Right Arcuate Fasciculus Abnormality in Chronic Fatigue Syndrome, 2014, Zeineh, Montoya et al

Andy

Andy

Retired committee member
Paper is from 2014, I thought I'd post this as it comes up in the Q&A with Dr Montoya.
Abstract:
Purpose
To identify whether patients with chronic fatigue syndrome (CFS) have differences in gross brain structure, microscopic structure, or brain perfusion that may explain their symptoms.

Materials and Methods
Fifteen patients with CFS were identified by means of retrospective review with an institutional review board–approved waiver of consent and waiver of authorization. Fourteen age- and sex-matched control subjects provided informed consent in accordance with the institutional review board and HIPAA. All subjects underwent 3.0-T volumetric T1-weighted magnetic resonance (MR) imaging, with two diffusion-tensor imaging (DTI) acquisitions and arterial spin labeling (ASL). Open source software was used to segment supratentorial gray and white matter and cerebrospinal fluid to compare gray and white matter volumes and cortical thickness. DTI data were processed with automated fiber quantification, which was used to compare piecewise fractional anisotropy (FA) along 20 tracks. For the volumetric analysis, a regression was performed to account for differences in age, handedness, and total intracranial volume, and for the DTI, FA was compared piecewise along tracks by using an unpaired t test. The open source software segmentation was used to compare cerebral blood flow as measured with ASL.

Results
In the CFS population, FA was increased in the right arcuate fasciculus (P = .0015), and in right-handers, FA was also increased in the right inferior longitudinal fasciculus (ILF) (P = .0008). In patients with CFS, right anterior arcuate FA increased with disease severity (r = 0.649, P = .026). Bilateral white matter volumes were reduced in CFS (mean ± standard deviation, 467 581 mm3 ± 47 610 for patients vs 504 864 mm3 ± 68 126 for control subjects, P = .0026), and cortical thickness increased in both right arcuate end points, the middle temporal (T = 4.25) and precentral (T = 6.47) gyri, and one right ILF end point, the occipital lobe (T = 5.36). ASL showed no significant differences.

Conclusion
Bilateral white matter atrophy is present in CFS. No differences in perfusion were noted. Right hemispheric increased FA may reflect degeneration of crossing fibers or strengthening of short-range fibers. Right anterior arcuate FA may serve as a biomarker for CFS.
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Full text available at http://pubs.rsna.org/doi/full/10.1148/radiol.14141079

Press release from Stanford, http://med.stanford.edu/news/all-ne...bnormalities-in-chronic-fatigue-patients.html
 
Forbin said:
Do we know that this is actually caused by the disease, though? Could it instead be a predisposition?
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Hence why I want to know what is happening with severity and duration. With differentiating from predisposition the disease duration issue is particularly important. However we might need to understand what causes ME and we might also need a study showing development of ME over time, and measuring things like fasciculus enlargement. If the enlargement is smaller in new patients, and bigger in patients who have been ill for a long time, then we might have a partial answer. A large prospective study might do it, but the cost and logistics are probably prohibitive right now.
 
If there is a structural change after onset, I wonder if it could possibly be related to the pattern of headaches seen in ME/CFS. Virtually all of the case definitions mention headache, with both the CCC and the CDC's Fukuda definition using this language:
"Often there are significant headaches of new type, pattern or severity."
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I certainly developed headaches of a new type after onset - a kind of continuous migraine, but they really were only a feature of the first few months of the illness.
 
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The authors conclude that "Right anterior arcuate FA may be a biomarker for CFS". What's about this? Could it? Why or why not?

So what would need to be done is a new study with a cohort consisting of ME plus other diseases and healthy controls to confirm this?

Does somebody know which chance there is for such a study being positive?

Can this diagnostic tool be applied in clinical practice?

What are the consequences of an increased/thicker right anterior arcuate FA?

(I have the slight feeling all this might have been answered during Montoya's Q&A... :confused:)
 
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So, can anyone explain to me why this isn't used as a potential biomarker, or even in the pipeline as one? Am I missing something as usual?
 
ivorin said:
So, can anyone explain to me why this isn't used as a potential biomarker, or even in the pipeline as one? Am I missing something as usual?
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The authors say in the paper this can be used as a potential biomarker but needs follow-up (small cohort, needs to be tested on a different cohort...).

Still, if this could be a potential biomarker, will there be a follow-up?
 
Inara said:
The authors say in the paper this can be used as a potential biomarker but needs follow-up (small cohort, needs to be tested on a different cohort...).

Still, if this could be a potential biomarker, will there be a follow-up?
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Exactly my thoughts, what happened with this :(
 
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