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Neuroimaging research from Adelaide.

Daisymay

Senior Member
Messages
754
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."
 

Marco

Grrrrrrr!
Messages
2,386
Location
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.
 
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A.B.

Senior Member
Messages
3,780
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.

What does this mean?
 

Amaya2014

Senior Member
Messages
215
Location
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?
 

leokitten

Senior Member
Messages
1,542
Location
U.S.
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?

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.
 

duncan

Senior Member
Messages
2,240
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.
 

Kati

Patient in training
Messages
5,497
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.
 

Kati

Patient in training
Messages
5,497
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)

Two subjects with CFS and their age- and sex-matched NCs were removed from the analysis based on their MR scan. One man, aged 30 years, had an absent right cerebellum without cerebellar symptoms, and one woman, aged 20 years, had a large frontal angiomatous tumour, again asymptomatic with regard to the tumour
 
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Kati

Patient in training
Messages
5,497
Here is an exerpt from the full text:

Two subjects with CFS and their age- and sex-matched NCs were removed from the analysis based on their MR scan. One man, aged 30 years, had an absent right cerebellum without cerebellar symptoms, and one woman, aged 20 years, had a large frontal angiomatous tumour, again asymptomatic with regard to the tumour

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.
 

barbc56

Senior Member
Messages
3,657
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
 

anciendaze

Senior Member
Messages
1,841
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.
 

JaimeS

Senior Member
Messages
3,408
Location
Silicon Valley, CA
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.

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
 

Gijs

Senior Member
Messages
690
I also have punctuate, nonspecific little white matter leasies. It could be due to infection or bloodflow problems.
 

Sea

Senior Member
Messages
1,286
Location
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.