A brain MRI Study of CFS: Evidence of brainstem dysfunction & altered homeostasis

[taniaaust1]

Hello Tania, did they actually send you the results of your scans etc in the study?

I participated in this study (a follow up?) in October/November last year, but I have not heard anything since, so I am really curious as to how I may have went.

When you look at the original link on the Me/CFS Australia (SA) website, the title of the article is "Publication of original Adelaide CFS MRI study" (my bolding). I am thinking by the wording of original, that this study, that is about to be published, is their first one - perhaps the one that you were in, unless you were also in a follow up study also?

I just seen the thread again. Yes they did send me my study results from the MRI, SPECT etc but as i said.. I was part of their study WAY back (so they must be taken AGES to do these studies and get them published). My results of my tests they didnt send for a very long time, many many months (I'd almost given up getting them when they suddenly came by the post).

Im still confused which study of theirs I was in.. I dont think it is that original study? as the numbers are lower then the numbers of partipants they were trying to get for the one I was in (unless they had trouble getting the number so went with less???). I remember the number 60 participants I think? (was that 30 controls and 30 ME or 60 each group? bad memory.. maybe I was in the original one?? maybe they used 10 less) They had some very sick ones of us in that study... I was much worst then (it was back in the time when I had trouble just sitting without collapse and had to nap every day) and the other partipant who was there when I was, she was too sick to drive herself there too and had been brought along by another as well. She looked quite sick and like she probably should of been in bed too, we both were unsteady on our feet.

Is there anywhere on that published study in which it says what year they actually started doing the study??? so I can look it up with when I had my study tests done and know?

IF I was in their second one? and not the original.. I assume they may publish a second one close after the first as as I said it was quite a time ago.. years, I dont understand why it wouldnt be finished by now.
................

I just looked up when I was part of the Dr Burnets study done in conjuction with the others, the MRI etc etc ME/CFS study. My SPECT was done for it July 2007. original study then???

 

[taniaaust1]

Hi, Tania--you are not alone in having high BP spikes--it was one of my primary symptoms for a couple of years. It usually followed a couple of hours after a walk--was a primary form of PEM; it could go as high as 200/100 on occasion, and was accompanied by considerable left chest pain--went to Emerg several times, no troponin, no heart attack, "go home." It would slowly resolve, but would remain somewhat elevated for a couple of days.

Interestingly, the first two occasions did reveal elevated myoglobin--I suspect the result of a viral attack on my heart? Recently, I have been taking AHCC and now a low dose of statin (10mg every second day), and this has pretty much stopped these spikes--there is now evidence that statins inhibit viral (and HIV) replication. I will post more on this (but see www.plosbiology.org, Mathieu Blanc, "Host Defence against Viral Infection ...", March 2011.

I was occasionally woken up after falling asleep and, feeling wired and weird, would take my BP and discover it was sky high... Slow meditative breathing could bring down my systolic 40 points in 15 mins sometimes. Clearly autonomic disregulation was involved.

Hope yours is normalizing--it is scary! Best, Chris

No idea if mine has normalised or not.. It was still spiking at times 6mths ago, I took it using anothers BP monitor and found I was having a spike (I dont have a BP monitor so dont know if it still does it now). I have a GP who isnt interested in such things at all and wont take it while Im standing so he dont see the issue, thou he did send me to immediately to the hospital from his surgery at start of the year after finding my heart rate or BP high (cant remember now which it was), it was caused by me standing up during that appointment to show him my arm then sitting down. It had normalised thou by the time the hospital put me onto its monitoring with the leads.

As i have heart issues in my family my CFS/ME specialist dont want me on statins but wants me to keep my good cholestrol (or whatever its called) up. Statins lower both kinds and the good kind is protective. Those who dont have enough of the good kind, if they have a heart attack they apparently more likely to have a more severe one and die.

ohh.. ive woken up on occassions feeling a bit like that, I did take my heart rate and it wasnt that which woke me up and put me on edge (over stimulated).. umm I hadnt considered it could of been my BP.

