cfs brain injury

Discussion in 'Fibromyalgia Main Forum' started by heapsreal, Feb 20, 2008.

  1. heapsreal

    heapsreal New Member

    The more I research this s__t condition the more i think its a brain injury, cause by a virus, bacteria etc etc, hit and run illness. Obviously some people have recovered from antivirals and antibiotics but many of us just seem to be going around in circles. Starting to think that symptom management is the best way to go, control pain and try to improve sleep, lots of antioxidants, pace yourself and wait/hope for the brain to heal. The last few weeks i have noticed improvement with lyrica and doxepin ie. less pain and better sleep, still up and down, more ups then downs though. Have just googled chickenpox and ebv brain injury and theres heaps of info on these conditions, they just dont mention cfs, but fatigue, pain, cognitive problems mmmmm sounds familiar. Maybe we should say we have post what it was we initially had. My new condition is post chickenpox/ebv complications(pcec), no such thing as CFS,LOL.
  2. meganp

    meganp New Member

    Hi Heapsreal,

    I've been worried at times about the brain injury thing. I'm not sure who else is pushing this theory (if anyone else knows can they post) but I know that this was the suggestion of the people who conducted the Dubbo trials in Australia and they recieved a lot of publicity here.

    I have recently reread their study and they looked for EBV viral evidence and couldn't find it, so they made what I think was a very illogical leap from that to suggesting it was a hit and run brain injury. Apart from this proposed hypothesis in the very last sentence of the paper there is no evidence whatsoever presented in their paper for this idea. They may have some other reasons for thinking this but I couldn't find them if they did.

    To give them credit I understand that their study was significant as it followed people from their initial infection stage for glandular fever (mono) and established the reality of post viral fatige in 10% cases. They also established a link between the severity of initial infection and CFS. However, now that I understand more about this I can see a number of reasons why their study might not have picked up the viral link. I am not a medical person, so this is just my opinion, but I do think my logical powers are as good as anyone's:

    1) The antibody test they used to test the level of antibodies was the EBV VCA ELISA test. According to the Stanford people, and Panbio the manufacturers of this test (of which I have a copy of their instructions), this test is no good for quantifying antibody levels.

    2) They did not test for HHV6. In my case I started with glandular fever but my results are now showing elevated HHV6 antibodies more than EBV. Perhaps they were simply looking for the wrong virus?

    3) They looked at the amount of the virus in blood cells and found that this was the same for CFS people as for people that recovered OK from glandular fever. From this they concluded that the virus was not the cause. However, what is really weird about this is that they acknowledge in the paper that there is also no difference in viral amounts between those that gain immunity to EBV without any mono symptoms at all(most of the population) as opposed to those who suffer full mono symptoms. It seems to me that if this indicator cannot distinguish between those who suffer full on mono from those that catch it with no symptoms, then it is probably not going to be a good indicator for distinguishing CFS cases from non CFS cases. Using this logic you would have to conclude that EBV is not the cause of glandular fever and no one is suggesting this. Also, if I understand correctly, the test they used would not have been able to distinguish active from latent viral infection (the HHV6 foundation have been stressing the importance of this distinction). Furthermore, does looking in the blood preclude it from infecting other organs such as the brain or heart? Perhaps they were looking in the wrong place?

    4) They also looked at the T Cell response and found no difference between CFS patients and those that recovered. Again I wonder if this indicator can be questioned because they also acknowledged that the T Cell response could not be correlated with the severity of symptoms for those who had mono. Again if this cannot indicate severity of symptoms for mono is it a good indicator for distinguishing CFS cases from non CFS?

    There were a number of other things the study looked at which I don't really understand and it seemed very thorough in many ways, but I can't help thinking that despite this they have still missed something important. I hate to sound like I am bagging them because their study is very important for us in other ways and I give them credit for researching the issue when such studies are few and far between.

    I don't know if EBV and HHV6 are the cause. If not, both my doctors are suggesting it is more liklely immune system damage that is the problem. This makes more sense to me than the brain injury thing, though I am hoping it is viral because this may make treatment more of a possibility. Furthermore I have recently seen another paper suggesting that permanent damage does indeed happen to the immune system following symptomatic glandular fever, so this would seem more likely.

