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

From my scan of it that seems relevant. My consultant tried to.out it down to lack of concentration, but I always correct him and explain that is is more like a processing issue.

 

Ah. So I took you to be encompassing sensory sensitivities for the reason that Twisk references sensory functions in the abstract (5), and goes on to include photophobia, hyperacusis and hyperaesthesia under Sensory Dysfunction further in. I was also thinking of sensitivities to touch and odour.

 

I know it was asked of @Graham , but I definitely experience this & some places are worse than others. I tended to put it down to my brain trying to filter out the background noise, the artificial light, the mental effort involved in keeping your balance while not bumping into people.....

The Invisible Man and I had to work out a strategy because he lost me too many times. I knew I would be okay, so wasn't panicking, but simply didn't have the cognitive capacity to cope. So I'd stay where I was and wait till he found me. Now he stays by my side and if I start to feel like I'm getting very confused, I clutch his arm, sleeve, back of his coat. Like a toddler .

Mostly he leaves me at home. . I don't blame him!

 

One word: Ocado

 

Yes, me too earlier on, but now I guess I tend to avoid walking unless I feel confident my legs will do what they are supposed to.
Another thing, in a similar vein, was trying to dance, or at least move in time to music; I used to have a really good sense of rhythm and loved a good 'boogie' but that went too. There appeared to be almost a delayed reaction between me wanting to move and my body actually responding.
This has improved a bit but if I attempt to dance it tends to be like a toddler; ie feet staying still and the rest moving a bit.

 

My daughter descibes this as feeling as a baby would, when it can see its hand but is learning how to control it , and she has to really concentrate to do something that is second nature for most oeople.

 

This ties in very closely with what my wife describes to me. See my post https://www.s4me.info/threads/mirro...s-a-day-m-e-nearly-killed-me.5418/#post-97740.

 

Sounds familiar, thanks!

 

But the tachycardia is driven by the autonomic system just as the blood vessel constriction is. If there was a blanket defect in the autonomic system there should be no tachycardia. There might be a selective defect so that constriction did not occur but tachycardia did, but then there should be some evidence of selectivity from studies. I worry that the people who propound these dysautonomia theories get a bit vague at this point.

 

I am talking of systematic research studies which ought to have picked at least something up in some cases and my impression is that they did not.

 

It seems like there are different causes of POTS, but yes I think it could be described as a selective defect. Eg the baroreceptors don’t accurately signal body position , so leg blood vessels don’t constrict (or EDS impairs this etc) what does get picked up is hypoperfusion/potential faint scenario and the tachycardia is a sort of emergency response. Although perhaps in a very literal sense this sometimes isn’t dysautonomia because the dysfunction precedes the autonomic response- the autonomic system is prevented from doing a good job but it might not be the perpetrator...

These old studies are what I can think of (older studies often use post viral labels). It’s definitely under studied. I did quite a bit of googling last year and I don’t think I found evidence that EMG is normal- there’s an absence of recent evidence rather than evidence this is normal. When I’ve asked around most people haven’t had EMGs.


75% had abnormalities on a type of EMG testing
https://jnnp.bmj.com/content/48/7/6...paign=J_Neurol_Neurosurg_Psychiatry_TrendMD_1

 

Politics versus science. The problem is when they clash, such as in the minds thoughts of politicians and bureaucrats, and even with doctors in the community. We need to study subgroups, we need diagnostic and treatment outcome biomarkers, and we need more funding all round for all the groups.

I have written before that all the definitions will undergo a rewrite, at least, once we have diagnostic biomarkers. Some will just disappear. The name might change. A stricter definition is about decreasing cohort variability. Its not guaranteed. Subgroup analysis is fine, but it seems to me that later studies often ignore subgroup findings and they do not get replicated.

This all costs money and other resources, including researcher time. We still don't have enough of these things.

My best guess is that ME costs the world around a trillion dollars a decade (not year). The world seems fine with that, or is acting that way. Throw in related diseases like fibromyalgia and what are the costs then?

 

I agree, Trish, but seems like Frank has some strong opinions:
https://twitter.com/user/status/1038801274014232577

 

This kind of advocacy will probably achieve nothing. I'm pretty sure that an illness definition centered on PEM has a better scientific basis than a definition centered on muscle fatiguability. Health authorities in the US went with a PEM based definition. Instead of trying to establish ME as accepted illness distinct from CFS, they should use their time and energy to make sure that good ME/CFS subtyping studies are done.

 

I had it both.

 

It seems like the right wqy to go, but I sometimes wonder if subtyping is at all possible at this point? From what I've read here on forums, it seems like every patient is quite unique, even though there are many overlapping symptoms.

 

Symptom variability is only one aspect of subtyping. The key feature in subtyping is to find a subgroup that gives stronger and more consistent results, and that depends on what you are studying. Not having validated subgroups means its an expensive exercise.

Subgrouping is actually easy. Effective and validated subgrouping is not.

Given the nature of what we know then I would expect huge symptom variation anyway. Too many pathways, genes and organ systems are affected in some way. Individual variation, right down to what happened that day, including what you ate, might affect symptoms. Comorbities, especially pathogens, would have an impact. Subgroups with definitive symptom lists are highly problematic.

I have long been intrigued with so many findings at about a one third to two thirds split. I really wish we knew to what extent these findings are stable. The development of open patient databases is probably the best way to address this, as many subgroups might be explored and tested without ever needing to enrol new patients, and at minimal cost. However they would still have to be further tested, to ensure they are not an artefact of all that analysis.

The one most relevant to me is how different are encephalitis survivors, given we know the cytokine profile might be different. This finding by Lipkin et. al. has not been replicated. Other things were not looked at. Is it only cytokines, or are there other differences? We just do not know. Similar questions can be raised with respect to POTS versus NMH, or those with EDS, or those with a Giardia trigger versus Epstein Barr or Coxsackie virus, and so on. Lipkin also identified a possible cytokine shift at about year three. Is this stable? Does it associate with other findings? If we split the above groups into under three years and over three years, does it make a difference?

 

I thought I would chime in on this, since disabling "vertigo" was a major feature in the first decade of the disease for me. I'm surprised that there is actually a name like "Supermarket Syndrome." Large, enclosed spaces, like supermarkets or "big box" stores like Walmart, didn't exactly trigger my vertigo, since it was effectively 24/7, but being in such places definitely threw it into high gear. I suspect that it has to do with being confronted by so much "perspective." The converging lines of sight just make it harder to ignore one's unsteadiness. I found that the repeating patterns of overhead lights was especially annoying. I learned to keep my eyes pointed at the floor. This didn't always work, as I discovered when my local library installed new carpeting with a particularly jarring repetitive pattern.

Apparently, dizziness in large open spaces is a symptom of agoraphobia, but, since dizziness can make you want to avoid such places, it's easy to get mislabeled with that kind of anxiety disorder when, in fact, you have a disturbance of the balance center. By happenstance back then, I ran across a newspaper article about someone who was leading a one-woman crusade against the labeling of people with vestibular disorders as "agoraphobics." She lived in my town, so I met her, and it was largely due to her that I sought out sophisticated vestibular testing that showed significant impairments in both of my ears. It was very important to me, as it was the first concrete proof I had that my symptoms were not "imagined."