate safety, to decide dosage and begin to measure how effective it was. At this point the main things being measured were hearing and tinnitus changes, although vertigo and fullness in the ear were also monitored. The most important trial, in terms of demonstrating if a drug works or not is Phase 3. This trial with the rather hopeful title of “STOP-MD3” began in June 2020 with over 200 participants, comparing the drug to a placebo, again mainly on hearing and tinnitus with the other symptoms being secondary outcomes. The results of that trial have finally just been released in June 2026. A long term safety trial of the drug is now underway, due to complete at the end of 2026. Links to all the trials are at the end of this article.

Alongside this, the FDA granted SPI-1005 the status of “breakthrough therapy” in December 2025, since it was seen as the most promising drug in development for Meniere’s. They had also previously “fast tracked” the drug in 2019, the goal of both statuses being to speed up the process of bringing the drug to patients. There is now the possibility that SPI-1005 could be approved by the end of 2027.

So what do the trial results say about SPI-1005? Links to all the trial data are at the end of the article, but I will do my best to summarise them, focussing on the Phase 3 trial as it was the biggest and the main one used to demonstrate whether the drug might help. That trial looked at hearing loss - improvement in low frequency hearing and ability to recognise spoken words. It looked at tinnitus, in terms of loudness and severity, as well as feeling of fullness in the ear, vertigo and a separate assessment of dizziness. In each case the thing being measured was assessed at the start, as a baseline. Then the drug (or a placebo that looks like the drug but has no active ingredient) was taken for 4 weeks. No measurements were made at this point. After a further 8 weeks without taking anything, the hearing or tinnitus etc was assessed again. What we are looking for is a bigger improvement for those taking the drug compared to those taking the placebo, compared to the initial baseline.

Hearing Low Frequencies: This shows the most promise. Only low frequency hearing was assessed, measured at 250, 500 and 1000Hz, and to be significant, a small 10dB improvement was considered enough to count. The results reported are the number of people that at the end saw an improvement of 10dB or more. The results don’t show if anyone had a large improvement or if all those counted had just small improvements. Bear in mind that most people’s hearing fluctuates much more than 10dB with Meniere’s. Mine changes by up to 40dB. However, these are the headline figures - out of 112 participants on the drug, 59 saw improvement in at least one of the three frequencies measured. So more than half. Sounds excellent. However, out of 108 taking the placebo, 40 of those also saw the same improvement. So we actually have 19 out of 112 who have potentially seen benefit from the drug. When looking at those who had improvement in two frequencies, things look better - only 16 people on the placebo saw two frequencies improve compared to 43 out of 112 on the drug. So roughly a quarter (26) of those on the drug saw some kind of benefit that might be down to the drug.

Hearing Word Recognition: For this, a standard test of recognising 35 spoken words in amongst noise was used. Again we do not get to see how much people improved by. The measure is how many people could recognise at least 4 more words than they could at the start of the trial. Of those taking the placebo, 30 out of 108 saw this improvement by the end, and 45 out of 112 on the drug. So 15 people or about 13% of those taking the drug can be said to have seen an improvement that could be down to the drug

Tinnitus: Here, the approach taken in Phase 2 trials had been similar to the hearing loss - counting people who improved. But in Phase 3 instead an average tinnitus score was taken across all people taking the drug or the placebo separately. Both groups saw tinnitus severity drop by around 7-8 points out of 100 with a small benefit of just over 1 point for those on the drug. When it came to tinnitus loudness, both groups saw an improvement of about 1 point out of 10, with the placebo group being a tiny bit better.

Vertigo: Neither group saw average improvement of any significance.

Fullness: Both groups saw a small improvement, with those on the drug averaging around 0.6 out of 10 better.

Dizziness: Both groups saw a small average improvement of similar size

Side Effects: 45 of those on placebo reported some side effects, whilst 59 of those on the drug did - some 13% more.

As I was writing this, on July 14 Sound Pharmaceuticals released a statement saying that the Phase 3 long term safety trial now had enough participants and enrollment was complete. What I noticed about this press release is that, unlike all their previous ones, it says nothing about how effective the drug has been found to be for Meniere’s. They say that this has been the largest trial of an experimental drug for Meniere’s. But most of the press release is taken up with listing all the other conditions that are not Meniere’s that the drug may help with. This feels like a very muted press release, almost a preparation for a pivot away from Meniere’s. Maybe it has to be as they jump through the FDA regulatory hurdles, and of course want to interest investors in the wider possibilities for the drug, but it is to me markedly more downbeat than any previous press release.

What do people say that have taken it?

In the many online support groups, people who have been involved in the trials have reported back. Recent phases of the trials have allowed patients to know if they were on the drug or placebo and those on the drug itself have given extremely mixed reports. They vary from ecstatic, seemingly miraculous improvement in all symptoms from day one of taking it to quite a number who felt there was no improvement at all. Here is a taste:

“Within 24 hours it was a game changer. This drug has gave me my life back. The floaty, brain fog, and anxiety is gone.”

“Been on it for about 6 weeks. No difference. I was told it takes weeks or months for the drug to build up in my body. They don’t do placebos and they said on some people it doesn’t work.”

“This will not be a miracle drug . More like something else to help along with other things. I have seen many people in the past trial have no change at all taking the med. Few people have minor changes . But nothing miraculous!”

“It does help. Ear ringing lessened about 50%, reduced vertigo by about 90%. It’s been a game changer for me. Yes, it has helped.”

“So far I don’t see a noticeable difference with tinnitus loudness or less stuffiness in the ear, but it’s still way too early.”

“I was in the clinical trial. Did nothing for my tinnitus. I didn’t have any vertigo.”

“I took SP-1005 for a year. I didn’t notice any improvement in vertigo, hearing loss or tinnitus (which is the least of the three), but after 8 months I went into remission for 8 months. I don’t know if it was the study pills or it just happened, but I would go on them again to find out.”

One person, who feels they have had hearing improvement, has been posting very detailed experiences, in a public Facebook group, for example here

Out of nine people, one felt it helped just with hearing, two felt it helped with everything and six felt it did little or nothing. Bear in mind that this could be for any number of reasons. For example, maybe those with negative experiences are more likely to write about them, or the improvements were too subtle to notice over the time scale of the trial. But these reports do match I think quite well with the trial results.

The results are not, for most people at least, any kind of miracle. But on the other hand, there is nothing at all out there that can help even a little with hearing or tinnitus for Meniere’s. Anything small but significant that can be demonstrated, any improvement even for a subset of patients would be a good thing. So is this going to be another betahistine situation? A mix of results across the Meniere’s population? Could be - and maybe for a good reason. It is becoming increasingly clear that Meniere’s is not a single disease - the work of Professor Lopez-Escamez who I interviewed last year makes that clear.

There are subtypes, that can potentially be identified by the right kinds of tests. It could well be that drugs like betahistine and SPI-1005 help one or more subtypes and not all. But as yet subtyping the patients is not part of treatment trials - it should be I think.

Role of diet

Whilst we wait for approval of the drug, could dietary changes provide similar results? The first thing to note is that selenium is essential for the body to produce GPx1 which mops up hydrogen peroxide normally. Studies have been done to see if increasing dietary selenium can increase GPx1 and it seems it can. Some people are also trying to see if they can support the antioxidant process by supplementing with glutathione, since this is required for GPx1 to work properly, or with NAC which is needed for the body to make glutathione. There are however no good quality studies that I am aware of for this approach in Meniere’s.

So we wait. SPI-1005 looks likely to come to market at some point in 2027. Whilst it is clearly no panacea, it may help some people with some of the hearing-related symptoms of Meniere’s. If those people turn out to also be the lucky ones that betahistine seems to help with vertigo, the combination will, for those people at least, be some relief from the full range of awful symptoms we all put up with.

References

Overall review of antioxidants for Meniere’s https://pmc.ncbi.nlm.nih.gov/articles/PMC7693733/

Role of GPx1 in health and disease https://pmc.ncbi.nlm.nih.gov/articles/PMC9586416/

Meniere’s patients show reduced antioxidants (glutathione) and markers of oxidative damage https://pmc.ncbi.nlm.nih.gov/articles/PMC11333795/

Oxidative stress may lead to hydrops https://pubmed.ncbi.nlm.nih.gov/21042850/

The trials (For results click the “Results” tab on the trial page)

Phase 1b https://clinicaltrials.gov/study/NCT02603081
Phase 2b https://clinicaltrials.gov/study/NCT03325790
Phase 3 https://clinicaltrials.gov/study/NCT04677972
Open label safety https://clinicaltrials.gov/study/NCT06859788

YouTube Channel

Meniere’s Without The Spin has an associated YouTube channel - a summary of this article will appear there. https://www.youtube.com/@MenieresWithouttheSpin

AI Statement

No AI was used in the production of the text of this article. AI was used at times to help with some of the background research and to help produce or modify images.

It is easy to see why people worry. Flying is when many of us most commonly experience some kind of ear discomfort. The idea of needing to “pop” your ears is something most will be familiar with, and we’ve all quite likely heard of at least one technique to help, like swallowing, sucking on boiled sweets, or holding your nose and trying to push air “into” your ears. So, I’d like to spend a bit of time discussing flying with Meniere’s, offer some advice gleaned from the support forums and compare flying with other ways that pressure might impact Meniere’s. Bear in mind, as with so much relating to chronic illnesses like Meniere’s, your experience may not be the same as those I’m going to discuss, and nothing mentioned here is in any way intended to minimize or dismiss what you may have been through—I’d be very keen to hear from you!

To understand why flying might cause issues for Meniere’s sufferers we should quickly revisit the layout of the ear.

I snapped a photo of this model in my audiologist’s office. The important thing to notice is that there is a sealed-off chamber in the centre called the middle ear. Air from outside is prevented from entering by the eardrum. If the outside air pressure goes up or down, the pressure difference from inside to outside will bend the eardrum, which makes it vibrate less effectively and can even cause pain and damage. So, we have evolved a roundabout way to let air into the middle ear from outside to equalize the pressure—the Eustachian tube. This connects from the middle ear into the back of the throat. It normally remains closed to stop nasty things like bacteria and viruses from the outside world infecting the middle ear. However, when everything is working well, swallowing allows the tube to open briefly so air can seep into or out of the middle ear, ensuring that there is the same pressure on both sides of the eardrum. If the Eustachian tube is blocked, maybe due to a middle ear or sinus infection, a cold, or allergies inflaming the tube, this process does not work properly and the tube cannot open, making equalizing the pressure difficult.

What might this have to do with flying? Here is where we need to bust a myth I’ve seen endlessly repeated in support groups: “Airplane cabins are pressurized, so there is nothing to worry about.” This is half-true. Typical commercial airlines fly at 30,000–40,000 feet or 9,000–13,000 meters altitude. That is higher than the summit of Mt. Everest. At 30,000 feet, the air pressure is around one-third the pressure you are used to at sea level, and you would be unlikely to survive. For the passengers to stay comfortable, airplane cabins are indeed kept at a higher pressure than the air outside when at cruising height. However, they don’t maintain the full air pressure they have at take-off. As they ascend, the air pressure in the cabin is allowed to drop to the equivalent of being at around 6,000–8,000 feet up a mountain, where the air pressure would be about three-quarters what it is normally. So, yes, plane cabins are pressurized, but they do still drop significantly in pressure as they go up, and on the way down, the cabin pressure must be rise back to normal, ready for you to get out at your destination.

Now we have enough to understand why flying puts a strain on your ears. As the plane increases in height, the cabin pressure drops. The higher pressure air still in your middle ear pushes your eardrum outward; maybe you notice your hearing worsen a bit. Then, usually, the excess air finds its way out via the Eustachian tube and you might hear your ears pop, although this is less likely on the way up as the air tends to seep out gradually. Where people sometimes struggle is as the plane descends and the cabin pressure rises. The eardrum is pushed inward, but the Eustachian tube might be less likely to open, as the excess outside pressure tends to push the tube closed. At this point, consciously swallowing, sucking sweets, or the Valsalva Maneuver of pinching your nose and gently blowing against the closed airway might be needed to help encourage air up the tube and into the middle ear. When this happens, you will almost certainly hear a pop or squeak and notice the change in your hearing as the eardrum relaxes.

What is the Meniere’s connection? First and most obviously, Meniere’s is an ear disorder, so it is natural to be wary of anything that in some way might mess with your ears. However, beyond that, many people have over the years found that for them, Meniere’s symptoms seem in some way connected to the weather, and more specifically, to changes in the local air pressure—so-called “barometric” pressure. Keeping track of the weather and tracking the upcoming pressure changes are a daily routine for some Meniere’s sufferers. There are even apps now that incorporate local weather and pressure forecast data in an attempt to predict when sufferers might experience attacks. I’m personally unsure of the value of these, as there is a danger of creating an expectation and anxiety that may itself bring on symptoms—it is a topic that would be ideal for a research study!

Nevertheless, the fact remains that many Meniere’s sufferers feel that for them air pressure changes are a major trigger for their vertigo attacks. For these people, flying may seem like a terrible idea, which leads to the hundreds of worried questions in the support forums.

What evidence is there? There are no good research studies on the topic that I have been able to find. Being a pilot is known to potentially make Meniere’s worse, but this is for a variety of reasons specific to being in that role regularly. It is also the case that having Meniere’s rules you out for being a pilot in the UK, but not the USA. But there seem to have been no studies on passengers with Meniere’s. However there is a huge amount of anecdotal evidence available.

First, my personal experience has always been that flying made no difference at all to my Meniere’s - being a Brit with a German wife I have flown a lot over the past 20 years and my flight here to England this week was no different. I struggle slightly more to “pop” my left ear than my right when we land, and coincidentally that is the first ear I had Meniere’s in and the worse one for symptoms now I am bilateral. I’ve no idea if there is a connection. But my experience alone is no way to draw any firm conclusions. What about the support forums? The question has been asked hundreds of times in the past few years, and my impression from the responses is that the vast majority of people have no issues at all. Some are anxious and take a variety of precautions, but overall I’d say at least 95% of people seem fine flying with Meniere’s (Maybe I should do a more detailed statistical analysis of the forums to try to get a more accurate figure). This does not mean it is the case that everyone is fine. Amongst all the positive stories are those who have had a bad time, suffering an increase in symptoms during or after a flight. It is of course impossible to know if the flight was the cause, but in most cases people seemed to feel it was. My impression then is that flying is rarely an issue for most Meniere’s sufferers. This is despite many people being concerned and anxious beforehand, which can often make symptoms worse.

This leads to what I am calling the “Flying Paradox” for Meniere’s disease. On the one hand we have large numbers of people reporting their experience of barometric pressure and weather changes as a huge clear trigger for their Meniere’s, on the other hand almost everyone can go through the pressure changes involved in a flight without issue. It is also worth comparing how much the pressure changes in each situation. Typical daily pressure change in the UK for example due to weather fronts might be 10-20mB (around 0.5 inches of mercury if those are your preferred units) and I’ve seen similar size changes on app pressure graphs being viewed with alarm.

This size of change is the same as driving up a 500ft (150m) hill, and is around one fifteenth the size of the pressure change when flying. Something else curious about the people’s experiences with barometric pressure is that no one can agree which direction of change is a trigger for Meniere’s. For some it is increasing pressure, for others decreasing, and for many, it is any change at all. As it happens this phenomenon has actually been researched in a few studies over the years, and the conclusion seems to be for those people in the studies who felt impacted, it was a drop in pressure that was more significant, although even there there is disagreement. The table below is from an AI-assisted deep research into pressure and Meniere’s and summarises the studies. All are linked in the references at the end of this article.

So what might explain the “Flying Paradox”? One thing that is different is the speed of the pressure change. Not only are weather-related changes a lot smaller than those encountered during flying, they happen much more slowly. Maybe that unexpectedly causes issues that a rapid change doesn’t. Similar rapid changes occur when ascending tall buildings in an elevator, or driving up large hills and mountains - neither of which I’ve seen regularly reported as triggers. So speed of change might be a factor. In addition, as I’ve written about before, expectation plays a big role in conditions like Meniere’s. The resulting symptoms are very real, and absolutely not purely psychological, but could be brought about at least in part by the expectation of an attack having seen a forecast. All we can say for sure is that right now the impact of pressure changes on Meniere’s is complex and not well understood.