    Sorry this is so long, but I had to get it all out.

    Cheers,

    Megan,
    Melbourne Australia
  3. aftermath

    aftermath New Member

    Megan,

    That was an excellent analysis of the Dubbo study.

    <blockquote>If not, both my doctors are suggesting it is more liklely immune system damage that is the problem. This makes more sense to me than the brain injury thing, though I am hoping it is viral because this may make treatment more of a possibility. Furthermore I have recently seen another paper suggesting that permanent damage does indeed happen to the immune system following symptomatic glandular fever, so this would seem more likely.</blockquote>

    Couldn't this essentially be damage to the part of the brain responsible for curing the immune system?

    The "hit and run" is indeed the scariest. Because, as other have said, the chances of ever recovering in that instance appear to be next to nil.

    What makes it so plausible is that researchers have spent the better part of 20 years looking for an active infectious agent with absolutely nothing to show for it. Granted, the research budgets for CFS are abysmal (CFS gets 4 million compared to 21 billion for AIDS). This is the reason that everyone from the US NEEDS to be part of the CFS association (the main group that lobbies for funding) with no exceptions. It really is the only hope.
  4. heapsreal

    heapsreal New Member

    Thats good info and yes i was refering to the dubbo study, also having a day where I have had enough and having a good winge. I think they also might be still making assumptions about all the information they got from the dubbo study. Im hoping its viral as it would seem easier to treat. I see my doctor in 2 weeks and am involved in a study he is conducting with doctor whiting (the doc who alister lynch saw)and how cytokines play a role in cfs, think this is where they are looking at an overactive immune system, so Im interested to see my blood tests from this and to hear about all other goings on in this testing.
    Have noticed small improvements with valtrex but had a couple of poor nights sleep, have cut back on doxepin and lyrica due to weight gain. Having such good relief with these meds so may juggle back and forth and try and keep my weight under control, also watch diet better.
    Thanks again megan, good luck
  5. aftermath

    aftermath New Member

    The one thing that the active viral infection theories can't seem to adequately explain in the role of a stress trigger along with an infectious agent at the genesis of CFS in many people.

    I was "burning the candle at both ends" and dealing with a 3 month long upper respiratory infection when I got sick. It was physical stress from abusing my body (sleeping 2 hours/night), not emotional, as I enjoyed the fact that I was progressing toward my goals. This formula is common for many people.

    The "brain blowing a fuse to protect itself" because of attack from all angles (infectious, stress, etc) seems to make a lot of sense.

    The following is from Dr. Jacob Teitelbaum. I haven't found much success with his treatment protocol, but the quote below makes a lot of sense.

    <blockquote>Chronic Fatigue Syndrome is basically like blowing a fuse.

    It’s like the circuit-breakers you have in your home. If you plug in too many heaters, for example, or blow-dryers—boom!—off go the lights because you’ve blown a circuit or a fuse. The fuse that you blow in Chronic Fatigue Syndrome is called the hypothalamus, and that’s a key control center in the brain. It controls temperature regulation, sleep, hormonal function, and the autonomic nervous system, which regulates blood flow, blood pressure, and pulse. Because the hypothalamus is blown, those four systems are off-line in Chronic Fatigue Syndrome.</blockquote>


    I suppose that the physical stress of not sleeping can also suppress the immune system to allow viruses to take hold.

    Still, the role of infection + stress --->CFS is all too common.

    It also would explain fibromyalgia, which from the accounts I read here, is often brought on by a stressor.[This Message was Edited on 02/21/2008]
  6. heapsreal

    heapsreal New Member

    hypothalamus problem explains alot of cfs problems like sleep etc and has carry on effects to other parts the body like the immune system etc. Also explain the hit and run theory. Now how do we fix it. I feel myself if i could get good quality sleep all the time i would get better. Having success with lyrica and doxepin, they seem to work off one another. Problems have been weight gain which im trying to remedy, and then i hope i dont get a tolerence to these meds. i do alternate with other sleep meds like ambien etc although not as effective but hopefully help me avoid a tolerence to lyrica and doxepin.
  7. LonelyHearts

    LonelyHearts New Member