Does recovery after CCI/AAI surgery exclude an ME/CFS diagnosis?

[ebethc]

I think a good analogy is HIV and AIDS. HIV does cause AIDS, but HIV is not the only way one can way to get AIDS.

what other ways can you get AIDS? you mean you can have AIDS but not HIV?

 

[panckage]

what other ways can you get AIDS? you mean you can have AIDS but not HIV?

Apparently. There a few studies on it from the 90's. I'm not sure if the other causes have been found
Eg. https://www.google.ca/url?sa=t&sour...Vaw1aH0OO6FyvGqV02-kRlHoc&cshid=1559147000552

 

[sue1234]

Regarding the having EDS vs. not having EDS issue, maybe we should classify it as having just a collagen issue. I do NOT have EDS, as I am quite the opposite. I have almost rigid joints compared to EDS. I could never do a back bend as a child, nor could a do a regular cart wheel because my hands did not bend back enough for leverage. I was born with hip dysplasia and by 12, had slight scoliosis. I was finally diagnosed with Multiple Epiphyseal Dysplasia(MED). I only was able to really understand what it was with access to Google decades later. It says it is a problem with the COL9 gene, which obviously is in the same family as the EDS COL3(?). My point being, we have different ways of getting to problems with our collagen, whether genetic variances, illness affecting gene expression, etc. I will be getting myself evaluated for CCI to either rule it in or out as a contributor to my 13-year illness.

 

[JES]

CCI can cause ME it seems but how common that is we do not know

This would be one of the key things to understand before people build their hopes up too much. There is a poll in another forum thread here, which currently has it at 18 people testing positive for CCI and 11 negative and we can probably assume at least most responders were diagnosed with ME/CFS, since they are members on this forum.

The next thing I would like to gain some understanding of, at least through anecdotal stories, is if there is a particular set of symptoms associated with people who get a positive scan for CCI and have been diagnosed with ME/CFS. The symptoms that Jen and Jeff had included many typical ME/CFS symptoms, but they also experienced symptoms not specific to ME/CFS like "head feeling too heavy", headaches, breathing problems, pressure behind the eyes, worsening/improving with head position change, etc. These seem to be typical symptoms of patients diagnosed with CCI, but the curious thing is that there is an overlap of both ME/CFS and CCI symptoms in these recovery stories. But what if one only has ME/CFS symptoms, does it make much sense to have any hopes about CCI being the cause? I have POTS, but I never had any symptoms related to my head specifically.

 

[Rufous McKinney]

If you're rich or live in a country w good/decent government coverage it's hard to understand how healthcare drives ppl to financial ruin.

In my case, I have Medicare. And I earned a supplemental Medicare Advantage plan thru work. What this plan provides me is: quite unclear.

I cannot access the two data bases they use to: determine whether you can obtain X for treatment Y. they use this for denials, but it costs money to subscribe so I cannot read it.

Calling on the phone several times: has not lead to any further clarity.

 

[ebethc]

I cannot access the two data bases they use to: determine whether you can obtain X for treatment Y. they use this for denials, but it costs money to subscribe so I cannot read it.

Calling on the phone several times: has not lead to any further clarity.

ridiculous, and way too common.... sorry you have to navigate that... I have piles of paperwork that needs to be filed and organized from insurance... it's too much for me, too.

 

[Hip]

But what if one only has ME/CFS symptoms, does it make much sense to have any hopes about CCI being the cause?

Although almost certainly not all ME/CFS patients will have CCI/AAI as the cause of their illness, once we get a better understanding of the basic mechanisms by which CCI/AAI might lead to ME/CFS, we may find that non-CCI/AAI ME/CFS patients are also affected by the same mechanisms — but arising from a different initial cause.

For example, if CCI/AAI is causing ME/CFS by impeding proper autonomic nervous system (ANS) functioning — ie, ANS dysfunction is the basic mechanism of ME/CFS — then non-CCI/AAI patients might also have ANS dysfunction as the basis of their ME/CFS, but arising from other causes, such as for example the old vagus nerve infection theory of Michael VanElzakker.

 

[ScottTriGuy]

HIV does cause AIDS, but HIV is not the only way one can way to get AIDS.

Yes, HIV may cause AIDS (usually only if the person does not have access to HIV meds).

There is only one way to develop AIDS, and that is untreated HIV.

Nothing else causes AIDS. AIDS by definition is a result of HIV and only HIV.

