Myalgic Encephalomyelitis (ME) or What? An Operational Definition, 2018, Frank Twisk

Yes that study was the epitome of why we need subgrouping. IIRC if you lump everyone together there was no significant difference from controls, hiding that under 3 years the direction of difference was *opposite* from over 3 years. And yet I can’t remember any subsequent studies from other researchers trying out this subgrouping split. Why not? This is easy info to collect. We could have a few studies which do analysis on the group as a whole and then split into under/over 3 years. It could be just a fluke or there could be substantial differences. I wonder if it could even be done retrospectively if researchers in old trials asked year of onset? *Anyone with access to the data and stats smarts could do this reanalysis*

Also a disease like MS has subgrouping eg primary and secondary progressive and relapsing remitting. They seem to have been able to keep an umbrella advocacy identity as MS though. We can have the best of both.

Yes I’ve had this and it showed I’ve got an inner ear lesion (probably due to ineffectual immune response to an ear infection?). Though my brain should have adapted to ignore the incorrect right ear info (dr thinks not consistently adapting is related to ME, I’m speculating due to cognitive attenuation problem). On a programme I watched (Medical Mysteries?) a woman has this type of bio issue and they went onto say she had this Supermarket Syndrome as a repercussion and they did some vestibular rehabilitation training for her. I’m not optimistic this would be effective for me though, if the problem is my brain lacking energy to filter out faulty messages.

 

I've wondered if this kind of thing might be related to something called "sensory gating," which is the ability to filter out extraneous sensory input. It's illustrated by the "cocktail party effect" in which it is possible to ignore all but the desired conversation. Perhaps defects in "gating" light, sound, image and balance inputs, etc. are related to the more familiar impairments in attention, focus and concentration.

https://en.wikipedia.org/wiki/Sensory_gating

 

This would describe something that I struggle with perfectly, and that definitely gets worse the more I do.

 

@Forbin @Andy yes this is the type of thing I mean, the same category of cognitive psychology (I’m rusty but I learnt about this stuff at uni). With the Cocktail Party Phenomenon it reveals that we actually do hear more than we think we do because we do hear whenever someone uses our name in another group of people talking at a party, even though we couldn’t consciously report what the conversation is about. In order to make the external world bearable we have to turn down (attenuate) almost everything happening around us and focus our attention. Think of it as a volume dial, but for all senses. At some level all of this information is still processed though (the metaphorical volume setting isn’t actually set to mute).

This isn’t an entirely conscious decision making process, though it is often conscious what we choose to focus on. At a party we could also choose to focus on the other conversation and attenuate down the person we look like we’re listening to though this would be rude (and that’s not what the Cocktail Party Phenomenon is referring to though - it’s hearing your name in the other group even when you didn’t think you were listening).

I would guess, from my lived experience and knowing about this, that effective ability to attenuate external stimuli is faulty in ME (or specifically in me ). For example if I go to a cafe I can both be overwhelmed by the sensory information AND be unable to decipher what my companion is saying to me to the extent I have to leave before eating, although everyone else is fine (and my ability to hear is within normal range).

It feels like I can’t attenuate the irrelevant sensory information and that is exhausting. If this is due to lack of sufficient brain energy (eg low ATP) it creates a vicious cycle because the full volume sensory experience is then more exhausting, and my ability to attenuate is even more impaired and so on until I lie in a dark room with noise cancelling headphones.

 

Exactly.

 

The first thing we have to be clear about is that something is going wrong in our bodies. It may be one thing or many but it exists and if it can't be found that is a problem with medicine and medical testing not in us. That is the basis for all our campaigning. This is all getting put down to psychology but the people claiming that are not offering any credible explanations for how that happens so we should be demanding answers rather than feeling we have to tweak the description of what is going on with us into something they will accept. Diabetics do not have to explain the biochemistry of insulin to be treated.

Ramsay said that one of the key points about ME was the variation in symptoms. Now I know that some people do not experience this but that it happens at all needs examined. I don't have such a variety since I stopped having to push myself with young children. I can now do less but I can stop before I reach my limits but I could easily have a day where I had severe pain in my joints at 9 o'clock, unable to remember how to get home 10, not able to speak at 1, forced to lie down exhausted at 3. Evenings were the worst with complete paralysis at 6 then a brief recovery with blindness most nights by 9 when I was helped to bed.

When I left the house I never knew how far I would get. No matter how I tried I could sense no difference on the days I managed to go shopping and the days I managed a few steps before hanging on the railings to get home.

