Discussion in 'General ME/CFS Discussion' started by knackers323, Dec 6, 2013.
Or is it found in other conditions also?
I'm under the impression it is one of the "hallmarks of CFIDS/ME, but I could be mistaken. Sure someone else will chime in eventually. FYI
I believe Post Exertional Neuroimmune Exhaustion (PENE) is unique to ME/CFS, although exercise intolerance is found in a number of other diseases/disorders. I think the term PEM is sometimes confused with exercise intolerance which is the reason some people think PEM is not unique to ME/CFS. But I could be wrong.
It depends on what you mean by PEM. We share some post exercise chemistry with fibromyalgia.
What is unique to strictly defined CFS and in ME by the ICC definition is that we have a measurable crash in energy production on day two after exercise.
Many diseases have exercise intolerance and post exercise problems. Many of those resemble ME. None show the day 2 post exercise crash. It may be an ME diagnostic marker.
I believe it's prevelant in many neurological disorders, but could be mistaken.
My guess would be that since other disorders have overlapping symptoms with me/cfs, this could be possible.
My step mom has MS and certainly seems to have PEM. We have even crashed at the same time after doing some activities together the previous day. Not sure this applies to all patients with MS or if it's the same type of crash but our symptoms are identical. She has a very mild case and her main symptoms are pain, tiredness and migraine headaches.
So far as I am aware, the specifics of the crash are different in ME and MS. At best its a different kind of PEM. Its the specific nature of the energy crash that seems to be unique to ME. See here: http://www.workwellfoundation.org/
Im guessing that the 2 day exercise test hasnt been studied in many illnesses, the design of the 2 day test seems to have arised from cfs/me but i dont really know. I dont really know if its important that its unique to cfs/me more so then it does happen in cfs/me and proves disability??
It would be helpful as a biomarker if it is indeed unique to us.
Sounds like more testing is needed where this is compared to other illness?
From Simon's article in July 2013,
Repeat Test Reveals Dramatic Drop in ME/CFS Exercise Capacity
In a Q&A session, Dr. Anthony Komaroff was asked how patients with depression compared to those with chronic fatigue syndrome. His answer below asserted that PEM differentiated CFS not just from depression, but from any other disease he had encountered.
The quote comes at 18:22 http://www.masscfids.org/videofiles/Questions/Questions.html
Yes @barbc56 and @heapsreal we really do need more testing. However I think (anecdotally) MS patients have been tested, and perhaps more. CPET itself is at least 50 years old. Who knows what other illnesses may lurk that have a second day crash as most testing is only one single test.
The question I want answered though is how every doctor from 1963 to 2007 missed this? Given Ramsay's description of PEM this should have been measured a long long time ago. Granted there is almost no research funding, and never has been, but they found five million pounds for the PACE trial!
Hi @SOC, this is why I am hopeful, but we need something more formal in a comparison to convince everyone. This will be our first diagnostic test I think, which also measure disability, but many of us will not be able to use it.
I agree. I think I read this before. However to get the 2 day CPET full recognized requires this be formalized, and results replicated other than by Workwell. That will then send a powerful message.
it would also be good to have a biomarker that pin points the dysfunction.
I think they need to make an effort to group several of these tests together to come up with a diagnosis. We keep saying it but they could use the 2 day test along with sveral tests on the immune system that would be far more accurate then just the list of symptoms such as the different criterias. Research takes time but gee it feels like we are banging our heads against a wall.
I don't believe that the 2-day CPET will be the ultimate clinical diagnostic test. One should not need to damage oneself in order to be diagnosed. Also, as has already been mentioned, the test is not even possible for the most severely affected.
