Do MEs cause CFS?

[Mij]

@Sidereal have you tried socializing lying down? I only do this with people I know well, of course I find it helps.

It feels as though this lack of balance and staggering gait is related to a lack of blood flow going to the brain?

 

[Sidereal]

@Sidereal have you tried socializing lying down? I only do this with people I know well, of course I find it helps.

It feels as though this lack of balance and staggering gait is related to a lack of blood flow going to the brain?

Interesting. I haven't tried lying down but it makes sense it would help.

 

[Marco]

Same here, it's a really debilitating & isolating symptom. I can't really socialise because the exertion of trying to keep my brain engaged with conversation will cause me to start slurring my words and get dizzy, confused and ataxic. I'm ok with brief one-on-one conversation or phone calls but anything more than that is exhausting and overwhelming to the senses.

Me three! That's exactly how I get with long phone calls or crowds.

 

[Strawberry]

My understanding is that the brain uses up more energy than any other organ. When I over use my brain, even when socializing it affects my gait. My equilibrium goes and I start to stagger when I walk. I also get sore calves. I don't know if this is true PEM though since the symptoms occur soon after. Either way, it's still debilitating.

I wonder if that is why I walk/stagger like I am drunk after driving home from work. I thought it was just that driving was too much physical effort after a day of work, yet I don't get punch drunk after doing a chore or two. I just pay for chores or walking the next day with getting sick and sore/fatigued. Driving must be both physical AND mental PEM.

And here I was thinking I didn't get mental PEM.

 

[MeSci]

I wonder if that is why I walk/stagger like I am drunk after driving home from work. I thought it was just that driving was too much physical effort after a day of work, yet I don't get punch drunk after doing a chore or two. I just pay for chores or walking the next day with getting sick and sore/fatigued. Driving must be both physical AND mental PEM.

And here I was thinking I didn't get mental PEM.

Even before I had obvious ME, I was finding driving mentally tiring. I couldn't drive any substantial distance, as my concentration just gave up. I have always marvelled at how people can drive long distances! I only started driving about ten years before I developed obvious ME, although I rode a small motor bike before then. I did sometimes have the concentration problem on the bike, I think.

 

[BurnA]

If infection can trigger then vaccine probably can. But we do not have any clear idea how the immune dysregulation of reactive arthritis arises from an infective trigger. It looks like some sort of persistent T cell activation but that is about all we know.

Is there anything relevant in this paper -
Toplak, N. et al. Autoimmune response following annual influenza vaccination in 92 apparently healthy adults
http://www.researchgate.net/publica...tly_healthy_adults._Autoimmun._Rev._8_134-138

Influenza vaccination did not increase the percentage of
positive autoantibodies in the general healthy adult
population.
• Increased level of autoantibodies or appearance of new
autoantibodies was observed in up to 15% of apparently
healthy adults after the influenza vaccination.
• Out of 92 healthy adults included in our study, 11
participants developed transient and 7 persistently had
elevated levels of autoantibodies after the vaccination.
• Newly synthesized autoantibodies after the influenza
vaccination had no apparent clinical significance.
• Prolonged autoimmune response following influenza vaccination
cannot be excluded.

 

[Jonathan Edwards]

Is there anything relevant in this paper -
Toplak, N. et al. Autoimmune response following annual influenza vaccination in 92 apparently healthy adults
http://www.researchgate.net/publica...tly_healthy_adults._Autoimmun._Rev._8_134-138

Influenza vaccination did not increase the percentage of
positive autoantibodies in the general healthy adult
population.
• Increased level of autoantibodies or appearance of new
autoantibodies was observed in up to 15% of apparently
healthy adults after the influenza vaccination.
• Out of 92 healthy adults included in our study, 11
participants developed transient and 7 persistently had
elevated levels of autoantibodies after the vaccination.
• Newly synthesized autoantibodies after the influenza
vaccination had no apparent clinical significance.
• Prolonged autoimmune response following influenza vaccination
cannot be excluded.

It sounds as if nothing much happened. Antibodies to everything may rise following an immune stimulus, briefly. Antibody levels are not black and white. We all have low levels of autoantibodies. What matters is if there is a chain reaction that produces permanent high levels and clinical disease.

 

[BurnA]

It sounds as if nothing much happened. Antibodies to everything may rise following an immune stimulus, briefly. Antibody levels are not black and white. We all have low levels of autoantibodies. What matters is if there is a chain reaction that produces permanent high levels and clinical disease.