These things happened when no one was there. Actually by the time I had my third child I was terrified that if anyone knew how bad things were he would be taken into care so I hid the worst things even from my husband.

With this amount of variation it is no surprise that all my tests were normal. Test my sight when I can see, what a surprise if I see the chart!

I think we try to fit what is happening to us into the words we are offered. I occasionally read something which captures what I have but a lot of time I don't partly because people seem to have things which last for longer than I experience.

My intuition is that my body runs out of something so it stops till it gets enough to start again. The way visual purple works maybe. Instead of the usual homeostasis where as soon as something happens the body produces a counter reaction, my system feels as if it takes a while to respond. For example if I get chilled it can take up to five hours before I get warm but I actually feel as if I am getting colder for the first few hours even though I am now inside with blankets and heat pads.

 

Here's one I made earlier (as they say) : https://www.healthrising.org/blog/2...xplain-chronic-fatigue-syndrome-mecfs-better/

 

Another one I made earlier : https://www.healthrising.org/blog/2...deficits-present-in-chronic-fatigue-syndrome/

 

@Marco I can’t read it all today but it looks really interesting and more developed than my random thoughts on this topic

 

@Forbin Very much what I experience. My gait gets much worse and I have to concentrate on walking. It's hard work and with the feeling like you aren't going to make it. The unsteadiness is awful.

 

Another name for ME was Epidemic Vertigo and it was a dominant symptom in some of the epidemics. From talking to people over the years and my own experience I think that problems with proprioception can be part of the disease. A positive Romberg test where you fall over if you close your eyes was suggested as part of a diagnostic set of symptoms.

In recent discussion I discovered I was not the only one who started using a walking stick to help know which way was up, rather than as a support.

 

Just asking because I have been wondering for a while and being just a mum with a child with ME is the most... Well you know I have no where else to go to get understanding and answers.

Dr Ramsay mentioned in severe cases acute muscle tenderness when with your forefinger you could detect minute “foci of exquisite tenderness” in the Trapezii and gastrocnemii. Is this a result of lactic in the muscles?

Dr Granet Simpson in Sydney Australia devised the same technique without prior knowledge of Dr Ramsay’s work.

Could this be the result of lactic acid? Julia Newtons work in the muscle would back this up? When you go for a run your muscles give way similar to how yours do Prof Edwards before the pain set in?

Understanding where lactic comes from is the key along with how and why. So I looked around.

They have found in brain injuries that the nerve cells cover their high energy demand with the glucose and lactate with the preference to lactate energy. This would also take in what Fluge and Meller findings with the Pyruvate problem.

So, if brain injury or inflamed brain along with oxidative stress is part of the ME problem, and we look at an injured brain needs Lactic to keep it going, is this where the vicious cycle of PEM comes from? A possible reason of the variability too? Lesser injuries take up less lactic? If the brain is calling for Lactic through the cerebral energy metabolism and we know the sun produces high burning lactic is this the reason some severe cases; like my son find that when they go out in the garden on a nice sunny say to zap up those rays in a hope they will feel better with a good dose of Vit D they crash, even if they are just sitting in the sun? Then take days of their Trapezii and gastrocnemii in pain feet feeling cold and neck pain?

Since 2008 Lactic has been looked at seriously as a biomarker with a new study last year https://www.tandfonline.com/doi/full/10.1080/21641846.2017.1280114

Fibro and ME have an overlap and both have lactic acid as a marker in a group of patients (I wonder if all ME/CFS/Fibro would have this problem if they were in the right place of PEM to show up?). Lactic is also a problem with diabetes.

Sepsis also has this problem

Another single-center cohort study including 830 patients with severe sepsis and septic shock admitted to the ED showed that initial venous lactate levels between 2.0 and 3.9 mmol/L, compared with initial lactate levels less than 2.0 mmol/L, were associated with increased mortality at day 28, regardless of the presence ...

Blood Lactate Levels Cutoff and Mortality Prediction in Sepsis—Time ...
https://journals.lww.com/.../2016/.../Blood_Lactate_Levels_Cutoff_and_Mortality.3.aspx

I think they have in the past looked at lactic to see how Heart Attach victims were doing too?

So, could lactic be a marker of severity or a marker of PEM?