 

[Wayne]

then non-CCI/AAI patients might also have ANS dysfunction as the basis of their ME/CFS, but arising from other causes, such as for example the old vagus nerve infection theory of Michael VanElzakker.

I've come to believe that vagus nerve involvement is a factor that ties a lot of varied causes for ME/CFS together. -- For years, I've done coffee enemas 1-2x/day, and for the longest time thought the significant benefits I got from them was the result of improved detoxification, and helping me maintain regularity. Just a couple of years ago however, I came to believe most of those CE benefits were instead from the ability of CEs to stimulate the vagus nerve, with one of its benefits being the activation of my parasympathetic nervous system.

I believe the primary reason for my own vagus nerve dysfunction was from it being compressed from a whiplash injury. But I also believe it was impacted by my chronic Lyme situation, and very likely other conditions going on in the body, particularly in areas through which the vagus nerve traverses. Which is just about everywhere from the head and neck all the way through the torso and ending in the colon.

My hypothesis is that any area of the body through which the VN traverses can become stressed by any number of reasons, such as infections, poor digestion, leaky gut, various kinds of structural imbalances, tight fascia, etc., etc. And when an area is stressed, the VN immediately sends this information back to the brain, initiating a "sickness response". So just about anything that causes stress in the body--in my mind--takes a person one step closer to becoming vulnerable to developing full-blown ME/CFS.

Accumulate enough of these stresors, combine them with the introduction of a traumatic event, and people with various susceptibilities (such as poor diet, or lack of exercise, enormous stress, mold exposures, etc.) can easily succumb to the ravages of ME/CFS. -- This is a very broad outline of my working hypothesis of different causes for ME/CFS. But I don't want to discount any number of other fundamental factors that can play a role as well, including genetics, epigenetics, various metabolic disorders, highly sensitive systems, etc. But in my mind, vagus nerve involvement is likely to be prominent in most cases.

 

[toyfoof]

@Mary @ebethc @Gingergrrl

I put a post about the CranioCradle with pictures from the pamphlet in my thread about neck issues here: https://forums.phoenixrising.me/thr...-me-cfs-experiences.62457/page-5#post-2207892

Since we were going off topic in here!

 

[nanonug]

It has been a terrible problem for the people that were misdiagnosed. Instead of getting the treatment they needed, they ended up with a label that, as of today, is still a medical cul-de-sac. For those who were finally correctly diagnosed with CCI, I'm happy for you. Also, envious.

Assuming that SEID/CFS/ME is a distinct medical condition for which one or more markers will be found, it has also been a terrible problem for people correctly diagnosed as well.

Many people with CCI were most likely included in many SEID/CFS/ME studies. Depending on the proportion of people with CCI included, the amount of "noise" introduced may have been enough to prevent these studies from reaching statistical significance. For this reason alone, many of the studies performed in the past will have to be trashed. A big "one step forward, two steps back" problem for people correctly diagnosed.

Some of you will feel the need to tell me that, if someone fits the criteria, whatever that might be, then that person has been correctly diagnosed with SEID/CFS/ME. Although it may seem a correct assessment, that is not the case. Most - if not all - diagnostic criteria include an exclusionary clause. We now know that many people with CCI present symptoms that mimic those of SEID/CFS/ME. The exclusionary clause is then fully applicable to CCI rendering the remaining criteria irrelevant.

If there is a lesson here for people diagnosed with SEID/CFS/ME, it is to never stop seeking alternative diagnoses that fit, even if imperfectly, the symptoms. One never knows who might get lucky.

 

[pattismith]

If there is a lesson here for people diagnosed with SEID/CFS/ME, it is to never stop seeking alternative diagnoses that fit, even if imperfectly, the symptoms. One never knows who might get lucky.

I understand your concern.
Mitochondrial diseases, D lactic acidosis, upper spine pathologies (not only CCI but stenosis, Chiari, etc), probably some auto-immune diseases and some genetic diseases too…. Many diseases can produce the ME syndrome, and are unfortunately still not correctly diagnosed. I am afraid that studies that are not able to segregate subgroups in their datas will not find anything consistant!

On the other hand, each time a subgroup is identified with a specific underdiagnosed disease, it helps a lot to better identify other subgroups!

 

[Pondering]

It has been a terrible problem for the people that were misdiagnosed. Instead of getting the treatment they needed, they ended up with a label that, as of today, is still a medical cul-de-sac. For those who were finally correctly diagnosed with CCI, I'm happy for you. Also, envious.

