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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of, and finding treatments for, complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia, long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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I agree that this study (like most CFS studies) need a 'sick' control group as well as a healthy one. Thanks for digging out the depression study, adreno, but note that it isn't looking at the same thing as the Unger study. Unger looked at basal ganglia activity while the Depression study looked a conectivity between the basal ganglia and the hemispheres so they aren't really comparable.This study doesn't tell us much, in my view. The same problems are found in depression:
Aberrant functional connectivity of cortico-basal ganglia circuits in major depression.
The aim of this study was to test the hypothesis that cortico-basal ganglia circuit dysfunction represents primary pathology in unipolar depression. ...Compared to controls, unipolar subjects exhibited altered connectivity between bilateral subcortical components of the circuitry (putamen-thalamus) and left hemisphere input and output components.
... These findings suggest that the cortico-basal ganglia circuitry is likely one of several loci of primary pathology in major depression.
"Chronic Fatigue Syndrome cures irresponsible gambling".
I agree that this study (like most CFS studies) need a 'sick' control group as well as a healthy one. Thanks for digging out the depression study, adreno, but note that it isn't looking at the same thing as the Unger study. Unger looked at basal ganglia activity while the Depression study looked a conectivity between the basal ganglia and the hemispheres so they aren't really comparable.
Just because the Unger study looked at the basal ganglia in isolation, doesn't mean that it works that way. The reality is that brain function works in circuits, and that it is pretty meaningless to look at isolated areas.
Meaningless in what way?
The extent of the lowered basal ganglia activtion correlated very well each patient's level of fatigue. This is pretty remarkable, because not only did they finally find a possible biological mechanism/marker, but it also shows the basal ganglia is probably involved in a linear way (lowered activation/fatigue severity). Wether this is a cause or a consquence of ME/CFS I don't know, but earlier research suggests it's a cause rather than a consequence.
I don't think we can conclude much from this study, but we can speculate that inflammation causes decreased reward (and fatigue). But this is hardly surprising.
Good question. I'm not a neuroscientist, so I have no idea honestly.And how does this differ from the lowered basal ganglia activtion seen in depression? What makes it specific to ME?
Well, we can conclude the basal ganglia is probably involved in ME/CFS. This is a pretty remarkable milestone in this disease with no known biological marker. Interestingly, this study was already announced at the Ottawa IACFS/Conference in 2011. Cort wrote a report about it where one of the authors speculates why the basal ganglia seems to be less effective in ME/CFS. (http://forums.phoenixrising.me/content.php?548-Ottawa) It definetely opens a whole new area of research which may ultimately lead to understanding the pathophysiology of ME/CFS and possibly a cure.I don't think we can conclude much from this study, but we can speculate that inflammation causes decreased reward (and fatigue). But this is hardly surprising.
Good question. I'm not a neuroscientist, so I have no idea honestly.
Well, we can conclude the basal ganglia is probably involved in ME/CFS. This is a pretty remarkable milestone in this disease with no known biological marker. Interestingly, this study was already announced at the Ottawa IACFS/Conference in 2011. Cort wrote a report about it where one of the authors speculates why the basal ganglia seems to be less effective in ME/CFS. (http://forums.phoenixrising.me/content.php?548-Ottawa) It definetely opens a whole new area of research which may ultimately lead to understanding the pathophysiology of ME/CFS and possibly a cure.
Unless you're completely sure the basal ganglia is involved in the exact same way in both ME/CFS and other disorders, I find your statement highly speculative. Most of this research is way above my head, but I suppose there is a reason why the authors refer to the similarities in ME/CFS and interferon-alpha induced sickness symptoms and not to MDD or another disorder.I don't find it that remarkable. We now know that the basal ganglia is involved in ME (also). But that is true of a range of disorders, and is not specific to ME.
Do you have any research to support your last notion? As far as I know, ME/CFS has only slightly increased parameters of inflammation and pro-inflammatory cytokines such as interleukin (IL) 1, IL6 and tumour necrosis factor (TNF)High inflammation is likely to cause fatigue and anhedonia. This is also known as sickness behavior. The fatigue and reduced reward (through reduced interest) will lead you to rest, which is what your immune system "wants". And since reward is mediated by the basal ganglia, these structures are necessarily involved. These are common findings in depression (that is inflammation, anhedonia and fatigue). So it is not surprising to see these findings in ME, as this is a disorder characterized by high levels of inflammation.
Do you have any research to support your last notion? As far as I know, ME/CFS has only slightly increased parameters of inflammation and pro-inflammatory cytokines such as interleukin (IL) 1, IL6 and tumour necrosis factor (TNF)
Since they used fMRI, like the study you quoted, presumably they looked at the whole brain not just at the basal ganglia (all the other fMRI studies I've seen scan the whole brain and look at differences between patients and controls). Assuming they did - I guess we'll have to wait to see the published paper to finbd out - then their findings appear to be different to the depression study.Just because the Unger study looked at the basal ganglia in isolation, doesn't mean that it works that way. The reality is that brain function works in circuits, and that it is pretty meaningless to look at isolated areas.
Thanks - this study looks altogether more relevant. I wonder if the Unger study excluded depressed patients from their sample? And what case definition was used (though I'd be surprised if they used the wacky Empiric criteria as Unger seems to be backing off that one).Here's another study that found decreased reward (hypoactivity in the striatum) in depression. The striatum is part of the basal ganglia.
"Functional magnetic resonance imaging (fMRI) data indicated that the MDD group was characterized by reduced activation of striatal reward regions during reward selection, reward anticipation, and reward feedback, supporting previous data indicating hyporesponsivity of reward systems in MDD."
http://www.ncbi.nlm.nih.gov/m/pubmed/19261334/
The CDC seem to be about 10 years behind the game. The study below below used MR spectroscopy and found elevated levels of choline in the L basal ganglia. That's along the lines of the Puri hypothesis.
http://www.cfids-cab.org/cfs-inform/Brainscans/chaudhuri.etal03.pdf
The CDC study seems to be an abstract from a conference presentation and not a peer-reviewed paper. I'm not going to take much away from it, as it's very easy to do bad brain imaging studies.
The headlines could easily read "Chronic Fatigue Syndrome patients unimpressed with gambling".