USA - NCHS/CDC Proposal for ICD-10-CM - adding SEID

I am speaking from the US perspective - See my other response regarding the behavior modification treatments promoted by the US CDC in my other response.

Also - I appreciate the clarification about differing points of view being expressed on here. At some point though, some basic agreement about what terms mean when used on here are necessary to avoid misunderstandings. When I say ME, I am referring to a specific disease which is well described in the ICC. If others are using the term ME but it doesn't look anything like the ICC, then misunderstandings will take over the threads.

I understood the goal of this group is to delve in to the science for myalgic encephalomyelitis. We can't discuss the science if we don't know what group of patients we are talking about.

 

Thank you. I understand better now.

I think, in principle, it's not a bad thing patients are "pro-active". I just know that in Germany, for instance, in most cases (ca. 95%) it will not work to ask doctors to use G93.3 or to educate them. They're simply God, end of discussion. Sadly.

Edit: I'm aware, at last , we're discussing about the US situation.

 

Honestly, I have info on some but when I say there are a LOT of efforts underway, I mean it. So I can't answer if any of them are based off of the IC primer. I've noted through my interaction with clinicians that they tend to trust large gov't-sponsored research, though, and that they scoff at CCC and ICC as 'too complex'.

I find this interesting and unusual, because clinicians in other disciplines don't seem to take issue with complex diagnostic algorithms or a wide variety of symptoms. In particular, I recall at the first Dysautonomia Conference -- which was a real game-changer for me in terms of how I conceptualize the way doctors CAN and SHOULD view illness -- they mentioned the wide variety of symptoms and emphasized the doctor should listen carefully and take down every little detail because you never know what might give a clue and help the patient improve. They all seemed to feel this way. What I get from mainstream docs is that if it isn't pared down, you lose them. They begin to believe that you're making it all up if you provide them with too much information.

Isn't this circular, though? We're trying to find a biomarker so we must use a specific definition of the disease -- but that definition may or may not include those with the biomarker we're looking for.

To be perfectly clear, I'm playing devil's advocate here -- I think CCC or ICC should always be the research definition -- but this is what researchers will say. In fact, they've said it to me directly!

 

Just to add to the confusion.David Systrom ( Harvard) started his research using invasive CPET with the symptom of exertional intolerance rather than any diagnostic label. He has found the same results for exertional intolerance in fibromyalgia, POTS and ME. He's a pulmonologist.If the term SEID serves to bring more researchers into the field that's great.

 

I have in the past paid relatively little attention to the ICC criteria and the IC primer document because they did not seem particularly relevant to research coming through. I had a look last night at the IC primer.

I think this is a very problematic document. It does not read like an information sheet based on careful analysis of scientific and clinical evidence. It reads like something cobbled together by a group of people who would like to believe in a particular way of looking at an illness that fits their research agenda or clinical practice but without any thought for consistency or justification. Sorry, I have to say it, it is just plain bad, and in the context of health care advice, worrisome.

The focus seems to be on the idea of a central 'multi-systemic neuropathology'. To start with this makes no sense in ordinary medical language. Neuropathology is pathology in one system - the nervous system. If the pathology is multi-system (not sure where the ic comes from) then it is more than neuro-. More importantly, there is no known neuropathology in ME. There are all sorts of symptoms but clinical assessment of people with ME does not point to any specific focal neuropathology and tests do not show anything consistent. There must be some sort of neuropathology to produce cognitive dysfunction and sensory intolerances but to imply that we have evidence of a particular pathology and call it near-immune exhaustion is just bad science and bad medicine.

Again, it looks to me that the group is making a false analogy - looking back to the claims made by Acheson and others about neuropathology and 'polio-like paralytic illness'. That is not what ME is about or ever was about as far as I can see. ME is a chronic disabling condition that at present we do not understand that shows no similarity to neuropathic viral diseases.

I realise that I may shock or upset some people by being as frank as this about ICC. However, I feel I have to because I am aware that the document has been taken as bona fide by a lot of patients and I think it is very misleading. It encourages people to look for treatments that are much more likely to do harm than good and to consult with alternative practitioners who are likely to be bad news for all sorts of other reasons. Everyone is free to make their own decisions but when children are involved things are not so simple.

 

We get nowhere if everything and anything about ME research is "crap". There's no money. So one can't expect to have high-quality research. (Even if there is money research doesn't have to be qualitative.) Still, sometimes you can get some info from bad research, too.

