Neural consequences of post-exertion malaise in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome - Cook, Light +

Sly Saint

Senior Member (Voting Rights)
May 2017
Neural consequences of post-exertion malaise in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
Dane B.CookabAlan R.LightcKathleen C.LightcGordonBroderickdMorgan R.ShieldsbRyan J.DoughertybJacob D.MeyerbStephanieVanRiperbAaron J.StegnerbLaura D.EllingsoneSuzanne D.Vernonf

Abstract
Post exertion malaise is one of the most debilitating aspects of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, yet the neurobiological consequences are largely unexplored. The objective of the study was to determine the neural consequences of acute exercise using functional brain imaging. Fifteen female Myalgic Encephalomyelitis/Chronic Fatigue Syndrome patients and 15 healthy female controls completed 30 min of submaximal exercise (70% of peak heart rate) on a cycle ergometer. Symptom assessments (e.g. fatigue, pain, mood) and brain imaging data were collected one week prior to and 24 h following exercise.

Functional brain images were obtained during performance of:
1) a fatiguing cognitive task – the Paced Auditory Serial Addition Task,
2) a non-fatiguing cognitive task – simple number recognition, and
3) a non-fatiguing motor task – finger tapping.

Symptom and exercise data were analyzed using independent samples t-tests. Cognitive performance data were analyzed using mixed-model analysis of variance with repeated measures. Brain responses to fatiguing and non-fatiguing tasks were analyzed using linear mixed effects with cluster-wise (101-voxels) alpha of 0.05.

Myalgic Encephalomyelitis/Chronic Fatigue Syndrome patients reported large symptom changes compared to controls (effect size ≥0.8, p < 0.05). Patients and controls had similar physiological responses to exercise (p > 0.05). However, patients exercised at significantly lower Watts and reported greater exertion and leg muscle pain (p < 0.05).

For cognitive performance, a significant Group by Time interaction (p < 0.05), demonstrated pre- to post-exercise improvements for controls and worsening for patients. Brain responses to finger tapping did not differ between groups at either time point. During number recognition, controls exhibited greater brain activity (p < 0.05) in the posterior cingulate cortex, but only for the pre-exercise scan.

For the Paced Serial Auditory Addition Task, there was a significant Group by Time interaction (p < 0.05) with patients exhibiting increased brain activity from pre- to post-exercise compared to controls bilaterally for inferior and superior parietal and cingulate cortices. Changes in brain activity were significantly related to symptoms for patients (p < 0.05).

Acute exercise exacerbated symptoms, impaired cognitive performance and affected brain function in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome patients.

These converging results, linking symptom exacerbation with brain function, provide objective evidence of the detrimental neurophysiological effects of post-exertion malaise.

https://www.sciencedirect.com/science/article/pii/S088915911730051X?via=ihub#t0005
 
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Thanks kindly for the bump @Sly Saint . You've saved me a job I was going to do later. On a brief read, seems that SMCI are ahead of the curve on this one, and seems to be the kind of approach many of us have been asking for?

I'll look forward to reading comments from folks more qualified than me to do so .. do your thing s4me ;)

Wishing everyone improved health and every happiness. John :)
 
While it's welcome to see research that appears to chime with personal experience (when subject to a stressor my brain turns to mush) unfortunately the results are open to interpretation that might support the BPS model. No criticism of the researchers - it's just the way it is.

I could imagine that a BPS interpretation would see the cognitive deficits found (errors made) as reflecting either top down executive function or attentional processes leading to PWME excessively focusing on normal symptoms to the detriment of cognitive processes (too much bandwidth taken up attending to normal sensations).

It may or may not be the case however that attentional processes in PWME's brains are overactivated because there is an earlier signalling problem (as per the Lights' work) that means they are being bombarded with sensory information. Unfortunately there's no way of telling from this study. We would need to show abnormal signalling at the pre-attentional level was driving the cognitive deficits and not some problem with top down control subject to 'conscious' control.

PS - I've just skimmed this paper for apologies if these issues were addressed.

Another small issue is that I do wish they wouldn't chuck in the kitchen sink when trying to make a case (e.g. 'white lesions' - barely relevant or Morris and Maes' 'feed- forward' theory - nice speculation I'm sure but hardly evidence). It just risks undermining their credibility.
 
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