I think this is misconceived and tends to take things in the wrong direction.
It is this sort of analysis that makes me think we should stop referring to 'outbreaks of ME' documented in the past, because they probably tell us nothing important about the illness people suffer from today. The 'neurology' of the Royal Free outbreak turned out to be not very much that could be pinned down with objective evidence.
The core of the definition given in this proposal is:
ME is a multi-systemic illness, which (1) often has a sudden onset, in most cases a respiratory and/or gastro-intestinal infection, but a gradual or more dramatic onset is also possible; (2) has an epidemic and an endemic form; (3) has an unique clinical pattern deviating from other post-viral states; (4) is distinguished by muscle fatigability/prolonged muscle weakness after trivial exertion; (5) is accompanied by symptoms relating to neurological disturbance, especially of cognitive, autonomic, and sensory functions; (6) can be accompanied by symptoms associated with cardiac and other systems; (7) is characterized by fluctuation of symptoms (within and between “episodes”); (8) has a prolonged relapsing course; and (9) has a tendency to become chronic.
The usual term is multi-system, rather than multi-systemic but that does not matter. The problem in using the term is that multi-system implies not just symptoms but pathology in several systems and we do not have that as yet.
The criteria themselves are not of much practical value.
1. If the onset can be sudden or gradual then a description of onset may be of interest but does not contribute usefully to a definition - because it does not narrow down possibilities. Th occurrence after infection is relevant but EBV is not really either respiratory or GI.
2. I do not think that it helps to talk of an 'epidemic form'. Of the hundreds of thousands of documented cases of ME maybe 1000 at most were documented as part of multiple case clusters. Since infections often come in epidemics and ME follows infections I cannot see that these clusters add anything useful.
3. ME may have a unique clinical pattern but we need to know what that is.
4. The idea of muscle fatiguability/weakness comes from Ramsay, I think. Ramsay was not a neurologist and I do not think neurologists would consider this a very helpful part of a definition because it is too vague and ambiguous. Fatiguability and weakness are different. Moreover, as far as I know no objective evidence has been documented for either muscle weakness or fatiguability in the sense that it has for myasthenia gravis.
5. ME is certainly associated with cognitive disturbance symptoms. Attributing symptoms to autonomic problems is a bit more tricky. I am not sure that any sensory abnormalities have been shown to be more common in PWME. I think from the neurological point of view it would be much more useful to focus on the cognitive deficit.
6. This is too vague to be useful. ME is not as far as I know associated with cardiac abnormalities per se, although there is a suggestion of low cardiac volume.
7. Fluctuation is also hard to use as a criterion. Moreover, I understand that for some people there is not much fluctuation.
8. A prolonged relapsing course is not very helpful as a definition that identifies people until it is a bit late!
9. This seems to add nothing to 8.
I appreciate that Frank Twisk has produced this in good faith as an attempt to document his conception of ME. However, it is not in a form that is going to be of use to medical practitioners, or to researchers.
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
). 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).