Some people do feel that they want to take precautions before flying. For the pressure changes, there are ear plugs that claim to help reduce the impact and many feel they help. Another thing people agree on is the need to keep hydrated. The dry conditioned air in planes makes that harder. So, it is important to drink enough. The next big issue is noise. Good advice is to try to choose a seat far from the engine, and if you have them, take noise-cancelling headphones. Then there is food—if you are one of those for whom the sodium in salt is an issue, try to avoid large spikes from snacks and, where possible, choose lower salt in-flight food options. Other advice from forum members is to ensure that you have rescue medication with you, maybe even take some as a precaution before the flight, and on descent, start trying to equalize the pressure early—aircraft often begin heading down earlier than you think—the moment you start to feel that slight ear pressure, use one of the techniques to encourage air into your middle ear. Leaving it all until near the end means the Eustachian tube is being forced closed by the extra cabin pressure, and it is harder to do one big adjustment than lots of little ones.

What can we say then about flying and pressure changes as far as they impact Meniere’s? Certainly it seems the vast majority of people fly without issue, and there are a few precautions you can easily take if you want. The “Flying Paradox” remains an area that could do with further investigation - understanding why so many fly with ease and yet suffer badly with weather and barometric changes might give us more insight into the complex ear issues we all live with. Now I’m off to the airport to fly back to Germany.

References

UK “Meniere’s Monitor” study into pressure changes https://pmc.ncbi.nlm.nih.gov/articles/PMC5224697/

Taiwan investigation pressure and temperature impact on Meniere’s https://www.researchgate.net/publication/362376300_Correlating_atmospheric_pressure_and_temperature_with_Meniere_attack

Munich study showing increase in pressure as trigger https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0152714

MRI study showing decrease in pressure making hydrops worse https://pubmed.ncbi.nlm.nih.gov/40155660/

AI Statement

No AI tools were used in the creation of this article other than for research and to help with one image. No AI generated text is used in the article at all.

Daniel has a PhD in auditory neuroscience with a focus on diagnosing excess inner ear fluid (hydrops), and in 2007 with support from the Australian Meniere’s Research Fund, he spent time in the USA working with renowned inner ear specialist Alex Salt on mechanisms for drug delivery for Meniere’s. Daniel then established a lab at Sydney University under the Meniere’s Research Group, where he worked until 2019. At that point he moved back to Perth, his home town, to start a lab there at Curtin University where he is currently Associate Professor, discipline lead for Human Biomedicine and course director for Human Biology.

I initially asked Daniel what areas relating to Meniere’s he has tended to work on. His focus has been understanding and measuring hydrops as well as taking a pragmatic approach to treatment. He said it was clear that the idea of a single “cure” for Meniere’s as a whole is a long way off, maybe not even possible due to the various potential causes each of which may need their own treatment.

“ What I'm trying to do is develop a very effective therapy. It's sort of a clinically pragmatic approach to what I think I can achieve in my life and how I can best contribute to the Meniere's community”

Daniel has therefore chosen to focus on treating the symptoms. In our discussion, he regularly made an analogy with psoriasis, a skin condition he suffers from. Whilst we might not know the exact cause or have a cure for psoriasis, it is extremely valuable to be able to dampen down the symptoms and make life more comfortable. The parallels with Meniere’s are strong - psoriasis also has periods when it flares up, treatments include steroids, and like Meniere’s we don’t exactly know what the cause is.

We then discussed endolymphatic hydrops, the build up of inner ear fluid which is the classic hallmark of Meniere’s. If you need a refresher on this or other aspects of inner ear anatomy relating to Meniere’s, check out this article:

For a long time the core theory of Meniere’s was that the excess fluid pressure caused hearing symptoms and some kind of rupture of the containing membrane caused vertigo. I have previously reported on the work of researchers who found strong evidence to suggest that these old theories may not be the correct picture. I was keen to hear Daniel’s perspective.

Daniel is firmly of the opinion that hydrops does indeed cause Meniere’s symptoms: the classic low frequency hearing loss, episodes of intense vertigo, tinnitus and fullness. He noted that the idea that maybe people can have hydrops without Meniere’s or similar symptoms seemed to stem from a 2005 study of temporal bones after people had died. That study concluded that everyone who had Meniere’s had hydrops but not everyone with evidence of hydrops had had Meniere’s. They had, though, Daniel said, had other inner ear disorders. He was happy to admit that it was possible to have mild hydrops which might go unnoticed if it doesn’t progress, but should it get worse it will become Meniere’s.

“So my view is that I think .. it definitely does lead to a lot of the symptoms of Meniere's disease and it explains why you can have sudden episodes of acute vertigo. It explains the low frequency (loss). It explains most, if not all, of the symptoms that you can get with Meniere's disease. People that sort of...dismiss it as just a side product never give an explanation of how you can have those types of symptoms, how you can have sudden vertigo attacks, or you can have low frequency loss and hearing loss, etc.”

Another advantage Daniel mentioned of focussing on hydrops is that it can be measured, which might give a way to really track if treatments are doing something. What we don’t have a good handle on though, he admitted, is the causes of hydrops. There are many potential causes, with good evidence to support all of them, including genetic, viral and autoimmune causes. So Daniel argued why not focus on treating and trying to measure the hydrops that they all seem to cause?

At this point I asked “What's the current state-of-the-art for measuring and imaging hydrops?”. He said that MRI specifically for imaging hydrops (with a specialised protocol and contrast dyes) has come a long way in the last 15 years, It still seems to depend a bit on which exact machine is being used, but you can, he said, definitely use the results as a clinical diagnostic tool for Meniere’s. The issue though is the cost and time - the chances are you may only get one such MRI in your lifetime if that, given that most doctors are likely to say they can tell just from your symptom history that you have Meniere’s. As Daniel said “It's just confirming the diagnosis, which is fine, but it doesn't offer much else beyond that. It's not like you can use that as a diagnostic tool to track …how your disease is progressing”

What interests Daniel is how we might monitor hydrops using some kind of cheap non-invasive approach, or regularly track some kind of biomarker that gives reliable indication of the way the condition is changing. That way it is possible to know if proposed treatments are actually doing something.

“There are tools, electrophysiological clinical test tools that …have been developed over the last 20 years, which are not invasive, can be done at the bedside and can provide the clinician a way of monitoring a patient's Meniere's disease whilst they're on a treatment, to work out if that treatment is working or not.”

So what tools are we talking about? The main alternative is currently electrocochleography which has been around for 80 yrs - this involves measuring electrical activity in the inner ear as it responds to clicks played into the ear, and usually requires an electrode injected through the eardrum to rest against the entrance to the inner ear. Professor Bill Gibson from Sydney university was a world-expert in this approach and used it on virtually all suspected Meniere’s patients but it is no longer routine. It is still invasive though - you wouldn’t want it done too regularly.

An approach that Daniel told me he has investigated alongside Bill Gibson in 2011 is “Otoacoustic Emissions”. When selected tones are played into the ear canal, some of the sound is reflected back from the structures in the inner ear and these echoes carry information about the membrane that carries the sensing hairs for sound. By examining recordings of the echoes, it is possible to see if the membrane has been pushed up or down and by how much which in turn gives an indication of the degree of hydrops. Daniel said he should revisit this - given that it is incredibly easy to administer, it could become the equivalent of the “blood pressure cuff” - present in all ENT clinics for monitoring hydrops progression.

At this point I had to ask - is hydrops reversible? I had heard and read numerous statements from researchers to suggest that it wasn’t, even if surgeries or treatments demonstrate symptom improvement. Daniel said “Even when patients have gone on to therapies that have effectively halted the progression of their symptoms for a long period of time, or even if they have had a surgical operation, like endolymphatic shunt surgery or ablation surgery, even then, it seems to be that majority of patients still demonstrate endolymphatic hydrops“ - so this does lead to a puzzle that probably demonstrates a gap in my understanding - what then would we be measuring if hydrops never reverses or improves? More to come on this topic I’m sure!

We then discussed the idea of cochlear and vestibular hydrops - is it possible to have excess fluid in either just the hearing part or just the balance part of the inner ear? Daniel’s response was that yes, some people seem to have hydrops in their semicircular canals and less in the cochlea, and vice-versa.

“Currently the clinical diagnosis of Meniere’s disease relies on having both cochlear symptoms and vestibular symptoms. And without that, you won’t get a diagnosis of Meniere’s disease. That’s not really much help for people who are suffering from recurring episodes of vertigo, but they haven’t got tinnitus or fluctuating hearing loss.”

He suggested maybe Meniere’s should be renamed Endolymphatic Hydrops, with subtypes of Cochlear Hydrops and Vestibular Hydrops.

So it was time to get into the weeds a bit to try to unpick exactly how hydrops might give rise to our symptoms, something I am always keen to find out more about. This will require us to know a bit about the inner ear structure.

This diagram shows all the spaces in the inner ear that contain endolymph, the fluid that we tend to have too much of in Meniere’s, The hearing issues in Meniere’s are thought to stem from the excess fluid in the yellow cochlea portion. The two green areas contain sensors that tell us about movement forwards and backwards and vertically whilst the blue region shows the infamous “semicircular canals” that inform the brain about rotations of the head in three different directions. The red area is the endolymphatic sac and its connection into the rest of the system (for convenience it is shown smaller than it tends to be). We have previously spent quite some time on this organ as some research shows that changes here seem to be connected to Meniere’s. However what interests us is a tiny flap called “Bast’s valve” that normally regulates how excess fluid from the green Utricle region is managed and potentially allowed to flow into the sac. Also there is a very narrow connection from the cochlea into the saccule. One way that hydrops could develop in only one section of the ear is that these very small tubes or valves could get blocked, maybe by loose crystals from the sensor organs, the same ones that cause BPPV.

Ordinarily the cochlear and saccule region is separate from the semicircular canals and utricle. Excess fluid in the cochlea might impact the saccule but not much else. However a theory put forward by Bill Gibson and potentially confirmed in experiments carried out by Daniel in 2013 suggested that maybe if the pressure of fluid in the cochlea becomes too much, Bast’s Valve may be forced open the wrong way or the duct between the utricle and saccule could suddenly open. This would lead to a spurt of endolymph arriving suddenly in the utricle and semicircular canals, resulting in an abrupt disturbance in those fluids and vertigo. A useful animated video of this proposed mechanism is linked in the resources at the end. Daniel’s experiments on endolymph in Guinea pigs were especially significant in establishing this idea. He found that as he artificially increased the volume of endolymph in the cochlea, hearing-related measures seemed to worsen but nothing much happened in the balance system. Then suddenly at a certain point there was a rapid recovery in the hearing signal and collapse in balance function. He then went further, using dyes that could be seen in real time during the experiments to show that no dyed fluid was initially entering the vestibular system as it was added to the cochlea, followed by a sudden influx at a certain point. It is worth quoting Daniel at length on this as it is significant:

“But cochlear function starts to get worse and worse and low frequency hearing gets worse and worse and then, as you continue to increase the volume of fluid in the cochlea, eventually you get this spontaneous sudden recovery of the hearing in the cochlea by 30 DB. Wow, I mean in almost in real time, you can almost see the core responses on the on the screen and then all of a sudden - bang. What the heck happened there? And it’s so immediate that it’s got to be a mechanical change. I mean, cell biology doesn’t work that quick. So it’s got to be a mechanical shift. So sudden recovery of cochlear function. But what you find is then in 30 seconds to a minute later, vestibular function takes a bit of a dive. So that got us thinking, well, how can that be the case?“

Daniel was keen to make it clear that ruptures of membranes and mixing of fluids in the cochlea (the old long-standing theory) could still be happening, and this could explain why hearing could sometimes suddenly improve in some patients without associated vertigo.

One thing that seems to characterise Meniere’s is that whilst there are these huge fluctuations in hearing and intense vertigo episodes there is also an overall progressive decline in hearing long term. Daniel speculated that this could be down to repeated disturbances of the potassium and sodium balance in the cochlea, or maybe down to the long terms impact of excess fluid pressure, but no one seems sure.

Treatments for Meniere’s Symptoms

It was time to discuss treatment since that was the other aspect of Daniel’s work. Steroids are the mainstay of treating flare ups in Meniere’s. The issue is getting enough drug into the inner ear. Taking tablets requires a super high dose which will impact other systems in the body so injection into the middle ear is the usual route, However this is very hit and miss - you can flood the middle ear and then hope some of the steroid diffuses across the membrane into the inner ear, but it is hard to control. This lack of consistency, said Daniel, may be one reason for the very variable results of steroid injection. Long term use of steroids is also not recommended, and there is evidence that people become resistant to them.

Previously Curtin University had been trialling a powerful antioxidant called “Probucol” for lowering cholesterol. The idea was formed that maybe it could also have an anti-inflammatory and antioxidant effect on the inner ear and treat Meniere’s. Like steroids, dosing the whole body was not a good idea so Daniel delivered the drug directly to the inner ear in animals. The trials were remarkably good - animals first had their hearing damaged and then as Daniel said “The animals who had received Probucol, the hearing was perfect and I was just like, I questioned it multiple times. I said, this doesn’t make any sense…results are never this good. But yeah, with the (Probucol) results were pretty good.”

Now these experiments were not about reversing or treating Meniere’s, and more trials would be needed to see if the drug might calm inflammation of the inner ear or reduce hydrops-related hearing loss. Currently there is no funding for such work.

The work that is ongoing and funded is on drug delivery into the inner ear. Daniel described the challenges:

“Getting a drug to where it (needs) to go to in the inner ear …is an art form and particularly with the inner ear, you’ve got several boundary membranes where you’ve got to get drugs through and then they go into big fluid compartments with high turnover rates that wash drugs away”.

The focus initially is trying to help get drugs across membranes using techniques called “nanocapsules” and “liposomes” - wrapping or attaching things to the drug that the membrane is happy to allow across. This could even result eventually in the creation of ear drops that could be administered into the ear canal and find their way right into the inner ear.

However longer term the really exciting work is on implantable delivery systems. This is a very active research area worldwide and involves devices that are implanted into the body, maybe under the skin or in the middle ear that automatically supply regular controlled amounts of drug to the inner ear. For example there have already been trials of a modified cochlear implant that not only provides hearing but doubles as a steroid delivery system. Daniel was very passionate about this topic:

“I really do think that topical drug therapy for the inner ear by transtympanic injections or some other means, drug delivery devices, is going to be far more effective than systemic therapies, taking a tablet, just because you can get so much more of the drug into the inner ear without all those other side effects that come with taking tablets for a long period of time.”

These ideas of drug delivery mesh well with some other work that Daniel has been involved with - devices to monitor the levels of essential chemicals such as potassium in real time in patients. The initial work is happening again in animals, but if it is possible to develop sensors that can be implanted into the inner ear, we may then be able to actually see sudden changes in potassium levels happening during attacks, or see slower changes that might allow prediction of when attacks are about to happen. This information could then even be used to drive drug delivery devices which might then prevent or diminish the attack.

As I always do with researchers, I asked Daniel his opinion on the drug SPI-1005 for Meniere’s that is currently in Phase 3b trials. Interestingly he said that the active ingredient in this drug, Ebselen had previously been compared to the Probucol he has worked on, since they are both powerful antioxidants. Ebselen mimics a chemical the body produces that mops up “free radicals” which cause cells to age and die. In theory it is therefore a promising drug to potentially protect the inner ear from damage that Meniere’s might be causing and Daniel expressed high hopes that if approved by the FDA it might be helpful. However, the challenge, as with all tablets, is getting enough of the drug to where it needs to go at the right time. If it is taken all day every day, which is what the current Phase 3b safety trial is testing, will it be possible to take high enough doses to get good amounts to the inner ear?

“I do worry about how long you could take a systemic therapy for at a high enough dose to get a high enough drug concentration in the inner ear. I mean, we are essentially a big vat of saline and that drug is going to diffuse through your body and it’s going to become dilute. Whereas if you can take that entire pill and then put it in your ear, it’ll be concentrated at the site.”