OK. I got the seasonal flu vaccine about 5-6 months prior to onset so I was wondering if there might be a link.

 

[Mij]

@Strawberry sometimes we compensate to preserve energy (mental and physical) without even realizing. When I first became ill I was asked by my M.E doctor if I had cognitive issues and I said no, not as far as I understood what that meant. But when he asked me several different ways we came to the conclusion that I did!

 

[leokitten]

I believe the basis of Fluge/Mella's theory, that fine tune control of blood flow is severely compromised, is a simple and very plausible mechanism explaining how both mental and physical exertion cause PEM. Muscles and brains require a lot of energy, i.e. rapid changes in blood flow to different areas.

I think we need to look at these more straightforward mechanisms tying together brain and body symptoms before delving into more complex ones. Even though this disease has been researched for more than a couple decades some basic questions still haven't been definitively answered.

 

[Chrisb]

As someone of now limited attention span I always fear that the ideas that come to me are platitudes fully dealt with years ago, and anyway of no interest. It's a risk that has to be taken.

There seems to me to be a corollary to the question of whether there are different sorts of ME, and that is whether, within the definition of the terms for the purposes of this Thread only, there are different sorts of CFS. There follows on from this the question of whether any changes which the sufferer experiences within his/her CFS are merely an "evolution" of the original CFS, or whether they amount to a new form of CFS. If they are a new form of CFS, which has arisen without the intervention of any new ME, could this, along with the failure of lazy practitioners (one can be sure that none of those referred to will be on this site, at least not with benign intent) to take or understand a full history, account in part for the biopsychosocial model of the condition?

I have no way of knowing how broadly my experience is shared. Over thirty five years my condition has progressed from mildish (after incomplete recovery from a July virus) to, at times, severe , at least in some major aspects. I borrow (steal, if you insist) Jay Gould's concept of "punctuated equilibrium" to describe the development. Although the condition fluctuates within certain parameters, one knows where one is in the cycle. Then something happens , the parameters change, and one is never as well again. Well, not yet anyway. Never is a long time-or perhaps not.

My subjective view is that the CFS experienced from year one to year eleven was clearly the same, despite being worsened by my attempts to recover full fitness. That from year eleven to about year thirty was a slightly different and substantially, in terms of degree, worse form. This was brought about by innovative therapy based on the advice of a leading expert. My present condition is something different again, but clearly related. It must be clearly related as my GP seems interested only in my blood pressure!

I do not wish to become solipsistic.The broader point is that upon presentation to a doctor uninterested in aetiology these different stages of CFS might appear as different idiopathic conditions.

A further question arises as to whether there might be any reason to believe that the different types of ME might lead to different and characteristic forms of CFS.

If I have misjudged this thread and am wasting your time, I apologise in advance.

 

[Jonathan Edwards]

If I have misjudged this thread and am wasting your time, I apologise in advance.

I don't think you have misjudged at all. What you say makes a lot of sense - it is all very complicated. Doctors are used to forgetting about the complications and latching on to some blood test that gives a nice number. Real life isn't much like that I think.

 

[MeSci]

It sounds as if nothing much happened. Antibodies to everything may rise following an immune stimulus, briefly. Antibody levels are not black and white. We all have low levels of autoantibodies. What matters is if there is a chain reaction that produces permanent high levels and clinical disease.

So you don't think it's significant that

7 persistently had elevated levels of autoantibodies after the vaccination

? (my bolding). I haven't read the paper, so don't know for how long the subjects were followed and thus for how long the elevated levels persisted.

 

[Chrisb]

I don't think you have misjudged at all. What you say makes a lot of sense - it is all very complicated. Doctors are used to forgetting about the complications and latching on to some blood test that gives a nice number. Real life isn't much like that I think.

Thank you for the response. It is most reassuring to know that you and those colleagues with whom you discuss these matters are open to our ideas. And that we are not entirely at the mercy of those whom I must try to avoid mentioning.

 

[BurnA]

If infection can trigger then vaccine probably can. But we do not have any clear idea how the immune dysregulation of reactive arthritis arises from an infective trigger. It looks like some sort of persistent T cell activation but that is about all we know.

Another one...
Autoimmunity. 2007 Feb;40(1):48-53.
Infection and vaccination in chronic fatigue syndrome: myth or reality?
Appel S1, Chapman J, Shoenfeld Y.

"The current concept is that CFS pathogenesis is a multi factorial condition in which an infective agent cause an aberrant immune response characterized by a shift to Th-2 dominant response. When the response fails to be switched-off, a chronic immune activation occurs and clinically expressed as the symptomatology of CFS."

