Which Way Wyller? CBT Proponent Finds Biological Signature in ME/CFS (?)

Cort

Founder of Health Rising and Phoenix Rising
Staff member
It's hard to figure out Wyller! He's been a strong proponent of CBT/GET and has reportedly made a lot of problems in Norway but in his last study he actually proposed that Epstein-Barr virus played a role in ME/CFS and urged more research in that area.


[*]See the Evolution of an ME/CFS Researcher?

From that blog:

Then Wyller suggested that inefficient viral clearance or reactivation or chronic viral infection-triggered immune dysfunction warrants further study in ME/CFS.

Then he referred to a remarkable 2014 German study which suggested that a deficient B- and T-cell memory response to EBV may be making it difficult for ME/CFS patients to control EBV infections. That's really no surprise to the ME/CFS community; it's long been clear that infectious mononucleosis is a common trigger for people with ME/CFS and FM“ but it's highly unusual for a CBT/GET proponent to make the connection.

Then, remarkably, Wyller, who recently criticized antivirals as he argued that CBT/GET should be the treatment of choice in ME/CFS asserted that this finding could reflect problems his ME/CFS adolescents were having with clearing latent herpesviruses. (Darn I miss the ability to put things in quotes...)

[fright]
[/fright] They might suggest less efficient viral clearance or reactivation of latent viruses such as members of the herpes virus family, in the CFS group Study Authors.

Finally, Wyller's study suggested that neither inactivity nor mood disorders had any effect on the biological findings presented. (One of his earlier studies discounted the idea that deconditioning was a relevant factor. )
Now Wyller believes he's found a distinct biological signature in the brains of his adolescent ME/CFS patients. We'll have to get the paper to know more but this statement "Immature FC of the right dAI-PPC in patients lacked associations with three known functional domains: cognition, pain and physical activity, which were observed in the healthy group" appears to suggest to me anyway that connections in the brain that regulate pain, cognition and physical activity are not working correctly in adolescent ME/CFS patients.

Wyller's tying it to a network that is involved in motivation. That may tweak some but I'm pretty much fine with that given that he's finding biological correlates. It suggests, after all, that something that has gone wrong in the brain is the answer.

PLoS One. 2017 Sep 7;12(9):e0184325. doi: 10.1371/journal.pone.0184325. eCollection 2017.Altered right anterior insular connectivity and loss of associated functions in adolescent chronic fatigue syndrome.
Wortinger LA1,2, Glenne Øie M2,3, Endestad T2, Bruun Wyller V1.



Abstract
Impairments in cognition, pain intolerance, and physical inactivity characterize adolescent chronic fatigue syndrome (CFS), yet little is known about its neurobiology. The right dorsal anterior insular (dAI) connectivity of the salience network provides a motivational context to stimuli. In this study, we examined regional functional connectivity (FC) patterns of the right dAI in adolescent CFS patients and healthy participants.

Eighteen adolescent patients with CFS and 18 aged-matched healthy adolescent control participants underwent resting-state functional magnetic resonance imaging. The right dAI region of interest was examined in a seed-to-voxel resting-state FC analysis using SPM and CONN toolbox. Relative to healthy adolescents, CFS patients demonstrated reduced FC of the right dAI to the right posterior parietal cortex (PPC) node of the central executive network. The decreased FC of the right dAI-PPC might indicate impaired cognitive control development in adolescent CFS.
Immature FC of the right dAI-PPC in patients also lacked associations with three known functional domains: cognition, pain and physical activity, which were observed in the healthy group. These results suggest a distinct biological signature of adolescent CFS and might represent a fundamental role of the dAI in motivated behavior.[/indent]
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