The IACFS/ME Conference in Ottawa: Sept 22-25, 2011

[eric_s]

I don't know. I also like it, but we've heard about this earlier already, like it says in the article. I think Hemispherx has a history of making big anouncements, not meaning to be negative, maybe somebody who knows more about their history could say more here.

 

[heapsreal]

Always politics involved, i dont think ampligen was ever going to be approved when there was no way to diagnoses cfs/me, now we are getting closer to a diagnostic test and the authorities are starting to take this illness seriously, then maybe there a chance of ampligen being approved. I do like the idea of an oral version as getting 2 infusions a week would be tough to organise. But i bet it will be priced out of my league anyway.

cheers!!!

 

[ixchelkali]

Jones from the CDC on interoception. It was a very strange study looking at signals going into the insula I think. About all I understood was that it suggested that sensory information was flooding the brain at high rates - that was the easy part. There was alot on self/non-self - honestly it was almost incomprehensible.

Miller from Emory/CDC who presented it said he didn't understand it either. The study was so 'different' that I imagine that it will get little play simply because few people can figure out what he's talking about. I imagine that Jones will be retiring soon and the CDC is giving him his last shot.

Is he still chuntering on about that? That was published about 4 years ago. It's just a dressed-up of version of the "sickness behavior" theories. It's saying that the interoception pathways in the brain that tell us whether we're sick or not are wonky. They get turned on during a bout of disease and don't stop when the disease ends, so we perceive ourselves as sick (even though we're not) because our brains are sending the signals that make us feel sick, or because we misinterpret the signals.

1. In infections that lead to disease and sickness, altered self can be considered a basis of recognition by and activation of innate, adaptive, and/or danger-driven immune responses and general self-maintenance responses.
2. The subsequent immune system and organ system functional changes induce physiological and biochemical alterations that are also recognized at multiple brain levels as extended altered self.
3. Specific organ-based signs, symptoms, and behaviors produced during an infection constitute expression of disease.

Based on these statements the following hypotheses can
be generated:

1. In diseases with sickness behavior, brain responses occur at the unconscious (physiological/subcortical or innate) level and the conscious (cortical or adaptive) level with the aim of restoring host stability and resolving the altered self state.
2. Resolution of disease or illness requires successful adaptation to the insult.
3. Disease and illness can occur simultaneously, but resolution of each may follow different time courses.
4. Continued disease is associated with uncontrolled infection, altered immune responses, or ongoing injury. Persistent illnesses such as CFS and post-infection fatigue are due to maladaptive biological (interoceptive) and/or cortical signal recognition or subsequent responses to them.

Thus in chronic illness following infection in the absence of readily identifiable markers of immunologically mediated injury or responses, the extended concept of altered self means the individual has strayed from their baseline stability or positive adaptive capabilities due to perturbations in the production or recognition of biological signals.

Here's the study: http://www.cfids-cab.org/rc/Jones-4.pdf

You know, it's going to be hard for CDC to convince patients that the winds of change are sweeping through the CDC's attitude toward CFS, as long as they keep letting Jones go on about his pet theory in public.

 

[Cort]

Is he still chuntering on about that? That was published about 4 years ago. It's just a dressed-up of version of the "sickness behavior" theories. It's saying that the interoception pathways in the brain that tell us whether we're sick or not are wonky. They get turned on during a bout of disease and don't stop when the disease ends, so we perceive ourselves as sick (even though we're not) because our brains are sending the signals that make us feel sick, or because we misinterpret the signals.

Here's the study: http://www.cfids-cab.org/rc/Jones-4.pdf

You know, it's going to be hard for CDC to convince patients that the winds of change are sweeping through the CDC's attitude toward CFS, as long as they keep letting Jones go on about his pet theory in public.

Its a very strange study and I can't imagine it will go far.

One part of it (if I got it right) - the idea of the brain being flooded with too much sensory information I like actually - Clauw thinks that's what's going on in FM, Baraniuk suggested that the information filtering gates may be broken in ME and the Lights think the dorsal root ganglia could be amplifying signals from the brain as well. I think that part of the theory (again if I got it right) works...Too much stimuli from the body upregulates brain activity resulting in glutamate toxicity, etc. and problems with concentration, 'willed action' - the brain is suffering...