How would this fit with your current thinking ?

 

[Jonathan Edwards]

Another one...
Autoimmunity. 2007 Feb;40(1):48-53.
Infection and vaccination in chronic fatigue syndrome: myth or reality?
Appel S1, Chapman J, Shoenfeld Y.

"The current concept is that CFS pathogenesis is a multi factorial condition in which an infective agent cause an aberrant immune response characterized by a shift to Th-2 dominant response. When the response fails to be switched-off, a chronic immune activation occurs and clinically expressed as the symptomatology of CFS."

How would this fit with your current thinking ?

Dear old Yehuda (Shoenfeld), bless his cotton socks, is the capo di tutti capi of popular 'autoimmunity'. There is no trendy theory he has not re-brewed for the masses. There is no such thing as a Th2 dominant response as far as I know. And there are no data in CFS so how does he know? I think he is muddling up autoimmunity with the chronic T cell activation of autoinflammatory disease.

In this case: myth!! (Or whatever they call it in Italian.)

 

[BurnA]

Dear old Yehuda (Shoenfeld), bless his cotton socks, is the capo di tutti capi of popular 'autoimmunity'. There is no trendy theory he has not re-brewed for the masses. There is no such thing as a Th2 dominant response as far as I know. And there are no data in CFS so how does he know? I think he is muddling up autoimmunity with the chronic T cell activation of autoinflammatory disease.

In this case: myth!! (Or whatever they call it in Italian.)

The idea is that once things have got started the immune system is dysregulated by the presence of antibodies that amplify the sort of cytokine or other signal responses that we usually make to viruses

Thanks, just trying to piece various bits together. How would the 'dysregulated' autoimmunity as you describe above differ from chronic T cell activation ? ie can you tell them apart ?

 

[Jonathan Edwards]

Thanks, just trying to piece various bits together. How would the 'dysregulated' autoimmunity as you describe above differ from chronic T cell activation ? ie can you tell them apart ?

Yes, normally that is easy. The autoimmune processes have antibodies which if you are lucky you can find. And they tend to cause disease through antibody effector mechanisms like Fc receptors or complement activation (as in RA or lupus) or interference with a particular tissue function (as in thyroid disease). T cell activation produces more local lesions that tend to be 'cold' - a term used to describe the 'cold' abscess of tuberculosis, which involves a local T cell response. Patches of psoriasis are typical of T cell lesions - local, patchy and 'cold'.

The problem comes when the effector mechanism is more subtle - as in the fatigue of Sjogren's syndrome (or other conditions with antibodies to nucleoproteins) and in the systemic symptoms that go with reactive arthritis or Crohn's diseas (T cell based). And if you cannot find the antibodies involved that makes things more difficult again. What is clear is that you can get severe fatigue in both B and T cell related diseases even if the specific immune or clinical signature of the disease is pretty hard to detect or short lived.

What I think may be an important difference is that we have very little evidence for B cell autoimmunity being triggered by infection or environmental stimulus. And that makes sense because B cells employ a chain reaction in their activation which can start up without external input. On the other hand there is a lot of evidence for disordered T cell activation after infection, of the sort seen in reactive arthritis or post-infective syndromes of other sorts. That also makes sense since after adolescence there is relatively little internal random generation of T cell clones - you really need an external trigger to change T cell behaviour.

 

[lansbergen]

I wish some severly affected would be tested for anti-PrPC-autoantibodies

 

[BurnA]

What is clear is that you can get severe fatigue in both B and T cell related diseases even if the specific immune or clinical signature of the disease is pretty hard to detect or short lived.

What I think may be an important difference is that we have very little evidence for B cell autoimmunity being triggered by infection or environmental stimulus. And that makes sense because B cells employ a chain reaction in their activation which can start up without external input. On the other hand there is a lot of evidence for disordered T cell activation after infection, of the sort seen in reactive arthritis or post-infective syndromes of other sorts. That also makes sense since after adolescence there is relatively little internal random generation of T cell clones - you really need an external trigger to change T cell behaviour.

Thanks for the very informative reply.

Would you speculate there is a subgroup of PWME with disordered T cell activation ? ( Based on the fact many people associate onset with infection) In this case would the onset be sudden - ie as soon as the disorder occured post infection ( or whatever stimulus ) ?

Or do you have an alternative suggestion why infection preceeds onset in many reported cases ?