I also asked Daniel’s opinion on as many common Meniere’s topics as I could - sorry Daniel, it was just such a pleasure to get to talk to an expert for a while. I will summarise the responses below:

• Meniere’s Subtypes (Work of Antonio Lopez-Escamez and others) - Excellent work, and knowledge that is probably essential for trialling treatments.

• Betahistine - Same issue as other drugs: how do we get enough drug to the inner ear? Could be why very high doses seem to work for some

• Dietary triggers - There are nice theories that could support the idea of salt being an issue, but it is not then clear why it would help some and not others. So it comes down to individual choice, people should try for themselves. However going very low with salt intake could sensitise someone to salt and make things worse. Daniel is a scientist and a natural experimenter, so what he said next might not be for everyone but it fitted with my approach too - “Being a scientist, what I’d probably do would be …go out and eat a high salt diet, just to see how sensitive I am to salt”

• Pressure and Weather triggers - Daniel began by admitting this is an odd phenomenon, and potentially could be an example of a “nocebo” effect and increased levels of anxiety (none of which is to say that the symptoms are not real - they very definitely are). However Daniel’s time with Alex Salt in the USA led him to think that it was possible for hydrops to lead to a blockage of the inner ear space that could in turn sensitise the ear to ultra low frequency sound and pressure changes. But beyond that no obvious mechanism seemed to exist for these kinds of triggers.

In conclusion we talked about funding, a very urgent topic in the Meniere’s research space. One of the biggest reasons that there has been so much great Meniere’s work done in Australia over the years was the former “Meniere’s Research Fund” founded by Bruce Kirkpatrick and others. As Daniel stated:

“Bruce Kirkpatrick passed away not long ago, which probably a lot of the Meniere’s community don’t know, but he was possibly, and arguably, one of the biggest donors to Meniere’s research in the world. He had given, I don’t want to give a number, but large sums of money to support Meniere’s research over the 15 year period.”

This was the source of funding that established Daniel’s original Meniere’s research position. He said that when he left, there was a chance that the remaining several million dollars might get swallowed up due to university reprioritization, and both Bruce Kirkpatrick and Bill Gibson fought hard to keep the money allocated for Meniere’s. The result of this was the recruitment of Professor Antonio Lopez-Escamez, whose work I wrote about before.

Now though, the charity group supporting the research fund has disbanded so the remaining money in the fund is being spent down, and continuation will require more donations. Daniel was keen to reinforce how vital the fund has been:

“I think it probably is under acknowledged the fact that at one level his position (Antonio) at his laboratory at the university really comes about because of the various generous donations from the people in and around Australia and around Sydney at that time.”

Bruce Kirkpatrick also helped provide startup funds for work at Curtin university that Daniel has been involved in, and Daniel pointed out how essential donors like that are for Meniere’s. The condition is not viewed as an attractive research topic as it is rare but not new, and competes for funds with things like obesity, cancer, mental health disorders and other significant causes of ill health. So we all need to be hugely thankful to those generous donors who have funded work, and look for any opportunities to spread the word about the need for support wherever we can.

This was a great discussion and I am incredibly thankful to Daniel for his time. I came away as always with lots more knowledge, a ton of new questions and the sense that the answers for Meniere’s are still elusive but smart people are working at the problem from many different directions and treatments will come.

Donate to Dr Brown’s Research

You can donate directly to support the work of Dr Daniel Brown here https://give.curtin.edu.au/menieres-disease-research-donate

The Full Video Interview

Additional Resources

Curtin University Article about Dr Daniel Brown https://www.curtin.edu.au/friends/curtin-research-is-music-to-the-ears-for-menieres-sufferers/

MRI In Meniere’s Disease https://jbsr.be/articles/10.5334/jbsr.1627

Electrocochleography for Meniere’s https://www.frontiersin.org/journals/neuroscience/articles/10.3389/fnins.2017.00301/full

Revisiting the cause of vertigo in Meniere’s https://www.jscimedcentral.com/public/assets/articles/otolaryngology-4-1186.pdf

It is for this reason that it is highly recommended for sufferers of conditions like Meniere’s to habitually log or journal their symptoms. This gives a record of how you really felt and can be incredibly valuable in many different ways. First it is a great document to take to doctors appointments - when they ask that dreaded opener “So, how have you been?” you can either use your log as a reminder to talk over what has been happening, or if it is readable enough just hand it over for them to scan through. It is also very useful if you start taking a preventative medication like a diuretic or Betahistine - after a few months on the new treatment you can look back and see if things really have changed. It was my journals that convinced me that Betahistine was not actually helping even though I had felt maybe it was. The facts were there - I was having roughly as many attacks as before and symptoms overall from my log did not seem better.

Dave Giugno who helps run a large Meniere’s support group on Facebook and also has a YouTube channel dedicated to his Meniere’s experiences has pointed out to me how useful journaling was to him in applying for Social Security Disability Insurance (SSDI) - something I had not considered but I can see it would be essential evidence for a case.

A final big use of journals is in spotting potential triggers. In the first instance you can just look back over your records and see if you can spot patterns - maybe comparing with records of the local weather and pressure changes, or seeing from your diary when you went out for a big restaurant meal that might have been loaded with salt or involved over imbibing alcohol. You could then take the journal one stage further and also separately log things you suspect are triggers, such as salt or caffeine intake. Dieticians suggest however that you do this more methodically - having logged symptoms for some time, exclude one thing that you consider may be a trigger for a few weeks, then reintroduce it and see what changes. Repeat with other potential triggers. If you want to hack this process to speed it up, you can eliminate all the suspect triggers (as much as is feasible - salt should not be reduced too low) for a few weeks or months, then reintroduce things one at a time over a long period. In all cases, the journal is your bedrock, the reference you will go back to again and again to see what has been happening and remove the uncertainty of your own fallible recollection.

So we need to be tracking our symptoms. What should we track and how? Consistency is key so doing too much will likely undermine your efforts and result in you not sticking to the journal. Given that the essential defining symptoms of Meniere’s are tinnitus, feeling of fullness in the ear and hearing loss plus bouts of vertigo, these seem like the things to track. I found that fullness and hearing loss tended to go together so I never bothered with fullness. Every day, sometimes more than once a day, I would try to write down a number for my sense of how much hearing loss and tinnitus I had on a scale 0-9 and also any attacks of vertigo with a “time spent in bed” and any medication taken. As soon as it became clear I was having problems with both ears I included a measure for tinnitus and hearing loss for each ear. The hearing loss I judged by rubbing my fingers together and moving them away until I could no longer hear the sound, just to give a rough and ready measure. I also added notes about anything else significant, subjective feelings or notable events, but these ended up being much less useful than the changes in the symptom measures. It soon became clear from this kind of journaling that I had a classic pattern - the hearing symptoms worsening for some days or weeks followed by bouts of vertigo after which things would improve. It was also clear that the flares came in clusters with longish periods of remission in between.

I kept my journal in a simple text file on the computer. If you prefer pencil and paper, Meniere’s sufferer and advocate Juliann Wallace has published the Daily Meniere’s Journal which you can find online, or if you message me I can send you a pdf copy. You could of course also use a spreadsheet or notepad on the PC or phone and these days cloud services will allow you to access files from multiple devices and keep them backed up. For a long time I thought some kind of app would be a nice idea and I tried a few over the years but they were all too complex and typically not tuned for Meniere’s. I used to be a software developer and had begun sketching my thoughts for my own app. Then all of a sudden in the past few months, a whole raft of new apps have appeared. I have seen at least five. I suspect the reason why may in part be down to Artificial Intelligence. AI coding has reached a point where it is much easier for someone with an idea to turn it into an app. This isn’t to say you don’t need skills - you do - setting up development environments is still a complex task. However the barrier to entry is lower and the speed with which something useful can be produced much less. So we suddenly have a lot of tracking and monitoring apps available or on the way. At some point I intend to review them, but at the moment they are mostly in my view incomplete and along with other people I am providing feedback to as many developers as I can. So rather than review any individual apps I wanted to list what I see as the useful features and where for me the apps are currently not quite there. This is of course my personal view and your needs from an app may well be different. I’d love to hear from you in the comments what you would like from a tracking or symptom journaling app.

It seems to me that there are three main focuses for tracking apps. First we have simple symptom logging like Menierly - open the app, click a few buttons to indicate your current symptoms and save. Then there are apps centered around doing a detailed hearing test - the authors of the Vestia and Meniere’s Biometrics apps want to make sure you understand that is their key focus. Finally there are apps that allow you to also track potential triggers - mainly sodium and barometric pressure, and even use that to predict when you might have an attack of vertigo. Balance:Vestibular Diary is in this category. Some apps mix all these approaches.

For me, the features of an ideal app should start from the classic presentation of the disease. There is a constant rolling landscape of fluctuating symptoms in Meniere’s - this is daily life for sufferers - decreases in hearing, increases in tinnitus, maybe the onset of balance issues. Layered on top of that are the spiky peaks (or maybe dread-laden valleys) of vertigo attacks. It is the shape of this landscape that I believe is the most useful thing. That means being able to consistently, quickly, note down key symptoms once or twice a day. Automated reminders are hugely helpful with this - I use an app called Daylio for mood tracking that has nailed this. I want a simple page where I can with one tap enter a subjective level for key symptoms for each ear. One value for left, one for right. I want not only a date but a time so more than one can be entered per day, and a way to edit them in case of errors or needing to add entries later (attacks can render us incapable of using any technology for a while). Attacks of vertigo should also be loggable including some way to estimate severity (I used hours spent out of action as my proxy measure) and rescue medication taken. With each log entry, an optional notes field would allow any special circumstances to then be added via text or voice. As far as essentials go, I’d then need to be able to see this data in a list, table or graph - spotting patterns is what we are good at but only if the information is presented in the right ways. This kind of ability to view the data in many ways is the main reason I always wanted a digital form of my log. Summaries of things like average attacks per week or month are also useful as is the ability to export or print the data for taking to a doctor.

Beyond that, for me personally, everything added needs to justify itself. Is it worth the extra complexity? Automating the process of adding the local weather or barometric pressure to the log might be valuable, as could be adding the amount of sodium consumed in the previous 24 hours if that data were available, maybe by syncing with a diet or fitness app. Trying to log potential triggers at the same time as symptoms doesn’t make sense to me - triggers need to be independently logged and then checked against the journal to see patterns. I’m not in favour personally of attempts to predict attacks. Firstly there is to my knowledge not enough good quality evidence in general of the impact of either pressure changes or diet to be able to do this kind of prediction across the board for any patient. There is also a big risk - that the prediction becomes self-fulfilling as anxiety and expectation play a significant role in conditions like tinnitus and vertigo as we saw last time:

One possible way that prediction could, maybe, make sense is if there were enough data on both symptoms and environment (logged separately) to then apply some AI pattern searching algorithms to the make an tailored, personal prediction. This could form the basis for an interesting research project. It would be very hard to do cleanly in a way that avoids bias but I think might be possible to at least determine if the idea has merit. However we aren’t there yet and apps saying they can already make predictions are, for me personally, making unsubstantiated claims.

What about hearing tests in apps? This is an evolving area. The iPhone paired with AirPod2 earpieces is capable of carrying out an FDA-approved hearing test which can then be used to set up the AirPods to compensate for hearing loss, so the idea of using the phone for measuring hearing is reasonable. The challenge with other phones and earpieces is that they are all going to produce different volumes and have different frequency characteristics. However as long as you use the same hardware each time and the same volume on the phone, you should at least be able to spot changes by doing at home measurements regularly. I can see some value in this. I am in the lucky position of having very regular professional hearing tests from my audiologist, but for those of you who aren’t, at home measurements through an app could be useful. The challenge here is the ease of use - I have tried these apps and found them very hard to get consistent results with and one hearing test could take from 5 to 10 minutes. But I’m open to being persuaded of their value - I’d certainly find the results interesting - to be able to see how the hearing fluctuates in detail every day could reveal a lot about how the fluid in the ear is changing and might even be a potential diagnostic tool. It has to be super easy to use for this to work though.

Journaling your symptoms, however you do it, is an invaluable part of your Meniere’s self-care. It is great that so many new apps are appearing, and we should end up with some truly useful tools to support the approach that best suits each of us. I’d love to hear from you about your experiences with monitoring and tracking your symptoms - what would you like to see in these apps? I know the developers are listening :)

A selection of apps under development

Menierly: Meniere’s Toolkit https://menierly.com/

Balance: Vestibular Diary https://alchemyg.com/balance-app/

Meniere’s Biometrics https://www.menieresbiometrics.com/

Vestia https://vestia.health/

AI Statement

No AI was used in the production of the text for this article. AI is sometimes used to assist researching areas but none of the resulting text is used. AI image generation has been used to produce or augment some images.

What is meant by “placebo”? It is a term that comes from medical science, from the testing of real drugs and treatments. One way to check if the active ingredient in a drug is really doing something is to give half of the people in a trial the drug and the other half an identical looking pill with no drug in it. To do this well, not even the person giving the drugs out knows which is which. The fake pill is called a placebo. Over years of doing trials, it has been noticed that sometimes people seem to report improvement even when taking the placebo treatment, and this has been called “the placebo effect”. The point of this article is to give a little overview of this and how it might be relevant to Meniere’s, rather than to dive deeply into what is a very complex topic.

So what might be happening? There are many reasons why someone might begin to feel better even though no active drug was taken. Maybe the expectation of being given a treatment really is somehow influencing the body, but this is not the only explanation. Many conditions have symptoms that come and go, so possibly it just got better naturally. Maybe having taken the decision to begin a treatment the patient also then takes their own rest and recovery more seriously. Or it could be knowing that they are taking a drug that should help means that the sufferer reports their symptoms differently, feeling that they really should be improving. However there are ways to get around some of this. For example, experimenters have tested pain relief by secretly giving some patients the treatment without them knowing, whilst giving the same treatment to others and clearly telling them what they were getting. Those that know they are getting treatment tend to report better pain control. So in that case the expectation does seem to be doing something.

There is another side to expectation - the “nocebo effect”. This is when you expect that a treatment might have an unpleasant side effect, and it does, even though you actually didn’t get the real thing. This seems to show that expectation of bad outcomes can somehow provoke those bad outcomes. Again, there are many possible reasons for this. Firstly we know anxiety has real physical effects on the body. Secondly, being told to be alert for unusual or new things might make the patient pay more attention to normal everyday aches or pains, hearing defects or other issues and have the sense that they must be down to the treatment. Whatever the cause, inactive placebo treatments can and do seem to have side effects!

How does this apply to Meniere’s and other vestibular and hearing disorders? First all the potential explanations for the placebo effect can be in play at once with Meniere’s treatments. Meniere’s is a notoriously fluctuating condition, with sudden spontaneous periods of remission that can last days, weeks or months, so it is very hard to know if the treatment you gave someone really worked. Then the symptoms such as tinnitus or degree of vestibular issues are not readily measured, relying instead on self-report. One exception to that would be hearing loss which can be objectively measured, but not if you do it yourself. The overall progression of the disease also means symptoms change through time with vertigo spells tending naturally to get less frequent or less intense, hearing loss tending to get worse and overall balance declining. So there is no constant background to compare to. This is why the landscape of medical trials for Meniere’s treatments is carpeted with mixed results and poor quality evidence.

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There is evidence that the both the placebo and nocebo effects are real in conditions relating to Meniere’s. An experiment was conducted in which participants were told that a tablet they were given would influence their balance. It did, even though it was a placebo. If told it would improve their balance, they walked more steadily, if they thought it would make their balance worse, they walked more unsteadily. Stress is also known to worsen tinnitus and impact vertigo. The impact of psychological state on Meniere’s has been well studied including the finding that vertigo is more likely in the hours directly after situations causing emotional distress.

