13th Invest in ME Research International ME Conference - 1st June 2018

But are they paying for people to travel, their carer, their carers travel, etc.? Are these people covered if they get worse and need to stay in the US until they improve a bit, which may never happen?

 

If cyclo works, hopefully they will be able to look more closely at why it works, and potentially find other alternatives that can have the same effect but not as severe side effects. I hope cyclo works if it can bring us closer to an answer, but I hope my health won’t depend on taking it for long periods

It is possible that for some patients one treatment will be enough to reset the system in some way, while for others it will only give temporary relief or none at all. In autoimmune diseases cyclo is used mostly as an early intervention to stop the disease progress in its tracks, before moving on to other more long term treatments.

 

This doesn't surprise me at all now after spending the last 3 years actively pursuing more accurate diagnosis, subsequent to 20 years of a useless CFS label.

The differential diagnosis challenge is staggering, there are so many overlooked conditions because not everyone presents in the classical manner. Even when they are suspected and investigated, tests are often not reliable enough. The whole thing is a complete guessing game.

It boggles my mind that any doctor can confidently give a diagnosis of exclusion when it is impossible to actually exclude even the basics properly, let alone the rarer diseases.

 

A differential diagnosis thread maybe?

 

Its kind of you to ask, thank you.

I will PM with more detail if you're interested? But as it's sort of related to my point above, in brief I've gathered a number of more specific but almost as poorly understood diagnoses.

Of course, if I ask each of the specialists in those fields about CFS or the other syndromes they say no it's not comorbid, your problems are explained by just <insert my interest here>. Such a mess of uncertainty.

I don't want to sound too pessimistic, so perhaps a better thing to end on is how much respect I have for the researchers that are genuinely trying to unravel it all regardless of the challenges. Most of the presenters at IIMER seemed to be doing that

 

I don't get the idea of M.E being hard to diagnose. I diagnosed myself and got it confirmed by two consultants within 6 months. Of course I had all the standard hospital tests done in the hope that it would be something else but I knew very early on. The crashes are the cardinal sypmtom. PeNE and PEM....I suppose I was a classic case, viral onset and I was low moderate to begin with so I would crash easily enough. The ICC was perfect. I don't see how M.E is hard to diagnose. The trouble is majority of doctors know nothing about it. Some think fibromyalgia and M.E are one and the same. I have met a lady diagnosed with.M.E who believes she has M.E but doesn't. She visited me to 'help' me. She never experienced a crash, had no idea what it was. Loved mountaineering. Her main symptoms were recurring throat infections and feeling tired after late nights out. She was.diagnosed 10 years ago. She assured me it was possible to live a full life with M.E......yes, as I type from my couch and my family are gone away to a hotel for the w.end......sorry this has turned into a rant. My point is M.E is easy to diagnose if doctors knew enough about it.

 

I couldn´t agree more. Not only interesting but essential.

I hope somebody raise this question officially to the NIH.

This may be happening in some other studies and it may contribute to the difficulty in finding answers to this illness since ME may turn to be different diseases, as many Researchers are already pointing out

And it could happen that identifying these conditions may help some patients to find treatments and improve their health ( I have in mind a young patient whose mother participates in the other forum and has been diagnosed with some other conditions)

 

Trying to be cautious in how I phrase this - at the conference I overheard several people within the American ME world express their concern about the selection criteria for Nath's study; that, in their opinion, a reason they are having trouble recruiting for it is because it's too strict.

 

@Sunshine3 Ive spent a little time in mitochondrial disease forums and I quickly realised that the symptoms people describe and the crashes are often very hard to separate from how people describe ME... meeting ICC/CCC criteria could absolutely be primary mito disease for some and I’m shocked it’s not the 1st thing on the possible differential diagnoses for ME.

 

You or anyone could email Nath. He said they do their best to reply to every email.

