A Tale of Two Studies

Last year there were two studies of MRI scans of CFS patients: one in Australia and one in the U.K.

Both used a technique called "voxel-based morphometry" (if you can say that several times quickly, you must be sober) to detect changes in both gray matter and white matter. Both concluded there are systematic changes in patients with ME/CFS indicating shrinkage.

Now, the big differences: the Australian study patients met both the Fukuda definition and the Canadian Consensus Criteria; the U.K. study used the CDC empirical definition; psychiatry was well-represented in the list of authors for the U.K. study. The Australian study has a hidden bomb inset in figure 2 showing a correlation resulting from linear regression of time since onset of fatigue and degree of shrinkage. The U.K. study makes no solid inference about rate of shrinkage, speculating that it must take place early in the disease.

That plot in the Australian study shows a definite trend of 1% shrinkage of white matter per year after onset of serious chronic fatigue, up to 15 years. You don't need any advanced training in statistics to recognize this. The result of linear regression is what you would get if you drew a straight line through the cluster of data points. This is consistent with reports of cognitive impairment. If this goes on very long, the end result must be dementia.

The U.K. study takes pains to emphasize the conflicting results of earlier studies. There is no mention of the effect conflicting diagnostic criteria have had. Considering the effect of inherited diagnostic incompetence from the empirical definition it is surprising they found anything.

In view of the way the PACE trial was handled we may expect two conclusions in the U.K.: 1) it is perfectly normal for people in their 20s and 30s to show CNS degeneration common in people 50 years older; 2) the source of these problems is clearly the unwillingness of patients to exercise, due to "faulty illness beliefs". There is probably a medical tiger team busy right now moving the goal posts before final publication of the referenced paper.

The Australian study seems to have a more useful message: the changes are consistent with altered cerebral hemodynamics and dysregulation in the autonomic nervous system. Thus, we have objective scientific data on changes in the CNS consistent with patient reports of cognitive deficits and orthostatic intolerance.

The problem of dementia is not exclusive to ME/CFS patients. Current estimates are that, unless you die young, you have about one chance in three of developing dementia. Medical and social costs associated with dementia are enormous. Personal costs are enough to drive people to suicide. We have to wonder at what point not merely the health care system, but the nation itself will break down under the load. How could we deal with 100 million dementia patients?

The only viable solution is to intervene early enough to prevent the condition from developing.


Hi anciendaze, this opens up a can of worms. While I have some reason to doubt that mental function cannot be dramatically improved in ME, if we are at very high risk for dementia then by ignoring us the authorities are deliberately allowing a very large number of potential dementia cases to go untreated. This is a bad idea, and represents a failure of public health measures, especially prevention. While we only represent a small proportion of the total population, I suspect this may show we represent a larger percentage of the dementia cases.

This is worrying for me as I have had ME since 1968, 1983 or 1985 depending on what level of symptom severity I choose to use. Since 1983 my functional capacity fits the case for mild ME under the ME ICC. My episodic memory is fubar, and my working memory is in decline. Only my semantic memory is holding up, which again points to ME being a special form of cognitive decline, deserving of its own research.

Bye, Alex
This is very worrisome for me. A brain scan I had done back in 2008 showed "mild atrophy unexpected for age" (I was mid-thirties). My neurologist and my physician both told me that it wasn't clinically relevant. I have great difficulty with word finding. It terrifies me to wonder what that image might look like today and worse, what it might look like ten years from now.
How could we deal with 100 million dementia patients?
Very easily. Everyone will be too demented to care or even realize there's a problem. Which is partly already going on.

Seriously though, the Australian study has been following patients for the past 15 years, taking "voxel-based morphometry" MRIs every year?
Where is this study?
Nielk;bt6589 said:
...Seriously though, the Australian study has been following patients for the past 15 years, taking "voxel-based morphometry" MRIs every year?
Where is this study?
Follow the embedded link, like this one. They haven't been following individual patients for 15 years. They just did a study of one cohort which recorded the length of time for unexplained fatigue. This was then correlated with the results of voxel-based morphometry. I don't think that technique even existed 15 years ago.
I wonder why there are no similar studies going on in the U.S? It sounds like it may point to a biological marker for this illness.
After a recent local spate of paid political advertisements I begin to doubt that evidence of dementia remains outside the range of what is currently considered normal in an American population.
This just makes me sad. My husband, now 75, has had ME for 11 years now and the dementia is moving right along. Of course at his age, one could just say it is senile dementia, so no one will ever really care about the 'why' in his case.

Anciendaze: agreed re political ads and American dementia. I decided 30 years ago there is nothing scarier to me (a Canadian) than the US election year. I do wish it did not come around quite so often.
Very interesting anciendaze - I had/have a strong feeling about shifting goal posts here (well they will have to where psychobabblers involved). Also interestingly from personal experience I recall (severe then) severe headaches, "high spots" in the brain from MRI imaging and cognative problems to the extent of inabilities to recognise people or things - also barely able to speak or move. However through years of personal recognised ME supplementation the position has reversed though not fully well my "little grey cells" are functioning very well thank you and planning to go back to the psychiatrist foisted on me then and ask him if he can do the Times Crossword. Just can't see ME as the same thing as the various types of known degenerative dementias.
Enid;bt6626 said:
...Just can't see ME as the same thing as the various types of known degenerative dementias.
In medical terms the primary disease is not purely progressive. We appear to be dealing with secondary complications of cerebral hypoperfusion due to dysautonomia. This is getting close to the primary disease, even if it may still not be there. Orthostatic intolerance is a key symptom, and thus is ignored in psychosocial models.

Problems with cerebral hypoperfusion are far more widely found than clinical ME/CFS. I recently met a friend for lunch. She was late, as has become a habit in recent years. (She has also lost two jobs for being late to work.) She seemed a little uncertain of herself (not at all characteristic), and complained of feeling sleepy or light-headed even after drinking hot tea.

After some questioning, I learned she had a reaction to her medication for blood pressure. She is hypersensitive to this, and can only tolerate half the prescribed dose. More questions revealed she has been on the medication for several years, about the same period as her troubles.

The problem in this case is internists and cardiologists acting like mechanics or plumbers. As long as the heart keeps pumping the patient is healthy. Episodic confusion, and even syncope, can be attributed to aging. No doctor is likely to say the problem is iatrogenic.

This patient needs to lower her blood pressure, but she should not do so in a way that periodically makes her a threat to others when she drives a car. It would also be nice if her medication allowed her to keep a job. If the recommended treatment makes it impossible for her to hold a job she should be on disability.

I think the financial implications of that last option would lead to quick improvements in officially recommended treatments.

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