Preprint Opposite white matter abnormalities in post-infectious vs. gradual onset chronic fatigue syndrome revealed by diffusion MRI, 2024, Yu et al

John Mac

John Mac

Senior Member (Voting Rights)
Abstract
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a complex and debilitating illness with an unknown pathogenesis. Although post-infectious (PI-ME/CFS) and gradual onset ME/CFS (GO-ME/CFS) manifest similar symptoms, it has long been suspected that different disease processes underlie them. However, the lack of biological evidence has left this question unanswered.
In this study, we recruited PI-ME/CFS and GO-ME/CFS patients based on consensus diagnoses made by two experienced clinicians and compared their diffusion MRI features with those of rigorously matched healthy controls (HCs) with sedentary lifestyles.
PI-ME/CFS patients showed significantly higher axial diffusivities (ADs) in several association and projection fibres compared to HCs.
Higher AD values in PI-ME/CFS were significantly related to worse physical summary scores.
In contrast, GO-ME/CFS patients exhibited significantly decreased ADs in the corpus callosum. Lower AD values in GO-ME/CFS patients were significantly associated with lower mental summary scores in commissural and projection fibres.
Distinct patterns of AD alterations in PI-ME/CFS and GO-ME/CFS provide neurophysiological evidence of different disease processes and highlight the heterogeneities of ME/CFS.
These results also help explain inconsistent findings in previous ME/CFS studies and guide future intervention design.

https://www.medrxiv.org/content/10.1101/2024.08.04.24311483v1
 
Interesting first pass study suggesting subtypes based on changes to neurological structures.

143 participants, including 76 patients with ME/CFS (mean age, 42.64 ± 12.71 [standard deviation]; 64 women) and 67 HCs (mean age, 37.51 ± 11.57 [standard deviation]; 52 women).
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Requires replication to be sure and corroboration by other studies like Decode ME.

Increased AD (axial diffusivities) in PI-ME/CFS patients might be related to acute inflammatory responses following an infection, whereas decreased AD in GO-ME/CFS patients may reflect chronic neurodegenerative processes.
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We hypothesise that inconsistencies in findings across studies may arise from differences in sample characteristics, patient criteria, or statistical methodologies.
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Diagnostic criteria once again proving imprecise. Meanwhile methodology has no standard.

Even if the reported neurological differences between infectious vs gradual onset ME patients were proved consistent, we still dont know whether their underlying disease mechanism is the same, or different.

For discussion, is it two manifestations of an immune related mechanism gone awry, one due to infection of the nervous system by say HSVs and the other due to slower acting infection of other tissues like immune cells by other viruses say EBV? Or is it two entirely different mechanisms which both happen to cause fatigue?

The decades roll past and still we have no clue because studies like this are done, go on the pile, are ignored, more studies done and ignored, rinse repeat. There is no deductive overview at work requiring replication, seeking certainty and identifying questions arising then tracking down answers. Its just "lets start here" over and over again.
 
Possibly results from this grant?

https://www.s4me.info/threads/australian-me-cfs-neuroimaging-project-receives-1-2m-govt-grant.12748/

See also this study

https://www.s4me.info/threads/absen...-by-task-functional-mri-2024-schönberg.39688/

On a quick glance this looks to be a good-sized cohort by ME standards, carefully diagnosed, and with well matched controls - notably including for activity

Maybe someone with relevant expertise can comment on the quality of the method and the interpretation of the results?
 
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