Additionally, ME research is holey. This starts to change I think.

But there are also the people who have ME; observations can be made. But it seems it is not done. Because observations from the past are crap. Observations from the present are crap. Well, observations are crap.

So the IOM report is crap. Why should SEID be added to ICD10-CM?

The ICC Primer is crap. (And from here it follows, CCC is crap.) Why should ME stay in ICD? Under neurological disorders? Due to some noise sensitivity? (I'm being cynical.)

Remains CFS-Oxford and Fukuda. Crap?

Altogether, all diagnostic criteria are crap - why diagnoze ME at all? And if one decides to diagnoze ME, how if all criteria are crap?

The authors of ICC or CCC had lots of experience with patients. My impression is they did something I barely met in a doctor (or many other people): They listened and they observed. This must be the starting point: observation. Then one has to describe the observation. We all know that different people describe their observations differently. This isn't physics where an observation can be put into a standardized language. We all know, for instance, how hard it is to describe PEM.

I think, those who suggested ICC or CCC tried their best to put their observations into words. I also think IOM tried this by reviewing papers - not exactly an observation, but it can add valuable information.

Those that suggested CFS-Oxford didn't ground that on an observation, it was motivated by politics.

You start with an observation. You try to collect more people that fit into this observation. You try to figure out what lies behind the observation - what's the process behind it etc.?

 

I may have misread this, but it seems you're arguing for crap to be included because we don't have anything else? But isn't that exactly what happened when we got CBT and GET on the guidelines last time? They had little else to go on and didn't want to publish a blank guideline, so published a crap one instead.

When it comes to a war of biomedical crap versus BPS crap, they win. That's because they have the titles, the positions of influence, and the governmental backing (either in the past, such as with PACE, or in the present, such as Wessely's current role in the mental health review). They also have traditionally had larger grants, which lends them a credence the smaller trials don't have.

There aren't any easy answers here. There are brief answers (we need more and better research, for one), but they're actually quite complex because they rely on lots of things falling into place. But I do think it will happen. Only, though, if we keep insisting for better research and point out how woefully bad past research has been.

 

I am not quite sure what point you are making with your first sentence Inara. Some ME research is very good - especially the stuff with bona fide negative results like the phase 3 rituximab trial.

My reason for criticising IC primer was exactly what you say in your second sentence. The problem is they did not do that. Rather than starting with observation they started with a belief in 'neuropathology' which had never been observed and 'neuroimmune exhaustion' after some doubtful immune findings that as far as we know have nothing to do with the nervous system. They assumed they knew what the process was and said we should fit the patients to that.

What they are proposing is a bit like assuming that ME is due to short-sightedness. You the take all the short sighted people with ME and say they have 'real ME' whereas the others don't.

 

Think ?Dr Koroshetz @ NIH has said it's too early to form subgroups. Is it up to researchers to look for subgroups within their data?

 

I see it can be understood like that.
CBT/GET and BPS are not about science or helping patients or understanding. It's about power. That needs to be addressed differently - it's another game with other rules. That's why they don't stick to scientific principles, in my view.

I think we have to be cautious to call everything crap, and too fast. For example: The NK cell studies aren't all crap - they're maybe not consistent. Lack of consistency or reproduction is not the same as crap. I think it would be more accurate to say "We don't know - we should look closer". We don't have deep analyses, with very few exceptions. That something isn't reproduced doesn't mean it's crap - it could be there was no money, or researchers realized they don't have the technology, or they find the topic not promising enough (again money). I also think, if it is looked at the immune system, this should happen at several points of time.

In the meantime, people with an ME diagnosis might find they have NK cell abnormalities. To say these are crap is denying part of reality, and maybe a person's reality. Obviously, there are people with ME who probably have these abnormalities, and others who don't. Does that mean the entire topic is crap? No. For some NK cells might play a role, for some they don't. Maybe we don't have the technology to know.

If we get down to it, we know only one thing for certain: There are sick and disabled people, whose disease was once called ME - it's not important if that name is correct, you could have chosen the name XYZ or KaKa - and other people tried to describe that symptom complex as best as they could. Some here say they were biased, seems everyone around ME was biased. Biased or not, sadly, that wasn't improved over time - which is the normal way - it was worsened by those who claimed the symptom complex is fatigue, by those power people.