When it comes to the placebo effect for treatments in Meniere’s the evidence is strong - ironically it may be one of the few examples of robust evidence for something in Meniere’s disease. There have been many trials of drugs such as betahistine where the drug is compared to placebo, and it is common for at least 50% of those taking the placebo to report similar improvements to those taking the drug. One of the largest ever betahistine trials (the BEMED trial) concluded that the drug was no better than placebo - not because no one got better, but because both real and placebo groups saw a huge 70% improvement in symptoms. The placebo effect extends to surgery too - maybe the much more extreme nature of such treatments increases the likelihood of an “expectation” based effect. In 1981 a study compared a common surgical procedure for Meniere’s - endolymphatic sac decompression surgery - with sham surgery where all steps of the surgery apart from the final decompression were carried out. Both groups of patients reported a 70% reduction in symptoms. So the actual decompression seemed, in that study at least, not to be the reason for the improvement.

A topic dear to many Meniere’s sufferers hearts is the idea that there are particular triggers that worsen symptoms or start the process that inevitably ends with hearing collapse and vertigo. The most common of such triggers are dietary, such as excess salt consumption or caffeine use, or weather changes especially swings in barometric pressure. It is clear from the huge numbers of reports I see daily in support groups that people really do feel that they experience fluctuations in symptoms that seem to match up with one or more of such triggers, and in the case of diet, many find that avoiding a trigger leads them to feel that they suffer less. If this is you, definitely keep doing what works for you.

There is another possible side to the trigger story though - we already saw that expectations really matter and anxiety is a known trigger in itself. So there is a danger that a heavy focus on triggers could potentially make things worse. For example, suddenly noticing from a packet or menu that the meal just eaten was a salt bomb may well totally stress many sufferers and that alone may worsen or even start symptoms. This is in no way however intended to suggest that salt or other triggers are not an issue for some people - clearly they are.

When it comes to barometric pressure as a trigger, it is an intriguing topic. Here the possibilities for the nocebo effect are worth bearing in mind - many people use apps to monitor the weather and pressure and to look for forecasts. Is there a danger that due to the very real impact that expectation can have these forecasts may worsen things for some people? I suspect there is but I’d love to see some studies on it. The interplay between what is really happening physically and the expectation will be complex and I’m sure there won’t be an easy answer. Again this is not in any way a suggestion that people don’t experience the symptoms that they report when weather or pressure changes.

There is an expanding range of tracker apps suddenly becoming available for Meniere’s, largely due to the huge advances in AI coding allowing more people to quickly write software. Some of these apps are beginning to try to “predict” when you might get attacks, based on automatically pulling in weather forecasts and pressure data, or dietary information such as salt consumption. I can see how this looks like added value and important information for people to have in planning. Based on what we know though about the power of expectation I also have concerns that these predictions could become, in some situations at least, self-fulfilling.

Meniere’s disease and related vestibular disorders such as vestibular migraine are heavily intertwined with the placebo and nocebo effects, both in trying to assess whether treatments really help and also potentially in thinking about and managing triggers. I would love to see a proper study of expectation in Meniere’s and one or more of these tracking apps could even form the basis for it. Could be really fascinating!

AI Statement

No AI was used to create the text in this article. AI was used at times to help with some of the research, but sources were always followed up and no AI output was used in the final text. AI was used to help generate the some of the images and thumbnail

So it is of course hugely exciting to be able to bring you news of a recently published paper that describes work from all three of these great Meniere’s researchers (alongside others). This study demonstrates quite conclusively that a fault in a gene that causes a rare issue with bone formation also makes it much more likely that the endolymphatic sac in the inner ear will not develop properly which in turn can lead to Meniere’s disease. It is worth saying from the outset that this gene fault is very rare, so this is not a discovery that has implications for most Meniere’s sufferers, but it is exciting confirmation of one genetic route by which Meniere’s can occur.

The paper is available here. The disease that the investigators examined is called “X-Linked Hypophosphatemia” (XLH). The last part means literally “Low (hypo) phosphate in the blood (-emia)”.

To understand what X-linked means requires us to remember some basic genetics. Every cell in our bodies contains genes, the instructions for making all the proteins needed to build and run a human. Those genes are gathered into packages called chromosomes, and we have 23 pairs of packages in most cells.

One package in each pair comes from mum and one from dad, so although these two copies contain the instructions for making certain proteins, the copy from each parent might be slightly different. This pairing makes genes robust - if there is a mutation in an essential gene in one of the pairs, chances are the other will be ok. One pair though is special, as they determine the sex of the person. Chromosome pair 23 consists of some combination of two chromosomes that are not the same, one shaped like a “X” and one like a “Y”. Females end up having two copies of the X - one from each parent, whereas males will have one X and one Y. The X and Y chromosomes do not contain the same genes - which is one reason males and females develop differently. This also means that males are at a disadvantage - if there are mutations in their X chromosome, there is no backup copy. This is what X-linked means - a condition that stems from changes in the X chromosome, making that change much more likely to have an impact on males.

So we have a disease caused by a genetic change to a gene called “PHEX” on the X-chromosome that is therefore more likely to impact males and leads to a shortage of an essential chemical - phosphate - in the blood. If the genetic change totally breaks the gene so that it no longer does any of what it should, it is called a “loss-of-function” mutation. Phosphate, along with calcium, is required to build solid bone - these substances convert the collagen mesh that initially forms as bone grows into rigid strong bone. Lack of phosphate leads to soft bones, risk of stress fractures, dental issues and arthritis in adults, and in children bow-leggedness, short stature and issues walking that are sometimes called “rickets”.

What did the researchers do?

The work of Andreas Eckhard and David Bächinger that I previously covered showed that a subgroup of about 30% of Meniere’s patients have a characteristic deformity of the inner ear. Their endolymphatic sac has not properly developed (termed “hypoplastic”). This can be seen by checking the bone structure of the skull from scans of the head. People with this issue tend to be men and to develop bilateral Meniere’s more often. (The other 70% of Meniere’s sufferers have a sac that has deteriorated or “degenerated” for some reason). The researchers suspected that maybe there was a connection between the XLH genetic disorder and this under development of the endolymphatic sac.

They recruited 33 people with XLH and examined them to see which had Meniere’s and of those, which appeared to have the under developed endolymphatic sac. Meniere’s is thought to impact around 2 out of every 1000 of the population, and only 30% of those will be in the "hypoplastic” subgroup we are interested in. XLH is even rarer, at around 5 per 100,000 people. So the chances of someone having both at random if they were not connected is a tiny 1 in 33 million. And yet of the 10 men and 23 women with XLH in the study, 6 had Meniere’s and showed an underdeveloped sac. This is incredibly unlikely to be down to chance alone, and is a strong indication of some kind of connection between the gene mutation and this form of Meniere’s. All were men, which fits with the previous work on hypoplastic sacs in Meniere’s.

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The “Gene Dosage” idea

There is some important nuance that I have so far missed out in order to simplify the explanation. In females, who have two copies of the X chromosome, which one gets used? The answer is that each cell seems to randomly switch off one or other of them, meaning that some cells get the faulty PHEX gene and some get the working one. This “mosaic” pattern means that although females can suffer symptoms from the PHEX gene they are generally not so bad. This study found exactly that, with those women that had Meniere’s suffering less severe vertigo and structural damage. It is also possible for the PHEX gene to be faulty but not entirely broken. In that case, it would still party do its job. This explains why there were also men who had Meniere’s but with less severe symptoms.

What this means for the future

This is the first study to link the PHEX gene to inner ear issues that can drive development of Meniere’s. It strongly suggests that men with fully broken PHEX genes are at a very high risk of developing bilateral Meniere’s disease. This means that early genetic testing combined with scans to look for poorly developed endolymphatic sacs can identify Meniere’s risk much earlier, before hearing loss or balance issues begin occurring. This in turn gives the possibility that targeted treatments may be able to prevent development of Meniere’s in these people. Just one example of the way that advances in genetic testing aligned with good quality science is pushing our understanding of Meniere’s ever further.

huge thanks to David Bächinger, one of the authors of the research, who checked the article for me.

Additional Resources

NIH Intro to Chromosomes - https://www.genome.gov/genetics-glossary/Chromosome

Wikipedia on SLH - https://en.wikipedia.org/wiki/X-linked_hypophosphatemia

Image attribution

1. NIH (Public domain)

2. 23 chromosomes ZBY360, CC BY-SA 4.0

3. Modified from https://www.frontiersin.org/journals/neurology/articles/10.3389/fneur.2025.1607435/full CC BY license

AI Statement

No AI was used to create the text in this article. AI was used at times to help with some of the research, but sources were always followed up and no AI output was used in the final text. AI was used to help generate the some of the images and thumbnail

I want to issue a caveat at the outset. I knew nothing about AIED when I began writing this and my knowledge is still far from deep or exhaustive. I am really trying to just present an overview of a topic which I am quite sure we will return to and it may be too shallow for those with a good understanding. If there are genuine errors please let me know.

AIED was first formally defined in 1979. Patients had begun to complain to Dr. Brian McCabe in Iowa of a rapid decline in their hearing over the course of just a few days or weeks, often in both ears. Taking high dose corticosteroids seemed to reverse some or all of this hearing loss. Given that one of the main features of steroids is that they dampen down immune responses, Dr McCabe reasoned that the cause was likely to be some kind of immune interaction in the inner ear. The assumption was that this was an autoimmune or autoinflammatory reaction where the immune system mistakenly attacks parts of its own body, in this case the inner ear. Since then AIED has gone on to be recognised as a distinct but rare inner ear condition, impacting less than 5 people per 100,000 every year. Like many autoimmune conditions sufferers seem to be predominantly (but not exclusively) middle-aged women.

Symptoms

The primary symptom of AIED is hearing loss, which may initially be one side but very frequently ends up eventually affecting both ears.

The kind of hearing loss we are discussing is called “sensorineural” hearing loss - that means it is something wrong with the fundamental sound sensing abilities in the inner ear and the nerves going to the brain, rather than some issue with the way the sound gets into the inner ear like a blockage or damage to the eardrum or middle ear, which would be called “conductive” hearing loss.

The defining feature is that this hearing loss comes on quickly. Anything between three days and three months for a substantial thirty decibel drop. This distinguishes it from both “sudden hearing loss” which might come on in a matter of minutes or hours, and the gradual decline that often accompanies Meniere’s disease and some other progressive conditions. Although most of the hearing loss is “sensorineural” in nature, up to a third of patients also show some conductive hearing loss, due to some additional eustachian tube or middle ear issue. It is though one of the few causes of sensorineural hearing loss that is reversible if treated early enough with steroids or other drugs to dampen the immune system. Around a half of sufferers also report problems with balance ranging from mild dizziness to intense vertigo episodes, and some also report tinnitus and feeling as if their ears are full or stuffy.

Progression and other illnesses

If untreated AIED leads to various forms of damage to the cochlea, the hearing part of the inner ear. The intense immune system activity can dump large amounts of debris, so called “immune complexes” resulting from the war it has mistakenly fought, and this debris can damage tissues especially the crucial boundaries of the inner ear that look after fluids passing in and out. The resulting damage can result in inflammation and build up of scar tissue (“fibrosis”) and even bone in places it shouldn’t be. Once this level of damage occurs, sometimes in just months, it is no longer reversible. The hearing loss can progress within three years to the point of needing a cochlear implant.

Some 15-30% of sufferers will also have one or more other autoimmune conditions, such as Lupus, Rheumatoid Arthritis, Cogan’s or Sjögren’s Syndrome - for these people flare ups of the AIED will often occur at the same time as increases in the other symptoms. The majority of people, up to 85% will have no other immune disorder and their inner ear is the primary site of autoimmune damage.

So why is this happening? The immune system is a highly complex and really rather incredible system. The outside world is full of tiny microbes that will do us harm if allowed to get inside our bodies and start copying themselves. The immune system looks out for these things and creates dedicated pattern-recognisers called antibodies to attach to them to label them as “bad guys” that need attacking, Normally this system works great, but every so often things don’t go to plan. The first thing that can go wrong is a simple case of mistaken identity. The "recognisers” have a pattern imprinted into them that accidentally also matches some essential element in the body. For example, exposure to a real bacteria or mould might prime the body to be ready to attack if more comes along, and the immune system attaches “kill this” flags to some similar-looking important inner ear protein by mistake. The other way things go wrong is a kind of collateral damage. Sometimes a major immune response to infection triggers autoreactive immune cells to go into overdrive, and pretty much attack anything around them, including the body’s own cells. Of course, neither of these things should happen in a properly functioning immune system, and the precise genetic causes for why they do occur in some people are being explored.

Diagnosis and Treatment

The immune system leaves significant evidence of its work circulating around the body in the blood. For example the kind of mistaken identity mentioned can result in a huge release of a substance called “interleukin 1 beta” (IL-1beta). There has also be found to be a big increase in antibodies to a protein called HSP70 in some AIED sufferers. These and other markers of inflammation and autoimmune illness can potentially be found in blood samples, providing one approach to diagnosis. However these tests are not especially reliable and so diagnosis becomes more about the symptoms and progression of the illness, in particular the rapid reduction in hearing in one or both ears. As with Meniere’s, an MRI is usually done to rule out other causes such as tumors and more recently with the right MRI approach and suitable contrast dyes, inner ear inflammation and damage can be seen too.

The other hallmark of AIED is how readily it seems to respond, in the early stages at least, to high dose steroid treatment. If AIED is suspected, this is usually the first treatment attempted, and if the hearing improves then AIED is considered much more likely. If high dose oral steroids don’t help, the other approach is injection of steroids through the ear drum into the middle ear in the hope that at least some of it finds its way into the inner ear.

Steroids are not a long term solution for most people as the body gets accustomed to them and they often become ineffective. High dose oral steroids are also not considered safe long term with side-effects such as weight and blood pressure increases, diabetes, osteoporosis, risk of infections, and mental health issues. There are other drugs that have been developed to target autoimmune conditions such as methotrexate, and these have often then been tried for AIED.

Comparison with Meniere’s

On paper, despite some substantial symptom overlap it initially looks as if Meniere’s and AIED are quite distinct. With AIED we have a focus on hearing loss which is quick and often bilateral, the condition is reversible in many cases if caught early, there are balance issues but much less of the full-on vertigo that is typical for Meniere’s, the cause is known and only about half of AIED cases show excess inner ear fluid (hydrops). Clear cut. AIED is not Meniere’s. In theory. That was until I started asking patients about it.

To get the patient experience I joined a Facebook AIED group and started reading some posts. My first thought was that everyone sounded like they had Meniere’s. The posts were impossible to distinguish from those in the many Meniere’s forums. Both on Facebook and Reddit many people offered their stories and it became very clear that, well, absolutely nothing was very clear. Few people fit into the nice separate diagnostic boxes that the doctors are trying to use to attach labels to the conditions. People have complex mixes of symptoms which are highly subjective, and even those easily measured like hearing loss seem to be hugely variable. I don’t envy the doctors trying to decipher this, nor the patient who wants answers and feels like they aren’t getting them. Here are a few quotes:

“I no longer care what disease it is called. What I am worried about is how it will develop in the long term”

“Take the marker tests and do a steroid trial. Be careful. I think many in the US over diagnose AIED and then prescribe highly toxic medication (methotrexate and the like).”

“I’m currently trying to figure out whether this fits better with Ménière’s (though not a typical case for me), migraine, or possibly AIED.”

“I see AIED as sitting under the umbrella of Ménière’s disease. It has the same symptoms, it’s just that it has an option to be treated by immune suppressants.”

“I’ve been diagnosed differently by different people and at different times over my 11 years since my first ear dropped, Ménière’s disease, autoimmune disorder of the inner ear, and vestibular migraine.”

Is Meniere’s really AIED?

So are they the same? Recent work that by Antonio Lopez-Escamez and others that I’ve written about has shown that there seem to be at least four distinct subtypes of Meniere’s with potentially different origins that can be identified by detectable markers in the blood.

Some have a high level of an antibody called IgE that indicates an allergic response. Around 20% have abnormally high levels of an immune signalling molecule called TNF-alpha suggestive of an autoimmune condition. And close to 15% of Meniere’s patients seemed to have excess of the marker IL-1beta we mentioned previously. The remaining patients have low inflammatory markers and probably have some direct genetic cause for their illness.