My son is now on a steep decline and because he is of school age I am hounded as a Fabricating and Inducing Illness potential. His Liver now is showing signs of damage which they have just picked up on a blood test. I was given no information or reason why but they will check on this in a few weeks time. Is it about time I looked at asking for a lactic test? Why is this not looked at as a matter of course? I cannot ask for too many tests due to FII and I am very sad to say I have lost all faith in doctors in my area and my son has been so badly treated it is always a risk of more emotional abuse lashed out on him and me if we go to the surgery.

The ironic thing is keeping active lowers your lactic, but with ME when they do any activity their lactic goes into overdrive? so this is not going to help? It's is the same with POTS which he has been diagnosed with.

Fluffy Duck how it is to be a mother with a child with ME I am dammed if I try and find out and we are both condemned if I don't. I know you will give me a good solid and no holds bared answer which would be much appreciated.

Tina Rodwell

Moderator note
The latter part of this post and responses to it have been copied or moved to this new thread:
Children with ME, schools and the problems of FII diagnosis

 

I think definitely not. Foci of tenderness in muscles occur normally anyway, unrelated to activity, particularly in the trapezius. I think this is a bit like the tender points of fibromyalgia - it does not mean anything useful. These are just the points that tend to be tender in everyone.

I understand how desperate people are to find answers but I cannot see that changes in lactate are going to explain the symptoms of ME. Levels of lactate that produce symptoms are easily measurable and nobody has come up with any consistent findings that would fit as far as I can see- certainly not for muscle. There were some interesting findings in brain but that would be something different. I think the metabolic ideas that some of the researchers are putting out are very oversimplified and not vey realistic.

I think the problem is that whatever the biological changes are that underly the symptoms we do not know how to test for them. The main reason to do tests is to see if there is some other condition that has been misdiagnosed as ME. And there is no real way to know what tests would be needed for that.

 

Are there tests that need to be developed?

If you could invent any test, what would it measure?

 

I wonder why those points are tender in everyone? There has to be a reason - a cause and affect.

Desperate is probably an understatement and can cloud our judgement that is for sure. Desperation along with hope can make a proper mess of the science. Asking and re-asking questions is a good thing to do.

Why does one thing have to explain the symptoms of ME? Is that my hope and desperation talking? What I observe in my son is a domino affect, a constant circle of activity increase in baseline symptoms, then added symptoms that always come in the same order the domino affect: tummy problems, heightened sense of smell, then taste, light lastly sensitivity to sound. He blacks out, but I think this is more to do with POTS/OI

Same goes for consistent findings. How can you have consistent findings in such a fluctuation of PEM. Again, what I observe is that domino affect, a crescendo of underlying symptoms and if he keeps on with activity (including doing a dot-to-dot that he could have done when he was five) new symptoms come on and then go away with rest, this may take months or years. So how can you get a constant reading? Its a bit like hitting a moving target? Like insulin with a diabetic?

Not only do we not know how to test for them, as far as I can see no one can agree on the symptoms themselves, not even patients? What would be your three top symptoms?

 

The problem is we have no idea.

 

It may be like insulin and diabetes but whatever it is does not look likely to be something like lactate. And the problem is not so much that findings are inconsistent. As far as I know measurements are just normal.

Maybe finding it impossible to do any significant activity, feeling ill, and sensitivity to stimuli including light and sound and standing up. I don't think there is anything very complicated in those terms. People without ME may not be able to understand quite what it feels like but we know enough to see that the problems PWME have do not seem to fit with the usual sorts of metabolic problems involving things like lactate. If they did I am pretty sure that MR spectroscopy study sin the 1980s would have picked them up.

I think it is a pity that certain doctors with an interest in ME have focused on metabolic issues or mitochondria without really knowing much about those. A couple of years ago Mike Murphy came to talk at IiME. He is a mitochondrial biochemist. His view was that the symptoms of ME do not sound at all like sings of mitochondrial malfunction, unless they are due to some sort of danger signalling.

 

It almost certainly has to do with sites of tensile force in continuous postural muscle action. Most muscles in the body are called on to do specific jobs intermittently. But trapezius and soleus (which is in the same place as gastrocnemius) contract almost constantly just to keep your body upright with slumping. The tennis elbow spot gets tender if you carry something for a long period with the arm slightly bent, and so on. Tender spots in trapezius are something casualty officers and rheumatology trainees get familiar with in their first clinics - and learn to reassure people that they do not mean anything. By the time I got to be a medical student I had already had episodes of tender trapezius and my father, who was a doctor, had reassured me.

 

Naviaux's view is that the cell danger response of the mitochondria is involved (if I've understood him correctly). I'm not competent to judge it, though.