 

[Snow Leopard]

They were recruiting healthy controls for the second study in April 2010.
If you were in the CFS study (as opposed to Fibromyalgia), this is likely to be the paper. They originally submitted the paper to the Journal of the Neurological Sciences, but apparently the referees didn't understand the computational methods used. So they had to withdraw and then submit the paper to NMR in Biomedicine, which is a more specialised journal.

 

[taniaaust1]

Dr Kwiatek been invoved in a few studies over the years, but most of them have been fibromyalgia focused.

nods.. he's a rheumatoligist

 

[taniaaust1]

They were recruiting healthy controls for the second study in April 2010.
If you were in the CFS study (as opposed to Fibromyalgia), this is likely to be the paper. They originally submitted the paper to the Journal of the Neurological Sciences, but apparently the referees didn't understand the computational methods used. So they had to withdraw and then submit the paper to NMR in Biomedicine, which is a more specialised journal.

ah thanks for explaining it .. You've cleared up my confusion. It must of been the original then, it was a ME/CFS study and not a fibro one.

I'd also wondered why different journals had been mentioned. ***feeling like I know what is going on now ***

 

[charityfundraiser]

This news article is from 2010 so the published study is probably the one they were recruiting for.

.............and they are evidently going to continue this study - check out this info from:

http://sacfs.asn.au/news/2010/04/04_22_adelaide_brain_scanning_study.htm

//////////////

Thursday 22 April 2010

South Australian rheumatologist Dr Richard Kwiatek is heading a follow-on study comparing brain MRI in CFS versus healthy controls.

Here is a message from Dr Kwiatek about the study:

I am the principal investigator of a follow-on cross-sectional study comparing brain MRI in CFS versus healthy controls to that originally conducted by Dr Richard Burnet, the (impressive and remarkable) results of which are currently under review for publication in the Journal of the Neurological Sciences.

This follow-on study is externally funded, and I have the allotted task of attempting to recruit 25 healthy controls to match the 25 individuals with CFS.

The purpose of the follow-on study is to both confirm and extend the original findings, the nature of which I hint at by the (to be published) abstract of a poster I have had accepted for presentation at the Annual Scientific Meeting of the Australian Rheumatology Association in Melbourne in May 2010.

I hope that you will be able to appreciate that these are very novel and seemingly highly significant mechanistic findings concerning the extremely vexing disorder of CFS.

Last Saturday, at the direction of the Ethics Committee of TQEH, I had published the attached advertisement in The Advertiser.

I attach the relevant Participant Information Sheet for your information as well.

Richard Kwiatek FRACP

//////////////////////////////

I added the bold for emphasis.

 

[Cort]

NMR Biomed. 2011 May 11. doi: 10.1002/nbm.1692. [Epub ahead of print]
A brain MRI study of chronic fatigue syndrome: evidence of brainstem dysfunction and altered homeostasis.
Barnden LR, Crouch B, Kwiatek R, Burnet R, Mernone A, Chryssidis S, Scroop G, Del Fante P.
Source

Department of Nuclear Medicine, The Queen Elizabeth Hospital, Adelaide, South Australia; School of Chemistry and Physics, University of Adelaide, Adelaide, South Australia. Leighton.Barnden@health.sa.gov.au.

Abstract

To explore brain involvement in chronic fatigue syndrome (CFS), the statistical parametric mapping of brain MR images has been extended to voxel-based regressions against clinical scores. Using SPM5 we performed voxel-based morphometry (VBM) and analysed T(1) - and T(2) -weighted spin-echo MR signal levels in 25 CFS subjects and 25 normal controls (NC). Clinical scores included CFS fatigue duration, a score based on the 10 most common CFS symptoms, the Bell score, the hospital anxiety and depression scale (HADS) anxiety and depression, and hemodynamic parameters from 24-h blood pressure monitoring. We also performed group??hemodynamic score interaction regressions to detect locations where MR regressions were opposite for CFS and NC, thereby indicating abnormality in the CFS group.

In the midbrain, white matter volume was observed to decrease with increasing fatigue duration. For T(1) -weighted MR and white matter volume, group??hemodynamic score interactions were detected in the brainstem [strongest in midbrain grey matter (GM)], deep prefrontal white matter (WM), the caudal basal pons and hypothalamus. A strong correlation in CFS between brainstem GM volume and pulse pressure suggested impaired cerebrovascular autoregulation.