So we have about 35% of Meniere’s sufferers having similar biomarkers to those found in AIED, showing the same kind of immune system malfunction as AIED. In Meniere’s though the immune system is thought to be attacking the part of the fluid regulation system - the endolymphatic sac, whereas in AIED it is thought the damage is being done directly to the hair cells and hearing mechanisms. If both were to be attacked then AIED and Meniere’s would truly be one and the same for that patient. In either case, the treatment is the same - steroids. Maybe this also explains why some Meniere’s sufferers seem to benefit from steroids and others don’t. If doesn’t seem like a stretch to suggest that for this 35% of Meniere’s sufferers, they effectively seem to have a form of AIED.

There have been great advances in the ability to isolate the immune system biomarkers and at the same time perform genetic testing. From these tests it is then possible to infer what may be going wrong with the immune system and choose a much more carefully targeted drug therapy, such as Anakinra, Etanercept, Rituximab and others.

Wrap Up

This is the extent of my current knowledge on AIED and its overlap with Meniere’s. I suspect that labelling Meniere’s as a single condition is a big part of the confusion and hopefully it will become much more common to try to work out which subtype people are suffering from. What is clear at the moment is that there is a gulf between the clean diagnostic boxes and labels coming out of many studies and research and that inform doctors, and the experience of patients who simply have a confusing, disturbing and life changing set of worsening symptoms. “I don’t care what you call it, just help me get better”.

Further Reading

• What is AIED (VeDA) https://vestibular.org/wp-content/uploads/2024/10/Autoimmune-Inner-Ear-Disorder-AIED_5_cobranded.pdf

• Autoimmune inner ear disease (AIED): A diagnostic challenge https://pmc.ncbi.nlm.nih.gov/articles/PMC6213300/

• AAO: Autoimmune and Autoinflammatory (Disease) in Otology: What is New in Immune‐Mediated Hearing Loss https://pmc.ncbi.nlm.nih.gov/articles/PMC5113311/

• Decoding the impact of autoinflammatory/autoimmune diseases on inner ear harmony and hearing loss https://www.explorationpub.com/Journals/ei/Article/1003129

• AIED Presenting as Meneire’s https://www.cambridge.org/core/journals/journal-of-laryngology-and-otology/article/autoimmune-inner-ear-disease-presenting-as-menieres-disease/B6DEEF935BE9E7D6FB30EF85834CE1B9

• Cochlear immunology and its therapeutic revolution https://pmc.ncbi.nlm.nih.gov/articles/PMC12644081/

AI Statement

No AI was used to create the text in this article. AI was used at times to help with some of the research, but sources were always followed up and no AI output was used in the final text. AI was used to help generate the some of the images and thumbnail

So what is this it? How is it thought to help and does it really do anything? Why is it not available in the USA? Let’s talk all things betahistine!

History

In the late 19th century, there was a lot of excitement when it was discovered that many systems in the body were looking after themselves outside of our conscious control - the so called “autonomic nervous system”. Things like the rate your heart beats, flushing of the skin when embarrassed or hot, blood pressure and many other body functions seem to react without being explicitly told to. As always when a new discovery comes along, people try to see everything through this new lens and feel that maybe it holds the keys to conditions and illnesses previously not understood. For example, cutting nerves that form part of the “fight or flight” nervous system was for a while a common treatment for glaucoma - excess fluid pressure in the eye. If this approach could help over-pressure in the eye, why not try it too for the inner ear condition “Meniere’s Disease” which by then had been thought to also possibly be a fluid pressure issue. A treatment for Meniere’s was developed that involved severing or clamping a branch of a nerve somewhere in the chest area of the spine. Like many many attempted Meniere’s treatments, some people felt this worked. In the end severing nerves for glaucoma was stopped in the early 20th century as long term outcomes were poor. However due to the hugely fluctuating symptom pattern of Meniere’s it was much harder to know what was and was not working, and such nerve cutting continued right up until the 1970s.

Many of the automatic systems that had been found related to circulation of blood and naturally people wondered if some of these afflictions related to blood flow issues. For example, a nasty problem that I happen to suffer called “Reynaud’s syndrome” causes the circulation in the fingers and toes to shut down due to spasms of the blood vessels in reaction to temperature changes. People began to think that maybe Meniere’s was a kind of “Reynaud’s of the inner ear” - some kind of blood vessel spasm or restriction. If some way could be found to improve inner ear blood flow maybe that might deal with the symptoms of Meniere’s.

Betahistine (in the chemical form betahistine dihydrochloride) was first synthesised in 1904 but as so often with such compounds, it wasn’t really known what it was or what to do with it and it seems to have sat around for nearly 40 years. Then in the 1940s it was found that it mimics histamine, which we spent some time looking at previously. In the 1960s experiments on animals seemed to show that the drug generated increased blood flow in the inner ear of guinea pigs so maybe it would help with Meniere’s. An advantage was that at the time, most drugs for vestibular disorders tended to be sedative and betahistine turned out not to be.

In 1966 betahistine, under the brand name Serc was initially licensed for use in the USA on the basis of a single study that seemed to show it was effective at reducing both vertigo and tinnitus. The drug was registered in Europe in 1970. At around this time however the USA began to tighten regulation on drugs and to demand a higher standard of proof than had been previously required. The single trial of Serc was heavily criticised. In particular there were only 18 subjects in the trial and it only lasted two weeks - far from what would be required these days to even hint that a drug for a highly fluctuating condition like Meniere’s “works”. The USA approval for betahistine was withdrawn in 1972 and has never been reinstated.

In the meantime Europe and other countries were taking a different more pragmatic approach to drug licensing. What mattered most was the safety - if a drug has a very good safety profile, there was little to be lost in offering it even when the evidence for it working may be mixed. Betahistine had been shown to be very safe in many different studies. A review of safety data in 2005 stated that over 35 years and more than 130 million patients only about 500 reports of adverse reactions had been received, most of them mild and not serious. Betahistine became a hugely popular “first line” drug for Meniere’s. A 2025 survey of treatments for vestibular disorders found that for Meniere’s 76% of doctors worldwide were prescribing it.

How might it be working?

Betahistine is often described as being like histamine - in other words it can trigger some of the reactions in the body that histamine does. As we will see there is a lot more to it than that but it is a good start. However it is not histamine, which matters for taking it as a tablet. If you want a drug to be effective taken as a pill, it has to make it into the bloodstream and histamine as we saw previously is for most people immediately broken down in the gut by a substance called DAO. Betahistine on the other hand was thought to make it through so that it could be delivered around the body by the blood, in particular to the brain and the inner ear where it might work some magic.

If you didn’t read the earlier article about histamine, and the histamine receptors, it might be helpful in what follows - if you have time it is here:

Over the years researchers have drilled into the specific action of betahistine and found that it not only behaves like histamine in some ways, it also acts like an antihistamine. To understand this we have to remember that histamine achieves its effects in the body by latching on to special receptors which then trigger the various responses. We have four such receptors (H1-H4), all of which histamine can attach to, each doing a different job. Betahistine was found to have complicated interaction’s with H1 and H3 receptors, and no real significant impact on H2 and H4. The lack of interaction with H2 is a bonus - it means the drug should not cause any release of stomach acid or cause digestive issues. For H1, it behaves in the much the same way that histamine does. We might then expect an allergic type response in the body, similar to histamine operating on these receptors. However the triggering of H1 by betahistine is very weak (maybe only one fifth as strong as the response produced by histamine).

The strongest effect is on the H3 receptors. Betahistine binds to H3 receptors as an “inverse agonist” - pushing the H3 receptor into an inactive state and preventing histamine from interacting with it. This receptor is found widely in the brain including the areas that process balance and eye movements, as well as in the inner ear hair cells and the all-important areas that manage the chemical makeup of the inner ear fluid (stria vascularis and endolymphatic sac). If the anatomy of the inner ear is new to you, check out these articles:

So we have betahistine attaching to and deactivating H3 receptors that are found in the brain and inner ear, and mildly triggering H1 receptors. Does this give us reason to think it might be helpful for Meniere’s? First the H1 receptors. One theory is that by taking up the place that histamine could otherwise occupy, but only giving a mild activation , betahistine might be acting almost as an antihistamine in the balance centers of the brain like a mild version of the typical antihistamines used for motion-sickness. In addition, triggering H1 receptors in the inner ear might open up blood vessels and allow greater movement of fluids across the various membranes. This sounds like something we might need if the “blood flow” theory of Meniere’s was correct (and would fit with the earlier experiments in guinea pigs). However the weak effect of betahistine on H1 makes it unlikely that this will be particularly significant. If anything, the real impact is likely to be due to H3. So what does that do? This is somewhat complicated so take a pause, grab a coffee and we’ll walk through it.

Stepping way from betahistine for a moment, H3 mainly controls the release of histamine and other essential brain messenger chemicals. More precisely, when triggered it reduces production of these chemicals. So this is like a self-controlling loop - some part of the brain releases histamine, some of that histamine binds to these H3 receptors and prevents too much more histamine being released. Part of a very finely balanced feedback system. Betahistine, by setting H3 inactive, may result in more real histamine floating around. Why might that help? In the inner ear we already saw that H1 could maybe help with blood flow and fluid regulation, and now we have more of the real deal histamine to bind to H1. Could this be producing more blood flow and better fluid management? And in the brain we have now more histamine to bind to H1 in the vestibular regions. Is that good? Previously we saw that reducing H1 activity in the vestibular areas of the brain can control motion-sickness, so how will increasing it help? During the period of a real attack of vertigo it likely won’t. However outside of that period, having more activity in the balance center of the brain is useful to help train these neurons to deal with the slightly screwy signals coming from your inner ears - a process called vestibular compensation. The antihistamines used to control dizziness can sometimes interfere with this process if taken too regularly. Since betahistine tends to be taken all the time, not just during vertigo, it may have a role in this “vestibular compensation” process, but that won’t directly prevent attacks of vertigo. Finally there is even some evidence that H3 might directly influence blood flow in the inner ear.

When looking at how betahistine might have benefits, there is one last possibility. When the drug is broken down by the body, the first thing it is converted into is a substance that may actually reduce the activity of neurons in the semicircular canals themselves - the things that are sending wonky signals giving rise to the vertigo in the first place.

What types are there and how much to take

Doses are hugely variable. It is common to start at around 24mg per day. The drug takes about an hour to peak in your body, and within 3-4 hours the level will be halved. Due to this very short “half-life”, it is usually taken 3 times a day to keep levels up. For example 8mg x 3 to make 24mg. However due to the safety profile, many doctors see no issue with increasing the dose if the patient does not see benefit, up to a licensed maximum in the UK and EU of 48mg a day. However studies have been conducted at much higher doses, and it is quite common especially in Europe to see doses as high as 144mg per day or even higher. This requires a doctor willing to prescribe “off-label”. I was on 144mg for over 6 months at one point. Doses up to 480mg have also been studied in Germany.

There are numerous brands worldwide, and the drug is available from many sources (although in the USA must be obtained from a compounding pharmacy). The brand doesn’t matter. The active ingredient will normally be betahistine (di)hydrochloride, although betahistine mesilate is also available, but typically requires a higher dose to get the same amount of drug into the body.

Given that the way the drug works is unclear, it is also not obvious how long it might take to work. The drug itself is quickly available in the body and only lasts there a short time, so that might suggest a fast response. However if the benefit were to come from vestibular compensation then it may take a long time for any improvement to show. Most people who say it helps seem to report needing several weeks to notice anything.

Possible Rare Side Effects

• Commonly listed include stomach and digestive issues (recommended to take with food if possible), headache and mild dizziness or drowsiness. The fact that these are listed as side effects does not necessarily mean the drug causes them due to the way side-effects tend to get reported.

• Rare - need medical attention

  • Allergy style effects - runny nose, stuffy etc - if the body is low on DOA it may be allowing more histamine from food into the bloodstream so adding betahistine might push the patient over the edge into having an allergic type response. Any allergic reaction needs raising with a doctor

  • Asthma - doctors need to know if you have asthma as the above allergic reaction may also rarely combine with the tendency to breathing difficulties.

  • Heart issues - palpitations, heart rate issues

  • Convulsions, confusion, hallucination (extremely rare)

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Possible Interaction with Antihistamines

It is often said that you should not take betahistine and antihistamines at the same time, on the basis that “one is histamine the other is antihistamine”. However as we have seen the way betahistine might be working is more complex and subtle. Antihistamines block H1 receptors. Betahistine may have a small direct impact on H1 although that is not clear. It may also (via H3 trigger) release of histamine that then might be having an impact through H1. Remember though that modern antihistamines don’t enter the brain, where betahistine may be having some impact. This all suggests a theoretical risk that antihistamines might prevent betahistine working to some degree, but since the way betahistine works is not at all clear, this is speculative. To my knowledge there have been no studies demonstrating this connection, but it is something you may need to try for yourself.

Does it Work?

“Doesn’t help me for anything”
“I can’t be without it”
“I take it for the extreme vertigo and it works miraculously.”
“Did not make a difference for me :(”
“The best thing I ever had in 48 years..”
“I’ve taken for over 13 months no side effects, unfortunately it didn’t work for me”
“Game changer for me.”
“Did absolutely nothing for me :( “
“Absolute miracle drug. I’ve been in total remission since starting 2.5 years ago”
“Dr took me off them, they made things worse”

This is just a tiny selection of the comments I’ve seen about the most common Meniere’s drug from years of reading support forums. Betahistine has been prescribed by some 94% of ENTs in the UK for Meniere’s patients, and yet seems to totally divide people about its usefulness.

There were early studies that seemed to show some effectiveness for reducing the frequency and severity of vertigo. It would be easy to write an entire article on the various studies and what their strengths and weaknesses were. The most obvious issue as with all treatments for Meniere’s is the hugely fluctuating nature of the condition, the fact that it naturally goes into periods of remission and then has flares that last some weeks or months. Add to this that most people try novel medications when they are feeling at their worst, so are quite likely to naturally start feeling better at some point after taking the new medicine. Then there are issues of standardising how to measure improvements in vertigo (what do we mean by “works”?) and the difficulty of finding a group to compare to given how wildly different peoples symptoms can be. So you need a lot of people in your study, but there aren’t a lot of people with Meniere’s. All of this makes studying treatments like betahistine very hard. The most comprehensive recent studies include the BEMED Trial in 2016 which looked at over 200 patients over 12 months and concluded there was no benefit to betahistine. In addition, the renowned Cochrane Collaboration in 2016 updated their review and looked at 17 previous studies with over 1000 participants. They concluded that there may be some benefit but the overall quality of evidence from all the studies they could find was low, so they could not state anything with confidence.

Why do studies not show a clear benefit?

One answer could be that the drug does nothing for Meniere’s. However the huge number of patients who feel that it does should at least force us to consider other options. Another issue as we have said is the huge fluctuations in Meniere’s and the problem of knowing if something is “really” working. All approaches suffer this, from dietary restriction to use of diuretics to surgical treatments. Then there is the underlying idea that Meniere’s is fundamentally a blood flow issue that betahistine can correct. This is far from agreed and recent evidence points more toward issues with the way the inner ear manages levels of sodium and potassium. There are though another couple of problems worth thinking about.

We said earlier that betahistine, unlike histamine, makes it into the bloodstream. But it turns out that more than 95% of drug seems to be converted in the digestive system into something else that is no use. This time the conversion is done by not “DAO” but a different substance called “MAO”. Experiments in animals that have shown increased blood flow have tended to use very high doses directly applied into the inner ear (or to samples in petri dishes). We may be getting a tiny fraction of those doses when we take betahistine as tablets. This may be a reason to consider very high dose regimes, or other delivery systems such as nasal sprays. To investigate this further, an experiment has been done using a substance called “Selegiline” that stops MAO from working that is taken alongside betahistine. This seems to increase the amount of betahistine available for use in the body 80-100 times. However to date I’m not aware that this has been tested with Meniere’s patients so the impact on vertigo is still unknown.

