Brainstem Abnormalities in ME/CFS: A Scoping Review and Evaluation of Magnetic Resonance Imaging Findings (Nelson et al., 2021)

[perrier]

https://www.frontiersin.org/articles/10.3389/fneur.2021.769511/full#h6

 

[Diwi9]

Yes, let's follow the evidence...more autopsies, more biopsies, improved imagining. Enough examination of blood!!!

 

[junkcrap50]

Can you, & everyone else who posts research on here, please post the Title, Authors, & Abstract whenver posting links to papers.

It saves a click (I, and many others, are that lazy), but it also enters the information to the Phoenix Rising knowledge base, so that searching can bring it up for someone who may need it in the future.

 

[junkcrap50]

Front. Neurol., 17 December 2021 | https://doi.org/10.3389/fneur.2021.769511

Brainstem Abnormalities in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Scoping Review and Evaluation of Magnetic Resonance Imaging Findings
Todd Nelson1,2, Lan-Xin Zhang1,3, Hui Guo1,4,

Luis Nacul5,6 and Xiaowei Song1,2*

Background: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a multisystem medical condition with heterogeneous symptom expression. Currently, there is no effective cure or treatment for the standard care of patients. A variety of ME/CFS symptoms can be linked to the vital life functions of the brainstem, the lower extension of the brain best known as the hub relaying information back and forth between the cerebral cortex and various parts of the body.
Objective/Methods: Over the past decade, Magnetic Resonance Imaging (MRI) studies have emerged to understand ME/CFS with interesting findings, but there has lacked a synthesized evaluation of what has been found thus far regarding the involvement of the brainstem. We conducted this study to review and evaluate the recent MRI findings via a literature search of the MEDLINE database, from which 11 studies met the eligibility criteria.
Findings: Data showed that MRI studies frequently reported structural changes in the white and gray matter. Abnormalities of the functional connectivity within the brainstem and with other brain regions have also been found. The studies have suggested possible mechanisms including astrocyte dysfunction, cerebral perfusion impairment, impaired nerve conduction, and neuroinflammation involving the brainstem, which may at least partially explain a substantial portion of the ME/CFS symptoms and their heterogeneous presentations in individual patients.
Conclusions: This review draws research attention to the role of the brainstem in ME/CFS, helping enlighten future work to uncover the pathologies and mechanisms of this complex medical condition, for improved management and patient care.

 

[Pyrrhus]

Can you, & everyone else who posts research on here, please post the Title, Authors, & Abstract whenver posting links to papers.

And just as a reminder:

Starting a discussion thread about a scientific paper: If you are starting a discussion thread about a specific scientific paper, please read this explanation of how to title your discussion thread.

 

[junkcrap50]

And just as a reminder:

Thanks. Didn't know of any guidelines.

 

[Consul]

I think next someone should try to determine what exactly is causing the O&NS (which then leads to the neuroinflammation). Why not look in the cerebrospinal fluid like they did in the recent MS study.

Some additional exerpt:

The review is in favor of the hypothesis that ME/CFS involves brainstem specific astrocyte dysfunctions, contributing to impaired brainstem cerebrovascular autoregulation and reduced blood flow (36, 56). Oxidative stress appears to induce ME/CFS symptoms, associated with reduced blood flow and neuroinflammation. An infection (the most frequently reported trigger for ME/CFS onset) has been linked to peroxynitrite production, a proinflammatory oxygen/nitrogen species (57, 58), triggering neuroinflammation. This can lead to the production of isoprostanes and cause vasoconstriction when the level of antioxidants is insufficient (59). Oxidative stress and increased isoprostanes in ME/CFS have been correlated with clinical symptoms (60). Reduced brain blood flow is common in ME/CFS patients, accompanied by lowered circulation and nutrient/waste exchange (61–65).

 

[godlovesatrier]

Also could it all be due to swelling and after swelling viral invasion of tissue and degradation of those tissue zones. Won't be for everyone of course, so that bodes the question do two subsets of ME look the same or do they look entirely different? Suspect there will be crossover between the subsets or we might have figured the disease out by now.

 

[perrier]

Can you, & everyone else who posts research on here, please post the Title, Authors, & Abstract whenver posting links to papers.

It saves a click (I, and many others, are that lazy), but it also enters the information to the Phoenix Rising knowledge base, so that searching can bring it up for someone who may need it in the future.

Pls change it; I’m not computer savvy; good point! Thank you

 

[Pyrrhus]

Pls change it; I’m not computer savvy; good point! Thank you

Thanks so much!

The moderators would be happy to change your discussion thread title if you report the first message in your thread to the moderators using the small "Report" link under the first message. The moderators generally try to avoid editing thread titles unless the original poster requests it.

You can also change it yourself rather easily:

Have you ever wanted to change the title of your discussion thread, but was confused about how to do it?