It can be argued that at least some of these changes could arise from astrocyte dysfunction. These results are consistent with an insult to the midbrain at fatigue onset that affects multiple feedback control loops to suppress cerebral motor and cognitive activity and disrupt local CNS homeostasis, including resetting of some elements of the autonomic nervous system (ANS). Copyright 2011 John Wiley & Sons, Ltd.

It looks like they are getting closer....the abnormalities are suggestive of autonomic nervous system problems, there is evidence of blood vessel problems (cerebrovascular autoregulation...) ,the hypothalamus is implicated......


They suggest that some insult (possibly during the early stages of infection) to the midbrain essentially resets brain functioning. A kind of generic insult makes sense given all the different pathogen triggers for ME/CFS that have been shown (and now SARS). This is similar to the 'sickness behavior' theory which posits that immune activation in the brain continues long after it should have been shut off.

 

[Cort]

NMR Biomed. 2011 May 11. doi: 10.1002/nbm.1692. [Epub ahead of print]
A brain MRI study of chronic fatigue syndrome: evidence of brainstem dysfunction and altered homeostasis.
Barnden LR, Crouch B, Kwiatek R, Burnet R, Mernone A, Chryssidis S, Scroop G, Del Fante P.
Source

Department of Nuclear Medicine, The Queen Elizabeth Hospital, Adelaide, South Australia; School of Chemistry and Physics, University of Adelaide, Adelaide, South Australia. Leighton.Barnden@health.sa.gov.au.

Abstract

To explore brain involvement in chronic fatigue syndrome (CFS), the statistical parametric mapping of brain MR images has been extended to voxel-based regressions against clinical scores. Using SPM5 we performed voxel-based morphometry (VBM) and analysed T(1) - and T(2) -weighted spin-echo MR signal levels in 25 CFS subjects and 25 normal controls (NC). Clinical scores included CFS fatigue duration, a score based on the 10 most common CFS symptoms, the Bell score, the hospital anxiety and depression scale (HADS) anxiety and depression, and hemodynamic parameters from 24-h blood pressure monitoring. We also performed group??hemodynamic score interaction regressions to detect locations where MR regressions were opposite for CFS and NC, thereby indicating abnormality in the CFS group.

In the midbrain, white matter volume was observed to decrease with increasing fatigue duration. For T(1) -weighted MR and white matter volume, group??hemodynamic score interactions were detected in the brainstem [strongest in midbrain grey matter (GM)], deep prefrontal white matter (WM), the caudal basal pons and hypothalamus. A strong correlation in CFS between brainstem GM volume and pulse pressure suggested impaired cerebrovascular autoregulation.

It can be argued that at least some of these changes could arise from astrocyte dysfunction. These results are consistent with an insult to the midbrain at fatigue onset that affects multiple feedback control loops to suppress cerebral motor and cognitive activity and disrupt local CNS homeostasis, including resetting of some elements of the autonomic nervous system (ANS). Copyright 2011 John Wiley & Sons, Ltd.

It looks like they are getting closer....the abnormalities are suggestive of autonomic nervous system problems, there is evidence of blood vessel problems (cerebrovascular autoregulation...) ,the hypothalamus is implicated......


They suggest that some insult (possibly during the early stages of infection) to the midbrain essentially resets brain functioning. A kind of generic insult makes sense given all the different pathogen triggers for ME/CFS that have been shown (and now SARS). This is similar to the 'sickness behavior' theory which posits that immune activation in the brain continues long after it should have been shut off.

 

[Wayne]

Cranial Nerves - Vagus Nerve - Digestion - Atlas Profilax

I feel I was able to improve my own brainstem dysfunction by having a structural procedure done called Atlas Profilax. AP Practitioners claim they are able to "reposition" the uppermost cervical vertabra (atlas), which in my case led to pressure being released on my cranial nerves/brainstem.

This procedure didn't "cure" my ME/CFS, but I noticed a number of improvements afterwards. I posted fairly extensively on my experiences on the ProHealth board in July of 2007 at the following link.