The last wrinkle may be the most important. It has become increasingly clear in the past few years that there are distinct subtypes of Meniere’s that have potentially different underlying causes. It may well be that betahistine is indeed effective, but only for one subtype. In that case every time a study is done on a big pool of generic “Meniere’s sufferers”, you will have mix of types and therefore a mixed muddy result. Future testing of drugs like betahistine would benefit from determining which sub-type each subject is in, or focussing on specific sub-types. The “allergic” type of Meniere’s is potentially thought most likely to respond if any.

Wrap Up

After all that what can we conclude? There is little good evidence from studies that betahistine works and it is not entirely clear how it might be working if it does do something. However it is safe, and it might just work if you are one of the lucky ones.

Quote from Doctor and researcher:
“In clinical practice I still offer a trial of betahistine to most patients. When I do, I usually opt for a relatively high-dose regimen. If there is no clear benefit, or if the patient remains attack-free for at least six months, I discontinue the treatment. I also think it’s important to emphasize that betahistine should not be used as a symptomatic or “on-demand” medication for acute attacks, despite the fact that it is sometimes prescribed or taken in that way.”

Huge thank you to Dr David Bächinger who helped to provide some of the references and scientific background, and also read a draft to check for errors and omissions.

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Additional Resources

The Role of Betahistine in the Management of Vertigo https://www.thieme-connect.com/products/ejournals/pdf/10.1055/s-0038-1676875.pdf

Betahistine Summary of Product Characteristics Sheet https://assets.hpra.ie/products/Human/30047/Licence_PA23355-014-001_20032026140428.pdf

Distribution of histamine receptors in the inner ear https://www.mdpi.com/2076-3425/13/7/1101

Real deep dive into Histamine in the vestibular system https://hal.science/hal-04790288v1

AI Statement

No AI was used to create the text in this article. AI was used at times to help with some of the research, but sources were always followed up and no AI output was used in the final text. AI was used to help generate the thumbnail

I know what you are saying. I don’t blame you, you can’t help it - I’m tempted to say it too - “But maybe it will stay this time, maybe it will be ok”. All I can do is look up wearily, broken and ground down, try to briefly hold your gaze long enough to say “I’ve been here before. Many, many times.”. This is the cruel chaos of an unpredictable chronic condition, never knowing what the next week, day or even hour is going to bring. No chance to find a new normal.

Not all illness and health issues are like this, and it is worth looking a bit deeper to understand just why Meniere’s and similar unpredictable long-term conditions are just so energy sapping, demoralising and why they might potentially give rise to additional health problems. We can start by looking at situations that should from the outside be awful and yet seem not to be.

I recently came across the “Disability Paradox”. I’d known the basic idea for a while but didn’t know it had a name. Studies of people with life-altering disabilities such as losing a limb go through a period of adjustment after which they typically experience a good or even great quality of life which is at odds with what most people imagine would be their situation. They redefine themselves, create a new life and adapt. This is not to suggest that everything is great, or to minimise the suffering, and of course there will enormous challenges. Humans though are incredibly adaptable, and form new habits amazingly easily and quickly. I would argue that a key part of that ability to adjust and adapt is the consistency and predictability of the changes brought about by the illness or disability. There is a new normal to become used to. When things follow a predictable path, even if the medical condition is serious and declining, we can build a model of it and find ways to think and plan around it. We can build a new life, even if it is one with different activities based on reassessing what we can and can’t do.

The work of a nurse called Merle Mischel in the late 1990s resulted in the “Uncertainty in Illness Theory” - this is the idea that patients will suffer high levels of uncertainty if they can’t work out what is going on with their illness. If they are unable to fully understand their symptoms or they constantly change, if they don’t know what a treatment will do or if it will be effective, and if they are unable to predict the future of their condition to any degree, they are likely to feel high levels of uncertainty. The original work of Mischel was around finding ways to reduce that uncertainty, which can arise for many reasons in various illnesses, maybe due to lack of information, poor communication, lack of structure in the medical system and so on. Our ability to mentally cope is impacted a lot by whether we can construct a good story about what is happening, why, and how we can cope, and with many illnesses and injuries, the treatments and symptom progression can be fairly well understood if communicated properly. But what if this uncertainty is actually inherent in the medical condition itself? That is where we are with Meniere’s. The unpredictability and uncertainty is baked in.

If by some chance you are reading this and are not a Meniere’s sufferer or are unfamiliar with it, I have described my personal experiences with it in one of the first articles I wrote, linked below. However there is nothing unique about Meniere’s - there are other unpredictable chronic illnesses, such as forms of Lupus.

Evidence suggests those of us suffering unpredictable, episodic conditions really are subjectively worse off than those with severe but steadily declining illnesses. We can’t adapt mentally or physically, we may not be able to work due to fluctuating patterns of our illness. We are constantly fearful of the next attack or relapse, and that fear is constant, ongoing and corrosive, leading to us avoiding activities and events and isolating ourselves. All of this results in high levels of stress and anxiety, and this is now known to be a potential cause of health issues. Our cortisol levels become continually unnaturally high leading to the chance of increased overall inflammation and poorer health outcomes.

If we look at data on Meniere’s, it has been suggested that some 74% of sufferer’s avoid specific social situations or physical activities for fear of feeling ill or not being able to hear, or due to the potential embarrassment of a vertigo attack that might have associated vomiting or worse. Anyone who has had one or more “drop attacks”, a particularly nasty feature of Meniere’s where an unseen force appears to literally shove you hard without warning to the ground, is likely to be traumatised and fearful of driving or even cycling. Three quarters of us feel that we are never free of discomfort, partly due to the ongoing symptoms and partly due to anxiety. Finally, up to 63% of Meniere’s patients show some form of psychological issue including depression which can form a vicious cycle as the stress itself can trigger vertigo.

Meniere’s of course plays fast and loose with our ability to work or hold down a job. If you can work, there is a good chance you will have periods of reduced productivity due to brain fog or tiredness. You will almost certainly need time off due to vertigo, and unlike most people who may fall ill at work, it is unlikely you would be able to easily get home without help if an attack strikes. You may well have anxiety about informing your employer about your condition. Should you end up without work, you then have the added anxiety of whether to inform a prospective employer when applying for a new job. All of this stress and anxiety… and you may have no issues at all for months, leading even those who know of your illness to begin to wonder what the fuss is all about.

What to do? How can we try to cope with this persistent uncertainty, to still live a life, and continue creating our personal story? I certainly don’t claim to have all the answers. First, if this resonates with you and you feel you may be suffering chronic anxiety or depression, please contact your doctor. These are serious issues but ones which do have the potential for treatment. For example, an approach with good evidence for managing anxiety is cognitive behavioural therapy, which will require the help of a qualified provider and would need referral through your doctor.

But there are a few other things you might consider doing. Firstly try to stay fit and healthy. Whatever you can find that fits with your current symptoms. Movement is good, movement outside could be even better. Exercise will help protect against the possible declines in health that stress can produce, can help reduce inflammation and can even be protective against depression.

Try to get good sleep - easier said than done I know with anxiety and fear of nighttime vertigo. But at least try to stack the odds in your favour by avoiding caffeine later in the day (assuming you drink it which many Meniere’s sufferers don’t), keeping the bedroom dark and cool, avoiding screens just before bed and sticking wherever possible to a regular sleep schedule (something else Meniere’s messes with - the number of times I’ve been unable to sleep at night having had to spend all day in bed with vertigo!). If you are managing to get some exercise in that will have the added benefit of helping with sleep.

Consider gratitude journaling - find something, anything everyday or every few days that you are grateful for, however big or small and write it down. The thing itself is less important than the habit you are forming of looking for good things when your default may be to see the bad.

Then there is mindfulness meditation. Mindfulness is another practice, like journaling, that is designed to build a habit of mind. You are training your mind to focus on this very moment, not dwell on the past or future. You are also learning to look at this current moment from the outside, like a curious alien scientist. Maybe there is stress and anxiety. Rather than living it and inhabiting it, mindfulness gradually helps you to step outside it and view it as just another leaf floating past on the river, a cloud in the sky that will pass. This can be a very useful skill to develop. There are numerous apps and videos that can help - I found the Waking Up app from Sam Harris especially good. I should say though that I suspect it would take a supreme level of ability in meditation to remain detached and separate during the throws of a full-on vertigo attack - the maelstrom of intense stimulation and emotion is too much. But the rest of the time, in my view it has something to offer.

You might also choose to rewrite your own story, to redefine yourself. I often see people who say that they don’t let Meniere’s define them. I understand the perspective, and I try to continue planning and doing things on the assumption that I’ll be fine. But I’ve actually done the complete opposite. I have consciously redefined myself as someone who has Meniere’s. I’ve become curious and want to learn as much as I can about it. And I want to help others who have it by talking to experts and bringing their knowledge to you. So I guess that is my new identity and each key I press in writing this is me writing more of that story. Welcome to the new me.

Additional Resources

CBT in chronic disease https://www.sciencedirect.com/science/article/abs/pii/S0272735823001113

Guardian - Seeing posibility instead of doom https://www.theguardian.com/books/2026/apr/19/how-to-train-your-brain-to-see-possibility-instead-of-doom

If intensity of pain is unpredictable it hurts more https://www.jneurosci.org/content/33/13/5638

Anxiety about pain makes it hurt more https://www.jneurosci.org/content/21/24/9896

Not knowing if you will keep your job leads to bad health https://pubmed.ncbi.nlm.nih.gov/19596166/

AI Statement

AI was used to help in some of the research and data gathering, and to find some sources and in production or processing of some images. No AI at all was used in the production of the text.

What is Histamine?

Histamine is a powerful single substance found all over the place in the body. It is one of those “signalling” molecules that the body makes a lot of use of - it is released to tell certain parts of the body to do things. Histamine in the brain keeps you awake and alert, in the digestive system it triggers release of stomach acid to help digest food. In the skin it helps the body defend itself against foreign invaders and causes itching, reddening and swelling, in the lungs it can cause narrowing of airways (asthma) to try to prevent unrecognised substances getting deeper inside, and in the nose and eyes it drives immune reactions that can lead to swelling of nasal passages and release of fluids (the classic runny nose and streaming eyes of allergies such as hay fever).

But if histamine is a single molecule, and is found all over the body, why don’t we get these symptoms all the time? And how can this single molecule have such a variety of different effects? By the time we’re done my hope is you’ll have answers to these questions and a deeper appreciation of a fascinating system in the body. For those of you with a good background in this I should say my focus is a high level overview, and mainly only of those areas that are relevant to understanding Betahistine in a future article. However, as always, if there are glaring errors in what I do cover, please let me know.

Something vital to know about histamine is that when released in the body’s tissues, it doesn’t last long. Two different substances (DOA and HMNT) break histamine down usually within a few minutes. This means that is has to be stored near to where it is needed, and must be protected from these substances when it is stored. The main place that histamine is stored is in the “mast cells” - an essential element of our immune system. Inside these mast cells, histamine sits wrapped in protective granules to stop it degrading. (Histamine is also present in some foods - more about that later).

So we have lots of mast cells full of stored histamine all over the place, but especially in areas where histamine might be needed. What might trigger it to be released?

The main job of histamine that we will concern ourselves with here is signalling to the body that some kind of foreign invader has been recognised, and to set in motion the processes to deal with it. So the mast cells have to spot bacteria, viruses and other particles that could do damage. When such bad guys first enter the body, it goes into overdrive making “antibodies”. These are specially shaped molecules that can recognise the invader and bind themselves to it. After a complex series of events that we don’t need to worry about here, the end result is that mast cells in the vicinity become armed with pattern-matched trip-wires - they bristle with these little Y-shaped receptors (antibodies of a type called Immunoglobulin E or IgE) which fit together with the target bad particles. A single mast cell can have many different triggers each set up to match a different specific invader and is all primed and ready to react when needed. When the right foreign invader fits onto the receptor, the mast cell quickly releases the stored histamine (“degranulation”). If the body is reacting overly-sensitively to something common in the environment, such as pollen, the mast cell will also respond to these allergens resulting in an allergic reaction.

So we have a way for the body to quickly react, rightly or wrongly, to something it wants to deal with, at the point where it needs to be dealt with. An allergen binds to the specially shaped receptor and histamine is released. In addition to this “antibody” triggered release, the mast cell can also be triggered by standard detectors that it has for signals coming from nearby damaged or dying cells - you get histamine released if the skin is cut or punctured for example.

Now we have a way to release histamine, but how do we end up with the different responses to it in different parts of the body? Why don’t we get all the reactions that histamine can produce all at once whenever histamine is present? One reason is the local release of histamine only where it is needed, and the quick removal of it. So for example, if you prick your skin on a thorn, there are mast cells right there in the skin ready to release histamine in response to the damage. But additionally, although histamine is a single molecule, there are four different types of histamine receptors that do different jobs. (A receptor is simply a special structure on the surface of a cell that can be triggered by a certain messenger chemical). Numbered conveniently H1-H4, they are found in different parts of the body . The H2 receptors, for example, found in the gut, release gastric fluids for digestion when histamine comes along. H3 receptors will be of interest us when we look at Betahistine in the future, as they are found in the inner ear. H4 was only discovered in 2000 and looks like it has a role in inflammatory processes, but is an active area of research. The H1 receptor probably does the most jobs and is found in the walls of the lungs and airways, blood vessels, skin, nerves and the brain, and when triggered causes tightening of airways, opening of blood vessels, sensitisation of pain nerves (itching), wakefulness and much more. H1 is also found in the inner ear.

Antihistamines

When you hear talk of “antihistamine” you might imagine that they somehow prevent release of histamine and reduce the amount of histamine in the body. This is not what is happening. Instead what is happening is a blocking of the receptors, especially H1 and H2, from doing their job. All histamine receptors are designed to do their stuff when histamine locks on to them. Histamine is then called an “agonist” for the receptor - just means that it makes the receptor fire. So one way you could imagine preventing the receptor firing would be to somehow attach something that fitted the receptor but did not cause it to fire. That would block the receptor from being used by histamine. Such substances are called “antagonists” - they bond to the receptor, taking the place where histamine should go, but do nothing. When substances were found that could damp down allergic reactions - the first antihistamines - it was assumed that this was what they were doing.

Actually histamine receptors are also capable of acting even without histamine present - a base rate of activity that goes on all the time at a lower level, and increases when histamine comes along. When examined more closely it turned out that the antihistamine substances were not just blocking the receptor - they were turning down the base level of activity pretty much to zero. They are not just dumb blockers of the receptor, rather they are stopping the receptor activity all together. This gives them their modern name of “inverse agonists”. Antihistamine drugs are generally “inverse agonists” - they bind to the H1 (or in some cases H2) receptor and effectively turn it off. Whatever it was intended to do (promote fluid release or itching or swelling or constriction of airways or stomach acid production) it can’t do anymore. Voila - allergy treatment (H1) or reduction of gastric distress (H2).

Some of the early antihistamines were small molecules that could easily get from the blood into the brain, which meant that they also turned down H1 activity in the brain leading to sleepiness alongside other side-effects. Modern second-generation drugs don’t so easily make it into the brain, so avoid these issues. However one useful side effect of some of the first generation drugs was a reduction of vestibular and nausea activity in the brain, so drugs like dimenhydrinate (Dramamine), diphenhydramine (Benadryl), meclizine (Antivert), and promethazine (Phenergan) are antihistamines that can help some people with Meniere’s symptoms.

Histamine - friend and foe

So histamine is essential and everywhere, sometimes usefully and other times causing a massive nuisance as the body overreacts to things like pollen or dust mites. The ultimate form of this overreaction is the most dangerous. Earlier we asked why we don’t get all the reactions histamine can produce all at once. Actually, sometimes unfortunately we do. The body becomes overwhelmed by histamine and there is swelling of tissues, streaming eyes, reddening of skin, and most dangerously narrowing of airways making breathing difficult. This is “anaphylaxis” and is an emergency situation. Antihistamines will not help at this point. The treatment is adrenaline, administered usually via an “Epipen” which many allergy sufferers carry.