 

I'm looking forward to the era of individualised medical assessments and treatments, and perhaps an increase in genetic testing may help with differential diagnosis, e.g. after watching the 2017 IiME Conference DVD (IIMEC12) I decided to have a DNA test and unexpectedly found I have two copies of a gene mutation giving susceptibility to a rare metabolic disease. Apparently, it is now included in newborn screening (not sure if that's in all countries) but symptoms can onset in adulthood, including muscle weakness and can be triggered by infection...my initial diagnosis over twenty years ago was post-viral fatigue syndrome "in the expectation of recovery" and changed to myalgic encephalomyelitis when I'd got worse after a year or so. I fit all the ME criteria and the ME ICC post-exertional neuroimmune exhaustion describes what I get more specifically than the ME/CFS CCC PEM, but whether ME is comorbid in my case or was a misdiagnosis, I won't know until there are tests for differential diagnosis.

 

https://twitter.com/user/status/1002937688255860736

https://twitter.com/user/status/1003226776338825216

 

I can totally relate to this. The "funny" thing is - even if you've made it to a specialist consultation for neuromuscular diseases (pretty rare in itself), and even if your symptoms sound very similar to a mito disease you won't be checked. At least that's what happened to me and I don't think I'm a huge exception. I think this is cruel and scandalous; you should get a chance to improve your health. It's not like we have lifestyle problems.

 

I agree it seems implausible to not suspect Mito disease based on symptoms but all the reports so far suggest Mito disease is just as rare in CFS patients as anyone else.

The topic came up in this conference and the speaker reminded us of a study (by Hanson or Hornig I think?), that tested 200 patients for Mito disease. Ironically they found undiagnosed mito disease in 1 of the healthy controls but in none of the CFS patients. As with all CFS research the criteria and selection bias may come in to it, but 0/200 is pretty hard to explain away...

 

This happened to me also, the myologist was very much on the fence over the need for a muscle biopsy. Luckily I returned a rather high blood lactate test so that forced her hand.

She readily acknowledged that mild Mito diseases can cause the sort of symptoms we experience, so perhaps the decision comes down to whether or not it's worth putting a 'mild' patient through a biopsy that ultimately won't lead to a huge amount of treatment options anyway.

I can see it from the docs perspective, she deals with people that are at risk of dying from these diseases everyday and we aren't going to compete with that. On the other hand you probably need to suffer chronic illness to know just how important a diagnosis and the validation it comes with is, regardless of treatment options.

 

I think also all the severe patients in Stanford study had gene testing and none had known mito disease causing mutations. I think its also quite possible that what you get diagnosed with depends on the type of doctor you go to where from my understanding Mito doctors will diagnose mito disease based on respiratory chain defects when this dysfunction could also be a secondary result of another disease such as ME.

 

I mean ME is criminally underdiagnosed, but if a lot PwME are actually false positives then that is really worrying. Would be really interested to hear more about this, because in the end ME/CFS is a diagnosis of exclusion, so how can they be certain that the patients don't really have ME/CFS?

Is it because they do not fit the strict ICC criteria?
Or is it because they found that the patients in fact, suffered from something else?

I am sure a significant part of ME/CFS patients are really worried that they do not in fact have ME/CFS, so would be really interested in hearing what they have to say about this.

I feel like this would be the best explanation. To be honest, I have never been a fan of using extremely strict criteria in ME/CFS studies. Because you inevitably just end up looking at more severely ill patients. Even in the body of someone with mild ME/CFS who fits Fukuda or SEID criteria, something is clearly going absolutely haywire, and it should be possible to find something severely wrong compared to healthy controls. Sure you get ''more'' results and more to report with the sickest ME/CFS patients with CCC or ICC criteria. But I figure there would be less ''noise'' with Fukuda / SEID patients, who would be less ill.

I don't have any scientific background, so sorry if I come off as a compelte newb.

 

SEID (current clinical diagnostic criteria in US) is not technically a diagnosis of exclusion. This change was made by the IOM to get more patients diagnosed.

But no one seems to be studying whether adopting SEID criteria has increased the rate of misdiagnosis. I doubt that's even possible to study today.