Cranial Nerves - Vagus Nerve - Digestion - Atlas Profilax

On one of my last posts on this thread, I listed all the improvements I had noticed, and gave an approximate percentage of improvement for each.

Best, Wayne

 

[Bob]

Here's a list of of all the links, in case helpful:


Published paper (11th May 2011):
A brain MRI study of chronic fatigue syndrome: evidence of brainstem dysfunction and altered homeostasis
Leighton R. Barnden, Benjamin Crouch, Richard Kwiatek, Richard Burnet, Anacleto Mernone, Steve Chryssidis, Garry Scroop, Peter Del Fante.
Article first published online: 11 MAY 2011
http://onlinelibrary.wiley.com/doi/10.1002/nbm.1692/abstract


Press Release:
http://sacfs.asn.au/news/2011/05/05...interdisciplinary_adelaide_research_group.htm
http://sacfs.asn.au/download/CFS_BREAKTHROUGH_ADELAIDE.pdf
http://www.mecfs-vic.org.au/ahmf-me...ugh-interdisciplinary-adelaide-research-group


More info:
http://sacfs.asn.au/news/2010/04/04_22_adelaide_brain_scanning_study.htm


A second discussion thread on the same subject:
http://forums.phoenixrising.me/showthread.php?11592-Aussie-cfs-study-MRI-scan-abnormalities

 

[ramakentesh]

all these brain / spinal studies are coming together
We also had Schutzer et al the other day, and Baranuik is coming
forget about retroviruses, I think its the brain / CNS where the answers will be found, and I think some of these guys are close
I'm optimistic

That or the circulatory system - but I agree.

 

[Sherrie]

Yeah, you were in the original study. I finally received my results for the current repeat study, well just the MRI and SPECT results and my MRI was ok but my SPECT showed reduced blood flow in the frontal cerebral cortices and frontal temporal cortices so I'm trying to read up a bit more on it.

I just seen the thread again. Yes they did send me my study results from the MRI, SPECT etc but as i said.. I was part of their study WAY back (so they must be taken AGES to do these studies and get them published). My results of my tests they didnt send for a very long time, many many months (I'd almost given up getting them when they suddenly came by the post).

Im still confused which study of theirs I was in.. I dont think it is that original study? as the numbers are lower then the numbers of partipants they were trying to get for the one I was in (unless they had trouble getting the number so went with less???). I remember the number 60 participants I think? (was that 30 controls and 30 ME or 60 each group? bad memory.. maybe I was in the original one?? maybe they used 10 less) They had some very sick ones of us in that study... I was much worst then (it was back in the time when I had trouble just sitting without collapse and had to nap every day) and the other partipant who was there when I was, she was too sick to drive herself there too and had been brought along by another as well. She looked quite sick and like she probably should of been in bed too, we both were unsteady on our feet.

Is there anywhere on that published study in which it says what year they actually started doing the study??? so I can look it up with when I had my study tests done and know?

IF I was in their second one? and not the original.. I assume they may publish a second one close after the first as as I said it was quite a time ago.. years, I dont understand why it wouldnt be finished by now.
................

I just looked up when I was part of the Dr Burnets study done in conjuction with the others, the MRI etc etc ME/CFS study. My SPECT was done for it July 2007. original study then???

 

[Dolphin]

I just sent the following to the corresponding author, for what it's worth.

As your paper found correlations with pulse pressure, I thought you might be interested in the attach figure which is taken from a paper which was just published:
------
Postural Neurocognitive and Neuronal Activated Cerebral Blood Flow Deficits in Young Chronic Fatigue Syndrome Patients with Postural Tachycardia Syndrome.
Stewart JM, Medow MS, Messer ZR, Baugham IL, Terilli C, Ocon AJ.
Am J Physiol Heart Circ Physiol. 2011 Dec 16. [Epub ahead of print]
------

Being seated is a bit of an orthostatic challenge - I know many patients who will try to be vertical a lot of the time - so perhaps a seated measurement is a bit like, say, the orthostatic stress at 30 degrees?
Anyway you can decide the relevance or otherwise of it yourself.

(Paper found a difference between CFS/POTS and control groups on pulse pressure with orthostatic stress).