Histamine in food

Histamine is produced by the body from the substance “histidine” which is found in lots of foods, so many that it is very unlikely you would not be getting enough. However, when food is fermented, or simply allowed to age or begin to decay, bacteria convert the histidine in the food into histamine outside the body. Then when you consume these foods, you are ingesting large amounts of histamine directly. Most people have no issues with this - they have enough of the “antidote” DAO in the gut to neutralise the excess histamine. If for some reason you don’t have enough DAO, the excess histamine could potentially lead to various unpleasant symptoms, such as stomach issues, a rash or hives, a stuffy nose, and possibly migraines [1]. This last connection is relevant to us Meniere’s sufferers as we are much more likely to also suffer migraine. Note that this is not an allergy but rather a response directly to too much histamine. The concept of histamine intolerance is controversial and there is a lack of good evidence. Some estimates suggest that 1-3% of the population may have the issue, most of which are middle aged women, so quite rare. [2] But I can not find a reliable source to back these estimates. However if you suspect you may have symptoms related to histamine intolerance, the obvious first step is to reduce high-histamine foods such as fermented and aged foods (for a full list see Johns Hopkins low histamine diet link at the end). There is also some limited evidence to suggest that DAO supplements might be useful if taken before consuming histamine-laden food. [3]

Histamine and Migraine

The potential link between histamine and migraine is controversial. There is quite strong evidence to support the idea of triggers for migraine, some of which are histamine-containing such as the aged and fermented foods previously mentioned. What complicates the picture is that antihistamines do not appear to help, and DAO supplementation seems only likely to help those with a DAO-deficiency that has already led to a histamine intolerance. Evidence in the wider population seems to be lacking - migraine is another huge topic for another time.

Hopefully now you have a better view of what histamine is, how antihistamines might be working to block the action of histamine when it gets released at times you’d prefer it wasn’t, and the potential, hinted at least, of a connection to migraine and also to the inner ear. This is going to help a lot soon when we talk about the most widely prescribed drug for Meniere’s - Betahistine. Until then, stay spin-free!

Image Accreditation

1. https://www.nature.com/articles/s41598-020-71901-2

2. Resources from biorender.com

3. Widely distributed online, unable to find source

References

1. https://pmc.ncbi.nlm.nih.gov/articles/PMC10218803/

2. https://www.aaaai.org/tools-for-the-public/latest-research-summaries/the-journal-of-allergy-and-clinical-immunology-in/2023/histamine

3. https://www.clinicalnutritionespen.com/article/S2405-4577(23)02122-8/fulltext

Additional Resources

The Pharmacology of Antihistamines - https://pmc.ncbi.nlm.nih.gov/articles/PMC3666185/

Johns Hopkins Low-histamine diet https://www.hopkinsmedicine.org/-/media/johns-hopkins-childrens-center/documents/specialties/adolescent-medicine/cfs-low-histamine-diet.pdf

Intro to Histamine and Antihistamines

AI Statement

No AI was used to create the text in this article. AI was used at times to help with some of the research, but sources were always followed up and no AI output was used in the final text. AI was used to help generate the thumbnail

I’ve had Meniere’s for nearly 20 years. For a long time it was a case of dealing with the terrible occasional bouts of vertigo and hearing issues and then living a normal life in between and trying to forget about it. This mostly worked. I was lucky - it was very very rare for vertigo to strike when I was out doing any of the things I loved. I even began to suspect that being out in the fresh air hill walking, mountain biking or swimming in the cold North Sea were some how preventative. Make no mistake, I had tinnitus, and hearing issues and my god the vertigo - “Kill-me-now world-spinning vomit-hell” I called it. But somehow it didn’t stop life in the periods in between. At that point I guess I hadn’t begun to think of any of it as “normal”.

When things began to go badly downhill a few years ago, it was initially hearing loss and other hearing issues that were the most troublesome. Some years ago I moved to Germany from the UK, to the home town of my wife’s family. My German language skills were poor and I wanted to improve them. Not long after moving, COVID arrived and we had two years of people having to hide their faces behind masks, and shortly after that it was clear my hearing was beginning to decline badly. Not ideal conditions for learning a new language! Still there were other ways to socialise.

I have been an amateur musican most of my life and on arriving in Germany, I was lucky to be able to quickly create a personal social circle through music. Folk music is a wonderful social network, and it turns out there is a really thriving Irish folk music scene in the area of Germany I moved to. Being able to just drop into a bar knowing I could join new people and play along with them was like a superpower. From that I joined a band and began playing gigs - things were looking good socially and musically. The music overcame the language barrier. Many Germans in the folk scene were able to speak some English, and since most time is spent playing, there is less need for talking to still feel “part” of things. In many ways there were more musical possibilites than there had been in the UK. It was all looking good. Too good.

Playing live music with others is a complex interplay between listening to yourself and listening to others, constantly being aware of how your instrument is sounding, correcting pitch and following melodies. As my hearing began to deteriorate this delicate dance began to break. The beginning of the end was noticing that I could not hear the pitch of some instruments properly, including my own, and was struggling to sing in tune. What I did play sounded awful to me. My confidence fell off a cliff. Playing was no longer something I enjoyed or wanted to do and I began pulling out of things. The band split up. That social outlet was shutting down. When one door closes, sometimes another one does not open.

I explored hearing aids. There is no doubt they help, especially when the hearing is stable, but they could do nothing for the distortion that was causing me to hear wrong notes. It is also increasingly evident that my left ear is too far gone for the hearing aids to provide good hearing - distored and robotic is the best I can hope for. For my native English this is just about OK, but for a new language this is hopeless. Social situations in German are really mostly just nod and smile.

Despite all this, during the initial period of hearing collapse I did not totally give in. I have a music “session” - a social gathering in a bar to play togther - that I run with another friend here in Germany once a month and so far have continued to go along. Sometimes the hearing is good enough to play and enjoy, sometimes not. It is close enough to home that I can run off if I have to. But the creeping seductiveness of withdrawal is ever present and I have to force myself to go.

Then the vertigo returned. It was carrying a big stick and promised to hit me repeatedly with the it until I just gave up curled in a ball in bed. I’ve tried ignoring it. The result - I had to pull over whilst driving back from a musical gathering I’d ventured to as it was too dangerous to continue. I had a drop attack in a ski apartment on the second day of a two day trip, spending 3 hours motionless on the floor and only crawling to the car because we had to vacate the apartment. I had vertigo in a supermarket and had to use the trolley to remain upright, and only yesterday I missed the 90th birthday meal for my aunt and godmother as vertigo struck an hour before we were due to leave. The vertigo is almost daily (which is why these articles are taking an age to assemble - apologies for that!). I’m visiting family for Easter and can hardly hear them all so have withdrawn from conversation and have to regularly retreat to bed with my ever-shrinking world spinning around me. This is my new normal.

The hardest part I think is this grinding wearing challenge of having no “normal”. There are enough occasional reasonable days that you begin hoping and thinking a sensible stable life might be workable. The constant dangling of the carrot of possibility and the daily demolishing of hopes and plans. Plans? What are they?

The withdrawal isn’t just a practical removal of myself from events and gatherings either. It is a drawing back from the person I used to be. I find myself much less patient, a lot more intolerant and quick to snap. Apologies to everyone in my support groups for the recent increase in the harshness of my tone. I am probably a constant dark cloud to be around - which of course increases the tendency toward isolation. All of this is insidious, a slow erosion, a cliff being eaten away by storm breakers. At some point it collapses and what was there once is gone. I feel my house teetering on the edge.

What to do? How do you keep up the fight, stop the collapse, prevent the isolation? Because prevent it we must. The evidence is clear - socialising and being around friends is good for you. Hearing loss is a major contributor to isolation and both hearing and balance problems now seem to contribute to cognitive decline. So we must not give in or give up. We must rage against the dying of the light. I am still making plans, still committing to things. If I have to cancel or work around hearing or vertigo then that is what I will do. I’m currently in the UK having driven here from Germany, but for the first time I would have thought twice if my daughter had not been with me to drive if there was a problem. I have committed to a music gig in the summer, in the knowledge that I have friends who would probably step in if I couldn’t make it. I have a list of articles I want to bring you and plans for more interviews with researchers. I have a summer trip to a music festival planned even though I may not be able to hear. But then again I might. And a walking trip in the mountains in October. Will I spend some of it in bed? Possibly. I may go for a swim in the cold North Sea later today even though right now I feel dizzy. Commit to things, work it out later. The alternative is the enveloping silent darkness. I’m not ready yet.

When I started writing I wondered if there was even enough to say to be worth bothering you with. Now I realise there is a lot that has had to go unsaid - particularly about the black dog in the room - depression, which would need several articles to itself, best left for another time.

I do still keep myself amused though - this time I thought I’d just use quotes from people called “Dylan”…

Further Reading

Cognitive decline and diziness - https://pmc.ncbi.nlm.nih.gov/articles/PMC12851631

Dangers of untreated hearing loss - https://www.hopkinsmedicine.org/health/wellness-and-prevention/the-hidden-risks-of-hearing-loss

There but not really involved: The meanings of loneliness for people with chronic illness - https://www.sciencedirect.com/science/article/pii/S0277953624000406

Images

1. https://www.flaticon.com/free-icons/isolation

2. Created by the author

Use of AI

No generative AI or LLM was used in the creation of this article nor the accompanying images.

Salt or Sodium?

When we say salt, we usually mean the ingredient that gets added to food to give it flavour and the stuff that makes sea water, well, salty. You might hear people say that our bodies need salt. What they really need is electrolytes sodium and chloride and fortunately these are easily found on earth attached tightly to each other. When sodium(“Na”) which is normally a highly reactive dangerous substance on its own gets attached to chloride (“Cl”), they calm each other down and form the “salt” that we are familiar with.

Since sodium is lighter than chloride, salt is roughly 40% sodium and 60% chloride. It has been incredibly useful for thousands of years, not just because our bodies rely on the sodium, or that it makes food taste nice (because evolution cleverly encourages us to eat what we need), but also because bacteria hate salty environments so it acts as an excellent preservative.

In the body, sodium is one of the most essential of the “electrolytes” - electrically charged chunks of stuff that are dissolved in our body fluids and without which the muscles, nerves and other tissues in our bodies simply would not work. A perfect example as we’ve seen in previous articles are the hair cells in our inner ears that let us hear. The nerve firing relies heavily on sodium. It is thought that we need around a quarter to half a gram of it per day to keep things ticking over properly. Since the sodium has heavier chloride attached, that ends up being just over 1g of salt. (It is absolutely essential when thinking about and reading about levels of salt to know if what is being discussed is really salt or sodium - even some research studies I read preparing this article mixed up the two! I will try to stick to discussing amounts of sodium - to get the equivalent salt, it is “near enough to just double the sodium amount) Oddly, despite how important sodium is to us, it has not been possible to establish a definite “recommended daily intake” - instead it has been shown that having 1.5g of sodium for most people is definitely enough, and that more than 2.3g could begin to have negative health impacts.

Most people will get their sodium entirely from their diet. Unprocessed food (fruit, veg, whole grains, seeds, dairy) tends to be fairly low in sodium but still contains enough that a diet of these things would generally be fine. However the vast majority of people end up consuming much more than a half a gram of sodium per day. In the USA for example the average is about seven times that, at 3.5g (over 8g of salt), most of which is coming from processed food where salt is added to improve flavour and lengthen shelf life. People also add salt to their food at the table, but this is not where most of the extra comes from.

Having enough sodium in your tissues and body fluids is essential. However having too much is bad - very fundamental things like nerve signalling in the body would quickly stop working. There is a “goldilocks” situation going on - we can not have too much or too little, it must be “just right”. So your body constantly monitors how much sodium is washing around. The sodium you eat is dissolved into your body’s fluids. If you have just the right amount and drink a lot of water, suddenly the sodium becomes more dilute, each bit of water has less sodium in it. Your kidneys will notice this, and try to get rid of the excess water through your urine, whilst keeping hold of the sodium. On the other hand if you have too much sodium your body will try to get rid of the excess. However the kidneys often can not remove the excess sodium fast enough, so they will also try to hold on to more of the fluid you drink to try to dilute the sodium you have eaten. This “fluid retention” is one of the possible reasons that excess salt consumption is associated with higher blood pressure and worse health outcomes (these associations sometimes seem to cause controversy on social media, but seem to be robust and well demonstrated[1]).

(If you see a number in brackets [] it means there is a link at the end for extra info)

You may know that a defining feature of Meniere’s disease is “too much fluid” (hydrops) - more precisely too much “endolymph” - the fluid that bathes the core of the inner ear. If this is news to you you might want to check these articles on how the ear works:

Even before hydrops was discovered, in 1929 salt restriction was suggested as a treatment for Meniere’s. The moment hydrops was connected to Meniere’s, the idea took off - since we know fluid retention can be caused by too much sodium, that could be the cause of too much fluid in the inner ear. Add in the ease with which this advice can be given, and that increasingly we know that too much salt is linked to bad health outcomes, it fast became the first line of attack for treating Meniere’s. Can’t do any harm, easy to do, simple to understand what is going on, could well help. Right?

What does the evidence say?

So what has research actually found regarding sodium consumption and Meniere’s? The topic has been studied quite a bit, from early experiments giving patients lots of salt in the 1970s, then 1980s research that began to suggest maybe it wasn’t helpful, up to more recent meta-analyses looking back over years of studies. The most trusted organisation looking over health research is the Cochrane Collaboration. In 2023 they gathered together all relevant studies about diet and Meniere’s and concluded there was no strong evidence that controlling any aspect of diet would help[2]. In 2024 a large study that found people with a genetic tendency to eat more salt were no more likely to suffer with Meniere’s [3]. So the current position based on the best available science seems to be that sodium reduction is unlikely to help.

What might be wrong with the idea? It was always an oversimplification of the complex ways in which the inner ear carefully maintains its own fluids and the quantities of sodium and potassium ions in the endolymph and perilymph. Most obviously, the simple fluid retention theory does not account for the fact that it is the potassium-rich endolymph that gains extra fluid whilst the sodium-rich perilymph does not. Also the whole inner ear is filled with cells that are designed specifically to keep the balance of sodium and potassium correct. The idea may not be entirely dead though. There are still ways that sodium could be impacting the ear.

First, researchers now feel that the key with Meniere’s is that the inner ear has lost control of its ability to look after its own chemical balance. It just about manages but is fragile. It could be that a sudden influx of sodium into the body overwhelms these systems temporarily, they just can’t deal with it quickly enough, and the hearing and balance that need the right ratios of sodium and potassium stop working properly. So it is the sodium itself, not the addition of fluid that might be the issue. This could suggest that what matters most is avoiding large spikes in sodium, rather than sticking to some very low level, and this is now the more common advice.

There is another totally different idea for the role of sodium. Levels of a hormone called aldosterone increase when sodium is low - it tells the kidneys to hang on to and not excrete sodium, and instead to get rid of potassium. There are aldosterone receptors in the inner ear and these have been found to drive aspects of sodium and potassium management - when aldosterone is present the amount of sodium absorbed from the endolymph may go up and the amount of endolymph may even go down[4]. So low sodium levels could release aldosterone and thereby aid endolymph fluid reduction.

Crucially though the majority of these receptors for aldosterone are in the endolymphatic sac and in previous articles we’ve seen that this organ is either under-developed or degraded in Meniere’s - if a lot of the sac was damaged or missing, sodium restriction would (on this aldosterone theory) be less likely to work. This would suggest sodium control might work better for some people than others, which is exactly what we seem to see.

Real World

Doctors who treat a lot of Meniere’s patients say controlling salt intake almost certainly helps some of them. I polled the members of two support groups, and had almost 600 reponses:

About 80% of the 600 were trying to keep an eye on their salt intake specifically for Meniere’s. Clearly still a very widespread approach. However the majority either felt that it wasn’t helping, might not be helping or had given up because it didn’t seem to help. Of the ones that felt it helped, some were very sure and support groups are filled with tales of salty foods triggering vertigo. As with everything “Meniere’s” we have a confusing picture of unclear theories, studies unable to show treatment working and patients totally split.

