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.
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.