However, the rest of it is just so strange that I can't imagine that anyone is going to pick up on it. It's just out way there. I couldn't figure out what in the world the presenter was talking about.

 

[Cort]

You know, it's going to be hard for CDC to convince patients that the winds of change are sweeping through the CDC's attitude toward CFS, as long as they keep letting Jones go on about his pet theory in public.

I would say 'gusts'....Mangan made it very clear that Unger picked up the ball with the CASA project and really pushed it forward when it looked like it might die. Having a CDC official work with the NIH and with the rest of the research community on something is pretty new.

They are sticking with the Empirical definition it looks like - Unger says a recent study shows its not so bad (but Jason's study on it was pretty bad). They are working with prominent ME/CFS physicians now instead of doing random sampling....and Unger has been talking to some patient groups.... There are some changes...They're doing their own thing - they're strong on the mind/body component, funded that nice basal ganglia work, the intriguing gynecological study and they're strong on NK cells too....They're never going to be the center of pathogen research that's for sure....

 

[WillowTree]

Cort, would you please remind me what CASA stands for. It escapes me right now. Thanks.

Also, I haven't heard anything about discussion of the ICC definition. Anything to report on that?

 

[CBS]

Cort, would you please remind me what CASA stands for. It escapes me right now. Thanks.

Collection, Aggregation, Storage and Analyses. Kind of a play on the Spanish term for home. It is a way to pool data from specialty clinics and across projects. But the empiric definition has to go. As pointed out earlier, it might be decent as far as sensitivity but the specificity is terrible and that's precisely why they keep persevering on the mind/body thing. One leads to the other.

Standardizing Data Collection in CFS/ME CASA Project
(collection, aggregation, storage and analyses)
Session Co-Chairs: Elizabeth Unger, M.D., Ph.D. &
Dennis Mangan, Ph.D.

 

[Ember]

They are sticking with the Empirical definition it looks like - Unger says a recent study shows its not so bad (but Jason's study on it was pretty bad).

Did nobody ask what they'll do for ME patients, removed from Reeves by the ICC?

 

[Ember]

These comments suggest that Jason is setting himself up in competition with the International Consensus Panel. Am I reading this correctly?

CortJohnson Cort Johnson
#IACFS/ME -#Jason - lots of symptoms are what doomed Holmes criteria. Jason's ME criteria had 4 parameters and required acute onset
24 Sep

CortJohnson Cort Johnson
#IACFS/ME - suggests using more symptoms (eg ICC) runs the danger of bringing in people with pscyh diagnoses (#Jasoneg Holmes criteria)
24 Sep

 

[meadowlark]

I don't suppose anyone's ever done a survey, but how rare IS slow onset? For the past ten years I've been able to check about 3/4 of the boxes for the CCC, and now about the same for the ICC. My onset took 17 agonizingly painful years. It would frighten me to be elbowed out of a diagnosis on that basis.

 

[Bob]

I don't suppose anyone's ever done a survey, but how rare IS slow onset? For the past ten years I've been able to check about 3/4 of the boxes for the CCC, and now about the same for the ICC. My onset took 17 agonizingly painful years. It would frighten me to be elbowed out of a diagnosis on that basis.

Here's a possible answer to this, that I posted on another thread:
http://phoenixrising.me/forums/show...Diagnosis-Poll&p=205109&viewfull=1#post205109

One thing that I think is important to point out to everyone is how Byron Hyde defines 'sudden onset'.

It's not as straightforward as you would imagine.

Some people think that they had 'slow onset', whereas Hyde always takes a complex clinical history and finds out for himself, and can come to the opposite conclusion.

'Sudden onset' can easily be missed by the patient because of the fluctuating nature of ME.

As an example, someone might have had a 'sudden' but very mild and short first episode of ME (this is just an example - it could be severe but short or mild and long or intermittent etc.), which then disappeared completely before the patient gradually became more ill again. So this type of onset could easily be considered as slow onset by the patient, but Byron Hyde would define it as 'sudden onset'. This type of 'sudden onset' could easily be missed by the patient, or forgotten about, or just mistaken for flu or similar.

Or there might have been a 'sudden' first episode many many years earlier (that possibly lasted for a few days or for a few weeks or months), that the patient had completely forgotten about or had decided at the time was just a viral infection, and then the symptoms returned again, slowly, long after the patient had forgotten about the original epidode. So this would also be mistaken for slow onset, whereas Hyde would call it sudden onset.