Here I want to quote directly from Stephen Rausch - formerly a very prominent Meniere’s researcher and doctor from Harvard Medical School [5]

Recommendation to restrict sodium intake was originally conceived as a way of reducing ‘‘fluid retention’’ in the inner ear. Although this notion might seem simplistic and improbable, the fact is that many patients with Meniere’s disease are sensitive to sodium intake and do better on a restricted diet.”

Reducing Salt - How much by and how?

If you decide there is nothing to lose by trying to reduce your sodium intake, what should you do? There are various target levels of sodium intake thrown around for Meniere’s varying from 1g to 2g per day (half to one teaspoon of fine grained table salt - more on how bad teaspoons are as a measure later!). This is total sodium, not just what you add to your food but everything cropping up in processed and packaged foods, snacks, drinks and restaurant meals too. This is where the stress and anxiety can creep in. If your doctor has made this a big focus and you believe that it is directly responsible for your awful symptoms you will naturally begin to worry. Vertigo is horrendous, and most people would go to great lengths to avoid it. So you start looking at every food with suspicion. Some people stop eating out as it is too hard to know what is in the food and inspecting packet ingredient lists becomes second nature. Avoiding salt dominates your life. This isn’t to say it can’t be done - it is a key element of many healthy eating plans and requires discipline and new habits, more fresh ingredients and home cooking, making some simple food swaps. But I know it is not easy for many and stresses them out. There are many resources out there to help and even recipe books from the Meniere’s community such as “Welcome to our table - Meniere’s Disease Cookbook” from Julieann Wallace. (This and other recipe links are in the resources at the end)

Before trying a dietary intervention like reducing salt, spend a few months keeping a journal of your symptoms. Pen and paper or a spreadsheet or dedicated app, it doesn’t matter. Consistency is key. Every day note for each ear the level of tinnitus, hearing loss, and any vertigo attacks and medications taken. I always also note number of hours I have to spend in bed unable to function - a good measure of how bad the vertigo was. Do this for months then try controlling sodium in the ways discussed. Don’t change anything else. Keep journalling. See if anything improves. Who knows, maybe you are one of the ones for whom it makes a useful difference.

Is it true that…

“You need to eliminate salt entirely”

Increasingly the advice from researchers and doctors is that what matters is the fluctuations in sodium level rather than the overall amount. What should be avoided are big spikes in consumption. A lot can be achieved using a “no added salt” approach and avoiding the obvious “salt bombs” like snacks. It is clear that for some people stress is in itself a trigger for Meniere’s, so having a simpler approach to salt control might be a good idea. Stephen Rausch again:

Although a very low sodium diet will achieve even distribution through the day, an even distribution can also be maintained on a ‘‘no added salt’’ (NAS) diet of 2000 to 3000 mg sodium per day. A target of 500 to 1000 mg of sodium per meal is relatively easy to achieve. Patient compliance is much better on the NAS diet than on a more severe restriction. There is an additional benefit of the more modest sodium restriction. If a patient is used to an extremely low sodium diet, a single handful of potato chips may double their day’s sodium intake, a spike that could easily trigger an attack. Alternatively, if the patient is equilibrated on the NAS diet of 1000 mg/meal, that same handful of chips may be only a 25% to 30% increase rather than 100% increase in daily sodium. The spike is relatively smaller and thus less likely to trigger symptoms.

“Himalayan Pink Salt is better”

…or Celtic Sea Salt or any number of other salts. Despite the marketing, it is hard to see how these are more than just salt. All salts taste different. I grew up not far from Maldon in the UK where one of the world’s famous sea salts comes from. For sure there are tiny amounts of different minerals in each salt depending upon where it originates. However these amounts are miniscule, and compared to the other foods you eat likely to be insignificant. Beyond those minerals, these salts are just sodium chloride. Of course if you are eating a type of salt that you personally feel is helping, stick with it. Sometimes though people will say that their choice of salt has less sodium in, and tables like this seem to suggest they do:

This is misleading. The measure here is a “teaspoon”. Notice the two lines for sea salt - the problem is that if the salt has coarse crystals, a teaspoon will actually contain lots of air in the gaps between the crystals, and less weight of salt! So adding a teaspoon of coarse sea salt to your food will make it taste much less salty than adding a teaspoon of fine grained salt. You may well then add the extra salt needed to get the flavour right. What matters is the total weight of sodium chloride being added to the food. (On the other hand if you always use teaspoons to measure and don’t notice the change in flavour, using a coarse salt may have accidentally resulted in you eating less salty food!)

“You can sweat it out”

There is some truth to this, but like everything about the body it is hard to make solid rules as there is so much variety. Sweat does contain salt but it is typically many times less salty than blood or body fluids. This actually means that if you sweat and don’t replace the fluid lost you will be making your body salt concentration go up! On the other hand if you replace the fluid lost with water you will be diluting the remaining salt in your body a bit. If you replace the fluid lost with an electrolyte drink you will replace some, all or possibly more salt than you lost. Studies on athletes [6] suggest that the average rate of sweating across all sports is 1 litre per hour and that the average sodium loss is about 1g. This will though vary enormously based on intensity of activity, temperature, and even individuals doing the same exercise can vary by factor of 10.

The Potassium connection

Another important electrolyte for the body is potassium. Again we get this from our diet (potatoes, bananas, leafy greens, beans, salmon and many other foods). Increasing potassium intake can reduce blood pressure and also encourages the kidneys to get rid of excess sodium. [7]. Most of us could do with eating more potassium than we do. One way to eat both less sodium and more potassium is to swap the salt in your kitchen for a salt substitute that contains potassium [8]

Round Up

• We need sodium

• We typically eat too much

• Some people find controlling salt seems to help with their Meniere’s

• Avoiding big spikes seems a better and easier approach than very low levels

• Journalling is essential

Good luck and let me know your thoughts. Do you find sodium control helps?

Please note that all of the above is provided for informational and educational purposes only and does not constitute medical advice. Dietary changes should be discussed with your doctor.

Links

1. https://pubmed.ncbi.nlm.nih.gov/41243115/

2. https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD015244.pub2/full

3. https://www.frontiersin.org/journals/nutrition/articles/10.3389/fnut.2024.1460864/full

4. https://www.sciencedirect.com/science/article/abs/pii/S0385814616300736

5. https://www.oto.theclinics.com/article/S0030-6665(10)00093-9/abstract

6. https://www.mysportscience.com/post/how-much-do-you-sweat

7. https://pmc.ncbi.nlm.nih.gov/articles/PMC11001572/

8. https://www.tctmd.com/news/massive-ssass-study-shows-switch-salt-substitute-cuts-stroke-cvd

Other links

Excellent summary of salt and sodium https://nutritionsource.hsph.harvard.edu/salt-and-sodium/

Reduced Salt Recipes

• BBC Good Food collection https://www.bbcgoodfood.com/recipes/collection/low-salt-dinner-recipes

• American Heart Association healthy Recipes https://recipes.heart.org/en/ - lots of online recipes and books

• Welcome to our Table - Meniere’s Disease Cookbook (Julieann Wallace and others) https://www.lillypillypublishing.com/meniereslowsodiumcookbook

Image Credits

1. NaCL “cartoon” - from abcteach.com

2. Salt shaker By Dubravko Sorić SoraZG on Flickr - https://www.flickr.com/photos/11939863@N08/3793288383/in/photostream/, CC BY 2.0, https://commons.wikimedia.org/w/index.php?curid=18125369

Before diving into the Lenire, it is worth revisiting the topic of what it means for a treatment to “work” - one that we will come back to again and again in these newsletters. In science-based medicine there is a well-established ladder of evidence to support the idea of a treatment “working”. At the bottom rung of the ladder we have people’s personal experiences - “I tried X and later felt better. It works”. Towards the top we have medical researchers trying to give the best answer they can by testing on many different people, comparing with other forms of treatment or none, trying to avoid bias and remove the impacts of other things that may influence the results. We even have a higher level that takes all the studies up to a given point in time and combines them to try to get a more accurate conclusion (so called “systematic reviews” or “meta-analyses”). So when thinking about whether something works or not, we have to see what lies behind the claims - where are we on the ladder?

The Lenire

This is a device from “Neuromod Devices Ltd” intended to treat tinnitus. It is a modified form of tinnitus sound therapy - a well established approach that uses various forms of sound and noise to both distract your brain from tinnitus and potentially allow you to “get used to it”. These approaches can take the form of apps or downloadable sound files, YouTube videos etc. The Lenire adds to this sound therapy a mild electric shock that is delivered to your tongue whilst the sound is playing. If you had to read that twice I wouldn’t blame you. You hold an electrode in your mouth and the Lenire device delivers mild shocks through the tip of the tongue in time with certain pulsing or changes in the sound delivered from the device to proprietary wireless headphones. This is based on an idea that the company calls “bimodal neuromodulation” - they suggest that having two simultaneous sources of stimulation will “drive neuroplastic changes in the brain’s processing centers”. Digging a bit further it seems that some studies have found tinnitus sufferers have excess activity in a brain region called the “Dorsal Cochlear Nucleus” and animal studies have shown that stimulating the “trigeminal nerve” can lead to modifications in this brain region. The tip of the tongue is one place that this nerve can be accessed. So the idea is that somehow this simultaneous stimulation of sound and the nerve “resets” the hyperactive brain region.

Does any of this make sense? Device manufacturers make all manner of claims, and it can be hard to know how true they are. There is some evidence from chronic pain and stroke rehabilitation research that this approach of simultaneously providing a nerve stimulus and some additional well-timed sense input to the body can lead to changes. The question then is - does it work for tinnitus? Does the device as described give improvement in tinnitus, and is the addition of this tongue stimulation giving any benefit over just using existing sound therapies? This second point matters, because the total cost of the Lenire device, including the required audiologist appointments to set it up, has been estimated at $4500-$6000. The company has done several large trials, and claims very significant effectiveness. However there has also been some criticisms of the trials, one of which is the lack of comparison with existing therapies. You can find a detailed appraisal of the device, the trials and some personal experiences from users here. I have not done a deep dive into either the underlying theory nor the trial quality - if you’d like me to, leave a comment - but as you will see below it may not matter for Meniere’s sufferers.

A quick read of the handbook for the Lenire device itself states that Meniere’s sufferers should not use it! As far as I understand it the reason is two fold. Firstly. the sound levels for the sound therapy component are important, and are set by the audiologist during the setup appointments. If you have Meniere’s chances are your hearing is fluctuating - every day it is different. This means one day you could find the therapeutic sounds too quiet to be effective and the next intolerably loud. Similarly, when suffering from Meniere’s, due to the fragility of the inner ear, it is common to have extreme sensitivity to noise. The second reason is that, as they say in the handbook, the specific case of tinnitus due to Meniere’s was not part of their clinical studies, and so they are not willing to claim that it can help, or even that it won’t make things worse - the loud sounds required plus the strange stimulation could potentially trigger vertigo attacks and trials would need to rule this out. What is interesting to me is that the warning against use for Meniere’s is only in the USA edition of the handbook, but missing from the European one - if anyone has any insight into this let me know!

So in the case of the Lenire device the topic of “does it work” has not actually been addressed for Meniere’s and use of the device is currently not recommended. Now we can look at a device that for quite some time was highly regarded and considered a useful treatment.

The Meniett device for Meniere’s vertigo

The Meniett is a handheld air pressure generator that delivers small pulses of air about six times a second into the middle ear. It was claimed to reduce the the number of vertigo attacks. The idea of the device is to try to use the air pulses to “massage” the inner ear fluid and somehow encourage it to move toward the endolymphatic sac to be reabsorbed. The device itself fits into the outer ear canal, so in order for the pressure pulses to be delivered as directly as possible to the inner ear a tube needs to be surgically inserted through the eardrum before the Meniett can be used. Like the Lenire, the total cost of the device plus necessary medical appointments could be several thousand dollars.

I won’t say too much about the way the device is intended to work - there is some limited experimental evidence to support various elements and maybe it would be worth a deeper look at some point, but the point here is to look at the “does it seem to work” studies as they hold lessons for Meniere’s treatments in general.

In the early 2000s things looked very promising - a number of studies concluded that the device was effective including some long term ones such as this or this. Such studies reported that users of the device said they had less vertigo attacks. This was the “holy grail” of Meniere’s treatment for those people that diet or medication was not helping - the only alternatives were significant surgical approaches or treatments that destroyed the balance of the impacted ear.

However by 2015, a study that looked at all available evidence at the time concluded that the device in fact did not work as advertised and more studies since seem to have confirmed this conclusion. In early 2026 the Meniett was withdrawn from sale. What changed? What did the early studies miss?

First, and most obviously, the early studies were not comparing the Meniett with anything. They were just reporting that patients seemed to be getting better, so surely it must have been the device. One study concluded that Meniett was effective and yet admits in the discussion:

“The present study is based on an unblinded protocol and, as such, may reflect the effects of therapy, placebo, and the natural history of the disorder.”

- in other words, no way to actually know if it was the device that was making things better. They also reported

“… the long-term data display a paradox: those who used the device the most had the most symptoms, and those who used the device the least across the long term had the fewest symptoms.”

- in other words using the device seemed to make things worse!

Yet in their conclusion they state

“Use of the Meniett device was associated with a significant reduction in vertigo frequency in about two thirds of the participants, and this improvement was maintained long term.”

- which sounds very convincing, until you realise that we now see similar levels of improvement for pretty much every treatment ever tested on Meniere’s, including doing nothing.

So there was typically no comparison treatment. In addition, to use the Meniett required a tube through the eardrum. This on its own is now a treatment that is sometimes used for Meniere’s - so was it just that causing the improvement? Early studies did not do that comparison. There were also no proper “placebos” used, or if they were they were not good enough. A placebo is a treatment that looks and feels like the real thing but actually does not contain the “active” mechanism of the treatment you are testing. So for a drug, it could just be a tablet of the same size, colour and taste as the “real” one but with no active drug in it. For something like the Meniett, a placebo could be a similar device that is inserted in the ear but does not actually pulse air (but emits some sound or flashes to suggest it is doing something). However this lack of pulsing could be noticed by some participants, which would invalidate the placebo. Later trials did compare the Meniett with both ear tubes alone and with good placebo devices and these trials showed that the Meniett seemed not to do anything significant.

Beyond these failings in the design of the early studies, there are other issues that make studying Meniere’s treatments very hard. Firstly the huge fluctuations over long periods and the constantly changing nature of the symptoms - this means any study needs to cover a very long period and to take into account the natural progression of the disease. In addition, there are psychological factors which mean that a placebo is essential - just knowing that you are getting given a treatment can reduce the anxiety that accompanies Meniere’s that vertigo or a drop attack is just around the corner. People also need to be encouraged to stick with the treatments being tested. A big issue in earlier trials was that due to natural fluctuations in symptoms, many people had less vertigo early in the study, at which point they felt they no longer needed the treatment and stopped using it. Since they drop out they are not included in the analysis. If there is a difference between drop out rate between placebo and treatment groups this can mess with the results. Finally, as already mentioned, of all vestibular conditions, Meniere’s is probably the hardest to investigate due to the fluctuation and remission, and in any trial well over 50% of patients receiving no treatment at all will report significant improvement in symptoms. This has actually been used to cast doubt on some trials that seem to show huge improvements - if you see the placebo group in a trial only showing a small percentage improvement it is worth looking more closely!

In the end, the Lenire might work for some people’s tinnitus, but should not be used for Meniere’s, and the Meniett was for Meniere’s vertigo but didn’t actually work and is no longer far sale. I’m not currently aware of any device that has been shown to help with Meniere’s. Our condition is a complex one and the search for reliable effective treatments goes on.

Links

https://pubmed.ncbi.nlm.nih.gov/27515294/

https://pubmed.ncbi.nlm.nih.gov/17178941/

https://pubmed.ncbi.nlm.nih.gov/18617868/

https://jamanetwork.com/journals/jamaotolaryngology/fullarticle/484604

https://www.cochranelibrary.com/cdsr/doi/10.1002/14651858.CD008419.pub2/full

https://www.lenire.com/

https://neuromedcare.com/lenire-device/

Image Accreditation

1. From https://www.nature.com/articles/s43856-025-00837-3 CC 4.0 license

2. Picture reprinted courtesy of Xomed