ME/CFS and LC at International Society for Magnetic Resonance in Medicine 2024

Assessment of Functional connectivity in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome using 7Tesla MRI

Maira Inderyas, Kiran Thapaliya, Sonya Marshall-Gradisnik, Markus Barth, and Leighton Barnden

Motivation: To assess Functional Connectivity (FC) differences between healthy individuals and Myalgic Encephalomyelitis or chronic fatigue syndrome (ME/CFS) patients using ultra-high-field fMRI.

Goal(s): Are there significant FC differences between brainstem and cerebellum regions comparing ME/CFS and healthy controls? Is there any association between clinical measures and FC in ME/CFS?

Approach: fMRI data were acquired on 7Tesla scanner during cognitive Stroop color-word task. Using a-priori regions, FC was assessed in CONN toolbox.

Results: Weaker FC was observed between brainstem and cerebellum regions along with altered FC within the intrinsic network hubs which supports our hypothesis of connectivities being defective in ME/CFS within those regions.

Impact: FC analyses using ultra-high-field MRI facilitates our understanding of the underlying patho-mechanisms of the cognitive deficits in ME/CFS and their progression.

Link (Presented at International Society for Magnetic Resonance in Medicine conference)

I don't know if there's a full text, but if there is, it's only accessible to conference attendees for one year, then only ISMRM members for one year, then available to the public.

 

Another presentation at this conference:

Investigation of hippocampal subfield volumes in long COVID and ME/CFS using 7T MRI

Kiran Thapaliya, Sonya Marshall-Gradisnik, Natalie Eaton-Fitch, Markus Barth, Maira Inderyas, and Leighton Barnden

Motivation: To study hippocampal atrophy in long COVID and Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS patients).

Goal(s): Our goal was to investigate hippocampal atrophy in long COVID and ME/CFS patients.

Approach: We used T1-weighted MP2RAGE data from 7T MRI and used FreeSurfer to estimate hippocampal subfield volumes in long COVID and ME/CFS patients.

Results: We found that hippocampal subfield volumes were larger in long COVID and ME/CFS patients compared to HC.

Impact: Our study showed atypical hippocampal atrophy in long COVID and ME/CFS patients indicating that existing brain research findings in ME/CFS patients may help better understand the neurological dysfunction in long COVID patients.

Link

 

Post-COVID Fatigue Relates to Bioenergetic Dysfunctions in the Posterior Cingulate Gyrus

Hye Bin Yoo, Hyeong Hun Lee, Serene Huang, and Jeong Hoon Lim

Motivation: Persistent fatigue after recovery from SARS-CoV-2 shows pathologies comparable to chronic fatigue syndrome or myalgic encephalomyelitis (CFS/ME). It is unknown if disruptions in mitochondrial functions caused by SARS-CoV-2 persists in post COVID fatigue as dysregulated mitochondrial homeostasis.

Goal(s): We aim to investigate if post-COVID fatigue relates to perturbations of mitochondrial function in the brain representing signs of neuroinflammation, redox imbalance, and neuronal dysfunctions.

Approach: Proton MR spectroscopy was performed on post-COVID fatigue patients targeting at posterior cingulate gyrus (PCG), one of the most metabolically active regions.

Results: We found reduced level of antioxidants and neuronal activity in post-COVID fatigue patients.

Impact: Proton MR spectroscopy in PCG of post-COVID fatigue patients shows signs of redox imbalance and reduced neuronal activity, suggesting of long-term dysregulations in mitochondrial homeostasis persisting after SARS-CoV-2 infection. SARS-CoV-2 infection may lead to further neurodegenerations post-recovery.

Link

 

Structural and Oxygen Metabolic Magnetic Resonance Imaging of long-COVID and ME/CFS

Xiang Xu, Puneet Belani, Dengrong Jiang, Rodophe Leforestier, Hanzhang Lu, and Benjamin Natelson

Motivation: Many long-COVID patients experience fatigue and post exertional malaise which are primary symptoms of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). Understanding the similarities and differences between long-COVID and classic ME/CFS could provide insights into the disease mechanisms.

Goal(s): To measure brain anatomy and oxygen metabolism between the two groups.

Approach: Clinical standard and advanced MRI techniques measuring the venous oxygenation were applied. The fatigue level was assessed by questionnaires.

Results: No differences in brain anatomy were observed between the groups, but the long-COVID group had significant lower venous oxygenation than the healthy control group and the classic CFS group.

Impact: Many long-COVID patients fulfill diagnostic criteria for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). Compared to structural changes, metabolism-related parameters, such as venous oxygenation of the brain, may be more sensitive to changes related to long-COVID and CFS disease mechanisms.

Link

 

Who's in a hurry?
I've only been waiting for 33 years as are miilions of other patients all over the world.
Two years embargo, that hurts.

 

Thanks for the warning.
Venous oxygenation caught my attention. I'd love to learn more about that.
I do remember though a bold signal turning into effort preference (NIH).

 

Wonder if this holds using deconditioned/unhealthy/sick controls.

 

Is it some difference in underlying disease mechanisms or does it reflect early onset of disease in LC-ME/CFS vs more established, longer duration non-LC-ME/CFS non-Covid related ME/CFS?

 

Could you explain what you mean by more established longer duration non-LC-ME/CFS?

 

Just that people with a diagnosis of ME/CFS from something other than Covid are likely to have had the disease for longer duration. Not least with delays to diagnosis and increased likelihood of being diagnosed with LC rather than ME/CFS since say mid-late 2020.

I'll edit to clarify.

 

What would your own n=1 answer be to your question?

 

I haven't done any brain imaging on myself (too sick early on, too risky for repeat Covid infection, no potential clinical management change), but potentially I could do it from now on. The low peripheral SvO2 measurements I've previously discussed might relate in a more global fashion. So if I repeated those 3-4 yrs down the line that might inform disease progression in terms of stabilisation and compensation.