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Possible Brain Biomarker for ME/CFS Found

zzz

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Fresh out of Stanford, a new study by Dr. Jose Montoya and colleagues:

Study finds brain abnormalities in chronic fatigue patients

“In addition to potentially providing the CFS-specific diagnostic biomarker we’ve been desperately seeking for decades, these findings hold the promise of identifying the area or areas of the brain where the disease has hijacked the central nervous system,” Montoya said.
Three key findings

The analysis yielded three noteworthy results, the researchers said. First, an MRI showed that overall white-matter content of CFS patients’ brains, compared with that of healthy subjects’ brains, was reduced. The term “white matter” largely denotes the long, cablelike nerve tracts carrying signals among broadly dispersed concentrations of “gray matter.” The latter areas specialize in processing information, and the former in conveying the information from one part of the brain to another.

That finding wasn’t entirely unexpected, Zeineh said. CFS is thought to involve chronic inflammation, quite possibly as a protracted immunological response to an as-yet unspecified viral infection. Inflammation, meanwhile, is known to take a particular toll on white matter.

But a second finding was entirely unexpected. Using an advanced imaging technique — diffusion-tensor imaging, which is especially suited to assessing the integrity of white matter — Zeineh and his colleagues identified a consistent abnormality in a particular part of a nerve tract in the right hemisphere of CFS patients’ brains. This tract, which connects two parts of the brain called the frontal lobe and temporal lobe, is called the right arcuate fasciculus, and in CFS patients it assumed an abnormal appearance.

Furthermore, there was a fairly strong correlation between the degree of abnormality in a CFS patient’s right arcuate fasciculus and the severity of the patient’s condition, as assessed by performance on a standard psychometric test used to evaluate fatigue.
The full article can be found by clicking on the title.
 

Marco

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I'm looking forward to reading the full paper but I'd be very surprised if the findings are unique enough (or sufficiently clearly discriminate ME/CFS from controls) to represent a "CFS-specific diagnostic biomarker".

Still interesting though.
 

Forbin

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Fascinating. Someone should do MRI's of ME patients who have "recovered" or are in remission to see weather these changes persist when symptoms abate. It might reveal whether the changes seen on MRI's themselves produce the symptoms, or whether the changes are "collateral damage" or perhaps even some kind maker of susceptibility present from birth.
 

A.B.

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The Stanford investigators compared brain images of 15 CFS patients chosen from the group Montoya has been following to those of 14 age- and sex-matched healthy volunteers with no history of fatigue or other conditions causing symptoms similar to those of CFS.
These findings need to be replicated in a larger study. It also sounds like the patients were hand picked, so this might apply only to a subset of patients. If they were hand picked, the obvious question is: based on which criteria?
 
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ME patiënts don't have afasie. This finding is not a biomarker at all.
It is true that distinct aphasia is not observed in most ME patients. (literally not being able to speak)

It might suggest something else but I too lack confidence that those results are going to be useful.
 
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Gijs

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It it well known that CFS patiënts have reduced white-and gray matter overall. Nothing new has been found. Nobody in the scientific world cares about these findings.
 

lansbergen

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Isn't aphasia due to problems with the LEFT arcuate fasiculus? This study found the abnormalities on the right arcuate fasiculus.
http://en.wikipedia.org/wiki/Aphasia

Classifying the various and differing subtypes of aphasia is difficult and has led to disagreements among experts. The localizationist model is the original model, but modern anatomical techniques and analyses have shown that precise connections between brain regions and symptom classification do not exist. The neural organization of language is complicated; language is a comprehensive and complex behavior and it makes sense that it is not the product of some small, circumscribed region of the brain.
 
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alex3619

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Isn't aphasia due to problems with the LEFT arcuate fasiculus? This study found the abnormalities on the right arcuate fasiculus.
Isn't it the case that they think the right arcuate nucleus might be enlarged due to suspected defects in the left arcuate nucleus? If I recall correctly, didn't the qeeg data show that the left arcuate nucleus was underpeforming? I could be wrong, its been a while since I saw the videos.

Also that the data on abnormalities arising out of the left arcuate nucleus is disputed and controversial?

PS While I was writing both @Snow Leopard and @lansbergen posted things that match with what I have read, even though I don't recall the specifics.
 

alex3619

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It it well known that CFS patiënts have reduced white-and gray matter overall. Nothing new has been found. Nobody in the scientific world cares about these findings.
Another thing that came out of the Stanford symposium where this was measured is we have reduced cortical thickness in most places, but one place that is increased in thickness. Specific symptomology also matches likely symptoms when brain abnormalities were found by qEEG, or quantitative EEG. Also its worth remembering that these findings are similar to what the Japanese found with brain inflammation in their modified PET scan.

Different lines of investigation are showing similar things, and it was the Stanford study which enabled this by using one cohort for many studies. Patients results can then directly be compared study to study. What is interesting here is NOT any individual study so much, but that collectively they tell a larger picture.

All this relates to pathophysiology though, and does not directly give us a handle on causation. Yet if these studies hang together with replication etc., then any model of ME is going to have to reach a much higher standard to be acceptable.

Edit: Its clear I misremembered cortical thickness for white matter thickness. Its white matter, the connections between neurons plus a soup of immune cells, that is decreased.
 
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Forbin

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Aphasia may be mild or severe. With mild aphasia, the person may be able to converse, yet have trouble finding the right word or understanding complex conversations.
http://www.webmd.com/brain/aphasia-causes-symptoms-types-treatments
Word retrieval problems are part of both the CCC and ICC definitions of ME/cfs.

ICC
1. Neurocognitive Impairments


a. Difficulty processing information: slowed thought, impaired concentration e.g. confusion, disorientation, cognitive overload, difficulty with making decisions, slowed speech, acquired or exertional dyslexia

b. Short-term memory loss: e.g. difficulty remembering what one wanted to say, what one was saying, retrieving words, recalling information, poor working memory
CCC
"Neurological/Cognitive Manifestations:
Two or more of the following difficulties should be present: confusion, impairment of concentration and short-term memory consolidation, disorientation, difficulty with information processing, categorizing and word retrieval, and perceptual and sensory disturbances--e.g., spatial instability and disorientation and inability to focus vision. Ataxia, muscle weakness and fasciculations are common. There may be overload phenomena [hypersensitivities to stimuli that have changed form pre-illness status]: cognitive, senory--e.g., photophobia and hypersensitivity to noise--and or emotional overload, which may lead to "crash" periods and or anxiety.
Anomic aphasia (also known as dysnomia, nominal aphasia, and amnesic aphasia) is a disorder which causes problems with recalling words or names
http://en.wikipedia.org/wiki/Anomic_aphasia.