Paper is from 2014, I thought I'd post this as it comes up in the Q&A with Dr Montoya. 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
Many thanks. I read the full text and it made a big difference to my understanding when Jose Montoya referred to it in his talk today. I was really pleased to hear that research in this area is being continued.
What I would hope they investigate is the degree of abnormality with respect to both severity and disease duration.
Do we know that this is actually caused by the disease, though? Could it instead be a predisposition?
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: 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.
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... )
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?
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?
