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.
Can you, & everyone else who posts research on here, please post the Title, Authors, & Abstract whenver posting links to papers.
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.
Thanks. Didn't know of any guidelines.And just as a reminder:
Pls change it; I’m not computer savvy; good point! Thank youCan 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
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"!
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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.
Oxidative stress and increased isoprostanes in ME/CFS have been correlated with clinical symptoms (60).
Why not look in the cerebrospinal fluid like they did in the recent MS study.
Makes sense. Weird that researchers would get that backwards.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/
I assumed thatPeople often look in the cerebrospinal fluid (CSF) for two reasons:
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:
- It's convenient. A lumbar puncture is a fairly easy procedure these days.
- People mistakenly think that the brain sits in CSF, so any debris from the brain would be detectable in the CSF.
But dont you think the fluid flow will sometimes go left also in the picture?
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.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 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).