Severe ME Day of Understanding and Remembrance: Aug. 8, 2017
Determined to paper the Internet with articles about ME, Jody Smith brings some additional focus to Severe Myalgic Encephalomyelitis Day of Understanding and Remembrance on Aug. 8, 2017 ...
Discuss the article on the Forums.

Neuroimaging research from Adelaide.

Discussion in 'Latest ME/CFS Research' started by aimossy, Feb 23, 2015.

  1. aimossy

    aimossy Senior Member

    Messages:
    1,068
    Likes:
    3,649
  2. alex3619

    alex3619 Senior Member

    Messages:
    12,244
    Likes:
    33,528
    Logan, Queensland, Australia
    Interesting. I have yet to read the full paper, but if they are right this implies we have considerable prefrontal cortex brain adaptation to poor brain function in the mid brain.
     
    merylg likes this.
  3. Daisymay

    Daisymay Senior Member

    Messages:
    709
    Likes:
    3,808
    http://onlinelibrary.wiley.com/doi/10.1002/nbm.3261/pdf

    "CONCLUSIONS
    The severity-dependent elevation of myelination in the internal
    capsule and prefrontal WM reported here, together with midbrain
    volume loss and midbrain neuroinflammation in CFS reported
    elsewhere (4,5), suggest that these midbrain changes
    are associated with impaired midbrain nerve conduction. Impaired
    brain–body and brain–brain communication through
    the midbrain could explain many of the autonomic and cognitive
    symptoms of CFS. Despite the observation here that clinical
    scores of CFS severity correlate with those of depression, in
    prefrontal WM the T1w variance associated with CFS severity
    does not correlate with the variance associated with anxiety
    and depression. Thus, although anxiety, depression and CFS
    may share biological similarities, on the present evidence,
    CFS appears to be a distinct disorder. T2w changes were detected
    in right middle temporal lobe WM which is relevant
    to cognition (47,48). This work highlights the potential of
    quantitative analysis of T1w and T2w MRI in clinical research."
     
    L'engle, Forebearance, merylg and 7 others like this.
  4. Marco

    Marco Grrrrrrr!

    Messages:
    2,360
    Likes:
    3,100
    Near Cognac, France
    Interesting (if you dig into the full text and references) that impaired mid brain function is associated with increased pulse pressure (the differences between systolic and diastolic).

    My pulse pressure (difference) was greater at an earlier stage when my orthostatic intolerance was worse despite other symptoms being much worse at a later stage.

    As an aside - I'm sure they had their reasons but I do wish they wouldn't use 'novel' techniques that require validation and are open to interpretation.
     
    Last edited: Feb 23, 2015
    JaimeS and aimossy like this.
  5. A.B.

    A.B. Senior Member

    Messages:
    3,527
    Likes:
    21,355
    What does this mean?
     
  6. Amaya2014

    Amaya2014 Senior Member

    Messages:
    215
    Likes:
    540
    Columbus, GA
    Interesting. I had several MRI's showing punctuate T2 hyperintense flairs in prefrontal region. The radiologist described it as "undetermined significance". Anyone else with similar results and interpretations?
     
    L'engle and merylg like this.
  7. alex3619

    alex3619 Senior Member

    Messages:
    12,244
    Likes:
    33,528
    Logan, Queensland, Australia
    I am not sure anybody knows. Its an inference from an empirical observation. I think they are implying that we have increased brain connectivity to compensate for decreased brain function elsewhere.
     
    L'engle, merylg and voner like this.
  8. leokitten

    leokitten Senior Member

    Messages:
    579
    Likes:
    1,874
    Maryland
    Yes I had the same results... there have been a number of studies showing that PWME have these "punctuate, nonspecific white matter hyperintensities" in their frontal lobes and that those are the only abnormalities seen using standard MRI.
     
    JaimeS and merylg like this.
  9. AndyPandy

    AndyPandy Making the most of it

    Messages:
    1,400
    Likes:
    6,047
    Australia
    My MRI report states "non-specific T2/FLAIR white matter hyperintensities in both frontal lobes"
     
    JaimeS and merylg like this.
  10. Snow Leopard

    Snow Leopard Hibernating

    Messages:
    4,566
    Likes:
    12,017
    South Australia
    I tried reading this paper again and I'm still baffled by the methods/results...
     
  11. duncan

    duncan Senior Member

    Messages:
    1,927
    Likes:
    4,157
    Similar results in brain MRI's of Lyme patients. Interestingly, these foci have been known to dissipate with abx treatment, only to return in some cases.

    Brain atrophy is also known to happen, also apparent with MRI's.

    I tried to get a SPECT scan to check cerebral blood flow. Even got two 'scripts, but still have yet to find a hospital willing to do those SPECT scans. The NIH flat out refused. But the NIH performed three MRIs, all within the space of 12 months, and two of the MRI's demonstrated abnormalities, including multiple foci and brain atrophy unusual for age. The third came back - read by a different radiologist and ordered by a different NIH team - marked as normal.
     
  12. Kati

    Kati Patient in training

    Messages:
    5,423
    Likes:
    19,303
    http://onlinelibrary.wiley.com/doi/10.1002/nbm.3261/full

    Evidence in chronic fatigue syndrome for severity-dependent upregulation of prefrontal myelination that is independent of anxiety and depression

    Open access.