Assuming that SEID/CFS/ME is a distinct medical condition for which one or more markers will be found, it has also been a terrible problem for people correctly diagnosed as well.

Many people with CCI were most likely included in many SEID/CFS/ME studies. Depending on the proportion of people with CCI included, the amount of "noise" introduced may have been enough to prevent these studies from reaching statistical significance. For this reason alone, many of the studies performed in the past will have to be trashed. A big "one step forward, two steps back" problem for people correctly diagnosed.

Some of you will feel the need to tell me that, if someone fits the criteria, whatever that might be, then that person has been correctly diagnosed with SEID/CFS/ME. Although it may seem a correct assessment, that is not the case. Most - if not all - diagnostic criteria include an exclusionary clause. We now know that many people with CCI present symptoms that mimic those of SEID/CFS/ME. The exclusionary clause is then fully applicable to CCI rendering the remaining criteria irrelevant.

If there is a lesson here for people diagnosed with SEID/CFS/ME, it is to never stop seeking alternative diagnoses that fit, even if imperfectly, the symptoms. One never knows who might get lucky.

I am a bit confused? Is there some research I am unaware of that says that CCI isn't ever associated with ME/CFS?

 

[Hip]

Some of you will feel the need to tell me that, if someone fits the criteria, whatever that might be, then that person has been correctly diagnosed with SEID/CFS/ME. Although it may seem a correct assessment, that is not the case. Most - if not all - diagnostic criteria include an exclusionary clause. We now know that many people with CCI present symptoms that mimic those of SEID/CFS/ME. The exclusionary clause is then fully applicable to CCI rendering the remaining criteria irrelevant.

I've always thought there is a slight logical flaw with such exclusion criteria: if the diagnostic criteria for ME/CFS excludes any other explanation for the symptoms, then when we do find the real cause of ME/CFS, that too will be excluded!

For example, if in future it were proven that ME/CFS is caused by chronic non-cytolytic enterovirus infection of the brainstem, then the exclusion criteria would say that you did not have ME/CFS, rather you had a non-cytolytic enterovirus infection.

So if you take such exclusion criteria too literally, it would be impossible to ever find the cause of ME/CFS, because as soon as you did find it, that cause would get excluded!



I think the hypothetical question to consider in these CCI/AAI cases is this: imagine in future if we develop some reliable biomarkers for ME/CFS testing. Then we can ask, would those with ME/CFS symptoms arising from CCI/AAI test positive on those biomarker tests? If they did, then we would say that they were suffering from ME/CFS, but just from an unusual cause. (Or maybe not so unusual, as it remains to be seen what percentage of those diagnosed with ME/CFS have CCI as the cause).

Whereas if they tested negative, we might conclude that they did not have regular ME/CFS, but had a very similar set of symptoms caused by their CCI.

The nearest we have to biomarkers at present are things like elevated IgG antibody levels to the ME/CFS-associated viruses, and low NK functioning. Both Jen and Jeff had such elevated antibodies, and I believe Jeff had low NK functioning.

 

[nanonug]

I've always thought there is a slight logical flaw with such exclusion criteria: if the diagnostic criteria for ME/CFS excludes any other explanation for the symptoms, then when we do find the real cause of ME/CFS, that too will be excluded!

Not necessarily. If a novel mechanism is behind SEID/CFS/ME then that will define the disease. But I doubt it will be called any of the current three acronyms.

For example, if in future it were proven that ME/CFS is caused by chronic non-cytolytic enterovirus infection of the brainstem, then the exclusion criteria would say that you did not have ME/CFS, rather you had a non-cytolytic enterovirus infection.

Not really. You'd simply rename the disease to something more appropriate. Simply, "the disease previously known as SEID/CFS/ME is now known as non-cytolytic enterovirus infection."

I think the hypothetical question to consider in these CCI/AAI cases is this: imagine in future if we develop some reliable biomarkers for ME/CFS testing. Then we can ask, would those with ME/CFS symptoms arising from CCI/AAI test positive on those biomarker tests? If they did, then we would say that they were suffering from ME/CFS, but just from an unusual cause.

In that case the biomarkers would not be specific enough. Additional tests, the kind people that are being diagnosed with CCI are being subjected to, would have to be ordered concurrently.

The nearest we have to biomarkers at present are things like elevated IgG antibody levels to the ME/CFS-associated viruses, and low NK functioning. Both Jen and Jeff had such elevated antibodies, and I believe Jeff had low NK functioning.

