The study used the Reeves 2005 population but remember that included assessment as:
The clinical visit included detailed medical history, physical examination, laboratory tests, psychiatric screen, and questionnaires to measure functional status, impairment and symptoms, and was completed by 783 persons. Participants were classified as: i) CFS cases, according to the 1994 case definition[22], [23]; i
Further the current study had an extensive exclusion process which included:
Subjects with a score >60 on the 20-item, self report Zung Self Rating Depression Scale (Zung SDS)(indicating more than mild depressive symptoms) were also excluded [25]. All subjects were required to be free of psychotropic medications including antidepressant, antipsychotic, mood stabilizer or anti-anxiety medications for at least 4 weeks prior to brain imaging procedures. No subjects were taken off psychotropic medications for the purposes of the study.
One of the criticism of Reeves work is that it didn’t distinguish between ME and depression, but it would appear that this study went to some lengths to avoid conflation. So as I read it, the study CFS cohort was Fukada, but with identifiable depression or other psychiatric confounders allowed by Fukada removed – so not a bad proxy for a wider ME/CFS population. That said I’d agree that the results are not overwhelming – another study that shows there’s ‘stuff going on’ but that the ‘stuff’ is all over the place. Some discussion about articulating the problems of definitions in the P2P context here: http://www.occupycfs.com/2014/05/22/p2p-agenda-fatigue/#comments
The clinical visit included detailed medical history, physical examination, laboratory tests, psychiatric screen, and questionnaires to measure functional status, impairment and symptoms, and was completed by 783 persons. Participants were classified as: i) CFS cases, according to the 1994 case definition[22], [23]; i
Further the current study had an extensive exclusion process which included:
Subjects with a score >60 on the 20-item, self report Zung Self Rating Depression Scale (Zung SDS)(indicating more than mild depressive symptoms) were also excluded [25]. All subjects were required to be free of psychotropic medications including antidepressant, antipsychotic, mood stabilizer or anti-anxiety medications for at least 4 weeks prior to brain imaging procedures. No subjects were taken off psychotropic medications for the purposes of the study.
One of the criticism of Reeves work is that it didn’t distinguish between ME and depression, but it would appear that this study went to some lengths to avoid conflation. So as I read it, the study CFS cohort was Fukada, but with identifiable depression or other psychiatric confounders allowed by Fukada removed – so not a bad proxy for a wider ME/CFS population. That said I’d agree that the results are not overwhelming – another study that shows there’s ‘stuff going on’ but that the ‘stuff’ is all over the place. Some discussion about articulating the problems of definitions in the P2P context here: http://www.occupycfs.com/2014/05/22/p2p-agenda-fatigue/#comments
@Simon , is it anywhere clearly cited as to what SF-36 PF scores are typically seen in clinics or outpatient studies? Has anyone reviewed the CFS and ME studies to determine what is commonly found (while acknowledging that most of these studies are primarily on mild patients). This would help us put studies like PACE into perspective.
I was wondering how this study would relate to ideas of the lack of blood flowing to the brain. From my very limited understanding the fMRI scan is detecting changes in the flow of oxygenated blood. I think the oxygenated blood affects the magnetic field more than once the oxygen has been released. Then they make an assumption that areas of the brain where processing is happening require oxygen and hence they look for the change between oxygenated and non-oxygenated blood.
So my assumption (although I've not yet read the paper) is that what they are detecting is less blood flow and less oxygen being metabolized in areas of the brain where people have fatigue. It made me wonder if this may relate to work that Julia Newton is doing at Newcastle finding increased acidosis in muscles which I believe is due to the lack of oxygen available to turn something (glucose?) into energy.
So my assumption (although I've not yet read the paper) is that what they are detecting is less blood flow and less oxygen being metabolized in areas of the brain where people have fatigue. It made me wonder if this may relate to work that Julia Newton is doing at Newcastle finding increased acidosis in muscles which I believe is due to the lack of oxygen available to turn something (glucose?) into energy.