My hope is that once the 2-day CPET is accepted, and that will take formalization as you say, that it can be used in a research setting to identify a clear ME/CFS sample for further research into less damaging tests which, while possibly less reliable, will be safer and easier. Having a test that (nearly) guarantees that the patients used in research really do have ME/CFS would be a huge step forward. It might clear up a lot of the ambiguities in the current research by removing patients who don't have ME/CFS from the patient samples. Some of the contradictions between research done by different groups may be the result of the inclusion of people with other illnesses with some similar symptoms. Our research is largely the living example of GIGO, garbage in -- garbage out. Once we can be sure we're getting genuine ME/CFS patients in the research, we'll get better research conclusions out.
Of course that means we'll have to wait for a decent clinical diagnostic test, but in the meantime those who can tolerate the 2-day CPET might be able to get it to prove disability -- or that they're really sick, which could be a major benefit in some cases.
They are studying further the pathways for this muscle cell dysfunction thankfully they might find something really useful.
Im thinking Julia Newtons work is very good from what I have read and seen she will make it impossible to argue. Is her work replicated yet?
The 2 day CPET can give us our first Gold Standard test, the test which will be a benchmark against every other test until its superseded. Having a benchmark test can accelerate research. Once we have one test, others will follow.
I have said elsewhere that we need a blood test, not exercise or spinal fluid, to be really acceptable. To this I would like to add that any non-invasive test would work too should we develop one.
On the subject of further testing, I'd also like to see the 2 day CPET done with other autoimmune disease type patients to see how they compare. I've had several docs (especially rheumatologists) tell me about how their patients "pay for it for days afterward" if they do too much but I wonder if those patient populations would show the same kind of findings on CPET. .
It seems PEM is also found in mold illness as Shoemaker describes it. There is a number of ME/CFS patients who've conquered this symptom and recovered much of their functionality through extreme mold avoidance. The writer of the blog http://ampligen4me.wordpress.com/ gives a great account of this. It's worth noting that he suffered an acute, viral onset and was also diagnosed by Dr Peterson. Unfortunately he has chosen to remain anonymous, but knowing his identity I can state he's been a very active member of our online community, and his credibility is unassailable.
I think Shoemaker has done a great job of detailing the immunological, inflammatory process in biotoxin illness. If this is the only other condition that has PEM, shouldn't we consider a similar immunological process is at play in ME/CFS? That PEM in ME/CFS could be the result of innate immune mediated inflammation. Particularly because C4a has been fairly consistently shown to be elevated in PEM, and according to Shoemaker's work is a strong indicator of biotoxin illness.
Increases of LPS in the blood appears to be universal in ME/CFS. Perhaps this could perpetuate PEM. I've wondered if those seeing improvements with Rifaximin also see improvements in this symptom. I didn't, but I think this approach might not be thorough enough. Those practicing extreme mold avoidance who see their PEM give way have to go to extreme lengths like following what Slayadragon calls the locations effect to achieve this. Those following her suggestions often see drops in their C4a from 25,000 or higher to under 2000. Maybe this is the marker to gauge success toward living without post-exertional malaise. It's worth noting that the writer of the blog above also took a course of Rifaximin at the outset of his experiment with extreme avoidance.
Sorry to keep banging on about lyme disease. I don't know how other lymers go, but i'm still getting PEM even though my general illness has improved on lyme abx.
I know some therapists recommend exercise for lyme.
http://www.ilads.org/files/burrascano_0905.pdf Joseph Burrascano for instance. Though he stresses no aerobic exercise.
This thread discusses PEM and lyme
I pulled this quote from Rich Van K
I wouldn't rule out other coinfections beside Babesiosis as causes for PEM. Actually, my current view is that Lyme disease can produce ME/CFS in those who are genetically susceptible, whether or not there are coinfections. Borrelia and at least three of the coinfections have been found to produce oxidative stress, which places a demand on glutathione. Borrelia depletes cysteine and glutathione in its host. Any factor that contributes to sufficiently depleting glutathione can contribute to producing ME/CFS, in my hypothesis, and if you have ME/CFS, you will have PEM/PEF.
I don't know how prevalent PEM is in other infectious diseases, or if it resembles me/cfs PEM. ?
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