    Abstract:

    White matter (WM) involvement in chronic fatigue syndrome (CFS) was assessed using voxel-based regressions of brain MRI against CFS severity scores and CFS duration in 25 subjects with CFS and 25 normal controls (NCs).

    As well as voxel-based morphometry, a novel voxel-based quantitative analysis of T1- and T2-weighted spin-echo (T1w and T2w) MRI signal level was performed.

    Severity scores included the Bell CFS disability scale and scores based on the 10 most common CFS symptoms. Hospital Anxiety and Depression Scale (HADS) depression and anxiety scores were included as nuisance covariates.

    By relaxing the threshold for cluster formation, we showed that the T1w signal is elevated with increasing CFS severity in the ventrolateral thalamus, internal capsule and prefrontal WM.

    Earlier reports of WM volume losses and neuroinflammation in the midbrain, together with the upregulated prefrontal myelination suggested here, are consistent with the midbrain changes being associated with impaired nerve conduction which stimulates a plastic response on the cortical side of the thalamic relay in the same circuits.

    The T2w signal versus CFS duration and comparison of T2w signal in the CFS group with the NC group revealed changes in the right middle temporal lobe WM, where impaired communication can affect cognitive function.

    Adjustment for depression markedly strengthened cluster statistics and increased cluster size in both T1w severity regressions, but adjustment for anxiety less so.

    Thus, depression and anxiety are statistical confounders here, meaning that they contribute variance to the T1w signal in prefrontal WM but this does not correlate with the co-located variance from CFS severity.

    MRI regressions with depression itself only detected associations with WM volume, also located in prefrontal WM.

    We propose that impaired reciprocal brain–body and brain–brain communication through the midbrain provokes peripheral and central responses which contribute to CFS symptoms.

    Although anxiety, depression and CFS may share biological features, the present evidence indicates that CFS is a distinct disorder.
    © 2015 The Authors. NMR in Biomedicine published by John Wiley & Sons, Ltd.
     
    Mel9, L'engle, SOC and 7 others like this.
  13. Kati

    Kati Patient in training

    Messages:
    5,423
    Likes:
    19,303
    What is staggering to me is of the 27 patients who qualified for the study and met both Fukuda and CC criterias, 2 were dropped from the study, one missing his cerebellum and the other with a large tumor in frontal cortex. (And how this was downplayed by the authors)

     
    Last edited: May 5, 2015
    ukxmrv, L'engle, JaimeS and 6 others like this.
  14. Kati

    Kati Patient in training

    Messages:
    5,423
    Likes:
    19,303
    Here is an exerpt from the full text:

    Only with ME gross abnormalities of the brains get only discovered during research. And yet these 2patients fully meet the Fukuda and Canadian Consensus criterias.
     
  15. barbc56

    barbc56 Senior Member

    Messages:
    3,524
    Likes:
    4,104
    It's an intriguing topic but tbh, other than understanding something was found in the brains of me/cfs patients that wasn't found in depressed patients or the other way around, Im clueless:thumbsup:.

    I'm interested in what others think of the paper and it's validity. It's implications are an important issue for us.

    Thanks.
    Barb
     
    merylg, Valentijn and Kati like this.
  16. anciendaze

    anciendaze Senior Member

    Messages:
    1,769
    Likes:
    4,477
    Irrespective of the fairly subtle changes in myelination they were looking for, the discovery of two patients out of 27 with gross neurological abnormalities suggests a fairly high rate of undiagnosed neurological problems in "CFS" patients. This parallels Byron Hyde's discovery that one of a series of some 53 patients referred to him as having "CFS" was missing a large chunk of brain. Several other patients in that series had undiagnosed physiological disease as blatant as syphilis or hepatitis. I am even aware of patients turning up elsewhere with undiagnosed TB!

    Even in the absence of any specific official test for "CFS" this suggests that this subpopulation is a reasonable group to test for exclusionary organic conditions. Some of these are treatable and even communicable.
     
    merylg, L'engle, JaimeS and 6 others like this.
  17. JaimeS

    JaimeS Senior Member

    Messages:
    3,105
    Likes:
    11,137
    Mid-Ohio Valley, United States
    This was what I was trying to think of in the newer thread. Hyde did a lot of neuroimaging with his patients. And Hyde was great at exclusionary techniques -- he often discovered some treatable condition over the course of examining 'CFS'.

    -J
     
  18. eastcoast12

    eastcoast12 Senior Member

    Messages:
    134
    Likes:
    397
    Long Island ny
    Same here.
     
    JaimeS likes this.
  19. Gijs

    Gijs Senior Member

    Messages:
    639
    Likes:
    1,288
    I also have punctuate, nonspecific little white matter leasies. It could be due to infection or bloodflow problems.
     
    JaimeS likes this.
  20. Sea

    Sea Senior Member

    Messages:
    1,209
    Likes:
    2,117
    NSW Australia
    I was a subject in their research. They told me that I would receive a report on my MRI that would most likely say 'normal' (which I did, though the hyperintensities were noted)
    The researchers said what they were looking at was only picked up by computerised measuring and that the differences between cfs and normal were seen statistically between the groups rather than on an individual patient level.
     
    JaimeS, Effi, Valentijn and 1 other person like this.

See more popular forum discussions.

Share This Page