You are relying on studies that have been done that most likely included people with CCI. There is no reason to believe that those same conclusions still apply if the CCI subset is excluded. Many (most?) of the studies done in the past cannot therefore be relied upon.

 

[Hip]

If a novel mechanism is behind SEID/CFS/ME then that will define the disease. But I doubt it will be called any of the current three acronyms.

Well CCI could be classed as a novel mechanism, as it has never previously been associated with ME/CFS. And this is also the first time to anyone's knowledge that corrective surgical treatment been shown to put ME/CFS symptoms into remission.


What interests me is whether the negative effects CCI has on the autonomic nervous system (ANS) might be the basis by which ME/CFS arises. Both Jen and Jeff had rapid remission from POTS after CCI surgery, suggesting that the surgery normalized the ANS. Then some weeks to months later, the ME/CFS symptoms cleared up as well.

There is increasing research interest in the way the ANS interfaces with the immune system, so this makes me wonder whether once normal functioning was restored to the ANS, this may in turn have resulted in a restoration of proper immune responses, allowing the immune system to finally clear viral infections, and/or rectify autoimmunity.



By the way, the NIH decided it was not going to adopt the name SEID, so I don't think that acronym is ever going to be used.

 

[nanonug]

Well CCI could be classed as a novel mechanism, as it has never previously been associated with ME/CFS.

If CCI were the novel mechanism behind SEID/CFS/ME, then the latter would no longer be a disease, it would simply be a set of symptoms associated with CCI. The disease would simply be CCI. If this turns out to be the case, then mostly likely I was misdiagnosed with CFS as I don't think I have CCI.

 

[nanonug]

Mitochondrial diseases, D lactic acidosis, upper spine pathologies (not only CCI but stenosis, Chiari, etc), probably some auto-immune diseases and some genetic diseases too…. Many diseases can produce the ME syndrome, and are unfortunately still not correctly diagnosed. I am afraid that studies that are not able to segregate subgroups in their datas will not find anything consistant!

I suspect that most studies wouldn't be able to segregate all subgroups anyway given the amount of people they typically enroll. Having one or two people in a subgroup very much kills any hope of achieving statistical significance. Not to mention that most researchers would probably not have the technical and/or financial means to identify all the subgroups. It's one big mess!

I am more and more convinced that being diagnosed with SEID/CFS/ME is useless. It is only Ron Davis's research that gives me some hope. Which reminds that it is probably time for me to leave PR once and for all. I have been here since March 2012 and PDH inhibition/dichloroacetate was the only thing truly helpful. I could have gotten the same info just perusing Pubmed, though.

 

[Hip]

If CCI were the novel mechanism behind SEID/CFS/ME, then the latter would no longer be a disease, it would simply be a set of symptoms associated with CCI. The disease would simply be CCI.

That assumes that CCI is the only casual mechanism of the ME/CFS symptoms. But what if, for example, it were a combination of chronic viral infection, plus CCI-caused autonomic disfunction which prevents the immune system from clearing the infection (which I actually suspect could be the case)?

Then you would have standard viral ME/CFS, in which CCI plays a maintaining role.

Perhaps similar to those ME/CFS patients who have IgG deficiencies, which may also be playing a role in maintaining an infection that cannot be cleared by the immune system.

 

[percyval577]

I suspect that most studies wouldn't be able to segregate all subgroups anyway given the amount of people they typically enroll. Having one or two people in a subgroup very much kills any hope of achieving statistical significance. Not to mention that most researchers would probably not have the technical and/or financial means to identify all the subgroups. It's one big mess!

1. I think , the main question must be, which structure in the body can only generate PEM, and can generate the somehow widespread plethora of different symptoms in different patients?
2. And only the next question were, by which and how many different impacts, this stucture could be somehow disturbed, to generate these potentilally very awful states.

Thinking logically, and best systematically. Still our research goes from 2. to 1. somehow. Not all bad of course, if you can´t get a prevailing idea.

Having read some articles on PEM, my philosopher approach would be this.
There is an article: "What does dopamine mean?" Yes, this whole strucure where dopamine is typicall would explain some plethora ... and also the common misconduct we do like so much, but we can say indeed, the Mechanism which might be involved in psychosomatics has gotten a huge impact.
However, call me an idiot, but I am slowly on my way out, here I tried a theory, short written.

@nanonug, your avatar ... sometimes I think the main possibility for our ilnness is indeed only that cells havn´t adapt to the new size of our brains, and our old friend the homo erectus wouldn´t suffer with mecfs.