All this doesn't get better with adding more and more names and more and more criteria. The ICC/CCC has one advantage: Many "experts" in the field agreed on them. That's quite an exception in the ME world. This could be further developed.

Imagine you all would have to describe your disease. How would you do it? How would you decide that another person has the same disease? In order to find out what's going on, you need to find people who resemble your disease as best as possible, not "a little". You can look at those separately to find if they share the same pathomechanism or another one, which would be quite enlightening.
I think that would be interesting.

Every human a new world.

 

I had to rethink about that.

What ICC/CCC/SEID share is something called PENE or PEM. The name is not important at this point. You could call it short-sightedness. This is supposed to summarize the experience of people with ME that their state worsens substantially after activity, noise/light/whatever exposure and so on. That's something we agree on: People with ME have in common PEM/PENE/short-sightedness. Therefore this is required to diagnoze ME. But it's not enough because this symptom is not ME exclusive. You need more to specify ME. Now it gets difficult.

So what to do?

Edit: I am not for the fight "ME vs. real ME". It's not constructive.

 

Maybe ME/CFS is nothing like any other illness and that's why we can't figure it out because we keep trying to investigate it like it's any of the kinds of illnesses we already know about.

Maybe we need to carefully and without assumptions look at every tissue in post morten studies.

 

In essence I agree. But we do not call PEM short sightedness because that means something else. PEM is an observed symptom in standard medical language - feeling like flu after exertion. But neuroimmune exhaustion presumes to give an explanation and I think that is uncalled for.

In fact it is very unclear what this term is supposed to indicate. It could mean a feeling of exhaustion that has a neuroimmune origin. Maybe, but we do not know that.

But it also seems to imply that somehow the neuroimmune system is exhausted or out of stock. This is obviously in some people's minds because the normal or low cytokine levels found later in the illness by Hornig and maybe others has been referred to as perhaps 'immune exhaustion'. But what would that mean? Running out of cytokines? Or cytokine RNA? or Cytokine DNA? None of those makes sense. Maybe running out of cells that make cytokines - but which cells?

What I object to is verbiage that sounds scientific but which is really just free-wheeling word association without any attention to plausibility!


I really don't think there is that much of a problem in defining people with ME. It seems a good idea to focus on PEM as a central requirement - but assuming that this is in the context of disabling fatiguability and sleep disturbance that is not obviously secondary toothed conditions that maybe include PEM. (I am actually not that sure that PEM occurs in other conditions.)

I think really that we agree that what matters is the observed clinical picture and the need to find out what its mechanism is without any preconceptions. And not get too bothered about names.

 

I shall not be commenting further in this thread as I am now retired, but this thread needs bumping.

 

Important update regarding proposals for ICD-11:

https://www.s4me.info/threads/updat...d-terminology-systems.3912/page-9#post-123205

 

Notice of upcoming March 5 - 6, 2019 meeting of the NCHS/CDC ICD-10 Coordination and Maintenance Committee

Federal Register Notice of Meeting issued 02/06/2019:

National Center for Health Statistics (NCHS), ICD-10 Coordination and Maintenance (C&M) Committee Meeting,

March 5, 2019 and March 6, 2019:

https://www.federalregister.gov/documents/2019/02/06/2019-01213/national-center-for-health-statistics-nchs-icd-10-coordination-and-maintenance-candm-committee

PDF: https://www.govinfo.gov/content/pkg/FR-2019-02-06/pdf/2019-01213.pdf



The Tentative Agenda includes discussions on the diagnosis topics listed below. Agenda items are subject to change as priorities dictate.

Matters To Be Considered:

ICD–10–CM Topics (Diagnosis topics):

Babesiosis
Congenital Vascular Hematomas and Hemangiomas
Corneal Dystrophy
Juvenile Osteochondrosis of Tibia and Fibula
Macular Hole Expansion
Neonatal Cerebral Infarction
Osteopenia of Hip
Sjogren Syndrome
Social Determinants of Health
Unspecified Use of Alcohol or Cocaine with Withdrawal

The full Agenda (known as the "Topic Packet") is posted a day or so before Dau One of the meetings.

It usually includes a greater number of topics that those listed in the early "Tentative Agenda":

Attendees who wish to attend the March 5–6, 2019, ICD–10–CM C&M meeting must submit their name and organization by February 22, 2019, for inclusion on the visitor list.