Simply click the down arrow at the top-right of the discussion thread, and select "Edit thread"!

 

[Pyrrhus]

Oxidative stress appears to induce ME/CFS symptoms, associated with reduced blood flow and neuroinflammation. An infection (the most frequently reported trigger for ME/CFS onset) has been linked to peroxynitrite production, a proinflammatory oxygen/nitrogen species (57, 58), triggering neuroinflammation.

I think the authors have it a bit backwards here. An infection would result in neuroinflammation, and the neuroinflammation would then result in the oxidative stress.

This is discussed in the interview with Dr. Komaroff:
https://phoenixrising.me/myalgic-en...ic-fatigue-syndrome/komaroff-research-me-cfs/

Oxidative stress and increased isoprostanes in ME/CFS have been correlated with clinical symptoms (60).

We all are tired of hearing it, but "correlation does not imply causation".

Why not look in the cerebrospinal fluid like they did in the recent MS study.

People often look in the cerebrospinal fluid (CSF) for two reasons:

1. It's convenient. A lumbar puncture is a fairly easy procedure these days.
2. People mistakenly think that the brain sits in CSF, so any debris from the brain would be detectable in the CSF.

In recent years, as researchers have uncovered a lymphatic system which drains the debris from the brain, people are starting to realize that we should have been looking for brain debris in the lymph nodes, not in the CSF:

 

[Consul]

I think the authors have it a bit backwards here. An infection would result in neuroinflammation, and the neuroinflammation would then result in the oxidative stress.

This is discussed in the interview with Dr. Komaroff:
https://phoenixrising.me/myalgic-en...ic-fatigue-syndrome/komaroff-research-me-cfs/

Makes sense. Weird that researchers would get that backwards.

People often look in the cerebrospinal fluid (CSF) for two reasons:

1. It's convenient. A lumbar puncture is a fairly easy procedure these days.
2. People mistakenly think that the brain sits in CSF, so any debris from the brain would be detectable in the CSF.

In recent years, as researchers have uncovered a lymphatic system which drains the debris from the brain, people are starting to realize that we should have been looking for brain debris in the lymph nodes, not in the CSF:

I assumed that

That makes the MS result less interresting.

But dont you think the fluid flow will sometimes go left also in the picture? For example CO2 has to go back to the blood, i would think more things also would do that. Could be a complicated back and forth system there dont u think?

 

[Pyrrhus]

But dont you think the fluid flow will sometimes go left also in the picture?

Yes, but only when the Blood-Brain-Barrier (BBB) is compromised, such as in acute encephalitis. In those cases, there is some back-flow, so the CSF might contain some debris from the brain.

Specific nutrients and metabolites, such as CO2, can diffuse or be selectively transported to and from the blood across the BBB, but that does not mean that fluid or debris flows backwards.

I hope this is clear.

 

[junkcrap50]

Yes, but only when the Blood-Brain-Barrier (BBB) is compromised, such as in acute encephalitis. In those cases, there is some back-flow, so the CSF might contain some debris from the brain.

I suppose some foreign bodies (virus, autoantibodies, debris, etc.) could get "trapped" between the blood brain barriers during flow, as the BBB heals or "the gates close." But I agree, lymph node biopsy or lymph fluid collection would be a good place to search.

 

[Violeta]

I think next someone should try to determine what exactly is causing the O&NS (which then leads to the neuroinflammation). Why not look in the cerebrospinal fluid like they did in the recent MS study.

Some additional exerpt:

The review is in favor of the hypothesis that ME/CFS involves brainstem specific astrocyte dysfunctions, contributing to impaired brainstem cerebrovascular autoregulation and reduced blood flow (36, 56). Oxidative stress appears to induce ME/CFS symptoms, associated with reduced blood flow and neuroinflammation. An infection (the most frequently reported trigger for ME/CFS onset) has been linked to peroxynitrite production, a proinflammatory oxygen/nitrogen species (57, 58), triggering neuroinflammation. This can lead to the production of isoprostanes and cause vasoconstriction when the level of antioxidants is insufficient (59). Oxidative stress and increased isoprostanes in ME/CFS have been correlated with clinical symptoms (60). Reduced brain blood flow is common in ME/CFS patients, accompanied by lowered circulation and nutrient/waste exchange (61–65).

Does anyone have good information about isoprostanes?

 

[VisualEffect]

I didn't understand the article. Researchers are saying that our brainstem's tissue degenerates for some reason, and this is the explanation for our symptoms??? I don't want to believe this, because tissue loss can't be fixed.
I am just some random guy compared to the these researchers, but isn't brainstem atrophy can be explained by chronic impaired cerebral blood circulation? And what about people with sudden symptoms onset? (Which is the most common pattern of disease onset) Their brain's tissue degenerated suddenly too?
Sorry for ranting.