So things are not clear cut, and all of the patient's clinical details need to be taken into account.

 

[Guido den Broeder]

It is also possible to suffer from the effects of a herpes virus for a long time, before getting ME.

 

[Tristen]

It's been my understanding that if the symptoms present as something other that ME in the beginning, but then progress over time into ME like symptoms, that would be "gradual onset". If the symptoms are ME from the start, that's "sudden onset". It's not the type of trigger (infectious, toxin, vaccine, etc), or severity (mild-severe) of the illness at onset that determines "gradual vs sudden onset". It's whether or not the symptoms are ME at onset.

I'm not sure if this is how Dr Hyde defines it, but I think he's right on with the use of "sudden vs gradual onset" to help tease out differential diagnosis'.

 

[meadowlark]

Thank you, Bob. I quickly lost two dress sizes in 1980 for no reason I knew of, and got frequent hemiplegic migraines after that. The migraines became daily (and ten hours long) in 1983, and continued til six weeks ago. The rest of my symptoms, including swollen glands, nausea, seizures, PEM and POTS, came in a deluge in 2000-2003. Before my diagnosis in 2000, I never had a doctor who thought those 9,000 migraines might be connected to a neuroimmune disease. I would find it odd (and somehow infuriating) if, through an overly narrow definition of onset, they were thought to be other than a very significant first act.

 

[Bob]

It's been my understanding that if the symptoms present as something other that ME in the beginning, but then progress over time into ME like symptoms, that would be "gradual onset". If the symptoms are ME from the start, that's "sudden onset". It's not the type of trigger (infectious, toxin, vaccine, etc), or severity (mild-severe) of the illness at onset that determines "gradual vs sudden onset". It's whether or not the symptoms are ME at onset.

I haven't heard that before. Do you think that's the difference between ME and post viral fatigue syndrome? (I don't know anything about PVFS.)

 

[Bob]

SOC, very interesting theories of the model of illness.

It's making me think about things.

 

[Ember]

I'm disheartened to learn that Lenny Jason is promoting his own ME criteria (with 4 parameters and required acute onset) over the ME-ICC. Does anyone know whether he's published his ME criteria? I assume he's based them on the CCC. Are they available anywhere for review?

I find this comment by Tom Kindlon, "I question claim more symptms brings in more ppl with psych diagnoses-a proper subset will have no extra cases." #iacfsme #cfs
24 Sep

 

[eric_s]

Hmmm... I don't know very much about Lenny Jason, but i think he has done a lot for us. But is it really smart to introduce yet another definition now, where we have the chance to abandon all the old definitions and try to replace them with the ICC? I think it's an obstacle for progress to have multiple definitions around.

 

[Dolphin]

Hmmm... I don't know very much about Lenny Jason, but i think he has done a lot for us. But is it really smart to introduce yet another definition now, where we have the chance to abandon all the old definitions and try to replace them with the ICC? I think it's an obstacle for progress to have multiple definitions around.

Maybe he did the work before the ICC_ME came out??

 

[Tristen]

I haven't heard that before. Do you think that's the difference between ME and post viral fatigue syndrome? (I don't know anything about PVFS.)

Well yes, going with my definition, I suppose that PVFS could fall under gradual onset. An example of this could be the HCV community that has a significantly higher rate of ME like illness than the general population. We all know that HCV doesn't cause ME, yet something like 5% of this community progress from a mild CFS like illness, to a more severe illness fitting ME criteria. I would suggest these folks have PVFS, not ME (But that's not to say that some may not have both). Their illness onset did not present as ME, but progressed into fitting much of the criteria over time, aka, gradual onset (and treatable).

I didn't get this idea for a definition from any particular professional source. It's just been my impression gathered over the years. If I'm understanding Dr Hyde correctly, on the type of onset being a helpful diagnostic tool for differentiating ME from CFS, I would agree. I also think that he's correct that many diagnosed with CFS have other treatable illnesses.

I also like what SOC says about there being some predisposing factor. Prior to my onset, I had been very healthy for decades. Never caught anything. Cross country runner, highly motivated, happy, on top of the world. Onset for me was mild but it was sudden and like a switch had been flipped. Obviously some weak link had just snapped. The disease began mild, but progressed non stop over the years into severe. Yet even though mild at onset, it was definitely sudden.