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Individual qEEG Research Assessments Released from Laurentian University

shannah

Senior Member
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1,429
Announcement From Millions Missing Canada
Research Results Released: qEEG Assessments for ME Volunteers From Laurentian University

During the summer of 2018, researchers from Laurentian University Neuroscience Department led by Andrew Pellegrini, visited 45 ME patients in their homes in Ontario. The purpose was to collect Quantitative Electroencephalographic (qEEG) data to investigate changes in brain functioning associated with Myalgic Encephalomyelitis / Chronic Fatigue Syndrome (ME/CFS).

The reports for all 45 of the volunteers in the study have been completed and will be sent out over the next few days. Every member of the study showed statistically significant brain anomalies compared to healthy controls on Quantitative Electroencephalography (qEEG) related to ME/CFS.

The reports are written so as to be primarily addressed to the physicians of each volunteer in hopes that the qEEG findings can be followed up with further testing as recommended for the benefit of the individual patients, and to help increase general medical understanding of ME based on hard neurological evidence.

Most importantly, Dr. Sonia Neubauer MD, who's lab in Chile generated the modern SPECT maps used by Dr. Hyde has graciously agreed to have her contact information included in the reports. She is willing and available to do the same work she did for Dr. Hyde and his patients for each member of the study. While qEEG has proven useful, SPECT still represents the gold standard for showing brain dysfunction in ME.

While Andrew had hoped to secure some method of funding as there is a fee associated with this analysis, unfortunately the cost will have to be borne by the individuals. This is also a medical test that will require a cooperative physician to make the referral and work with Dr. Neubauer. Given that many of the volunteers are clustered close together in Toronto and Ottawa perhaps the same physicians may see enough individuals with reports from the study to be open to this approach which is both somewhat unconventional and at the same time scientifically sound.

Therefore, volunteers choosing to share their reports with their physicians should also include a copy of Andrew’s thesis document showing validation of Dr. Hyde's findings, as well as the technical details of how the study was conducted. A PDF copy of Dr. Hyde's 1992 text book (which is now freely available on his website) will also be attached as a reference material for physicians. While nearly 30 years old, the SPECT images shown in colour at the front clearly show that PEM is characterized by a dramatic worsening of cerebral blood perfusion above and beyond the pathological baseline. Modern researchers are still working to define PEM (Post Exertional Malaise) and Andrew believes that Dr. Hyde's findings are of essential importance even though they have not, as yet, been widely recognized.

Andrew writes in his email to us, “This project has been one of the most interesting and rewarding experiences of my life and I am proud to be able to offer this small service to the ME/CFS community.”

With our deepest thanks to Andrew for his dedication to this project and his commitment to the community. Congratulations Andrew on completing this milestone in your research. We wish you good health and much success in the future.

Questions concerning your individual reports can be directed to Andrew. For those who want to know the backstory, the complete past history can be seen at:
https://bit.ly/3hFD1G9

Andrew’s thesis, ‘Quantitative Electroencephalographic Assessment of Myalgic Encephalomyelitis / Chronic Fatigue Syndrome: Support for a Novel Diagnostic Protocol’, by Andrew Pellegrini can be found at:
http://bit.ly/2kn1LM5

The textbook, ‘The Clinical and Scientific Basis of Myalgic Encephalomyelitis Chronic Fatigue Syndrome’ by Bryon Hyde, Jay Goldstein and Paul Levine is free to download at the following link.
https://www.nightingale.ca/publications

Dr. Hyde’s new book ‘Understanding Myalgic Encephalomyelitis’ and other publications can be ordered at this link.
https://www.nightingale.ca/publications

A preview of Dr. Hyde’s new book ‘Understanding Myalgic Encephalomyelitis’ can be viewed or downloaded from the Nightingale Research Foundation at:
https://www.nightingale.ca/

The ‘Definition of Myalgic Encephalomyelitis is available in four languages, English, French, Norwegian and Danish. It can be viewed or downloaded here:
https://www.nightingale.ca/understanding-m-e

Description of Attached Images:

Figure 9 The Left Temporal Lobe: The aggregate of 45 ME brains is shown on the left, compared with NRF SPECT maps of individuals on the right. The same left temporal hypoperfusion pattern shown here has been demonstrated by Dr. Mena and colleagues in 13/13 children with ME/CFS (Goldberg et al., 2011).

Figure 12 The Right Temporal Lobe: Regions of hyper and hypo-perfusion in the frontal, temporal and occipital cortices in this individual’s SPECT approximately cover the inferior half of the right hemisphere. Likewise, the aggregate of 45 brains, shown on the left, includes approximately the same area.


SM Temporal Lobe Sept 2020.png
 
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Wishful

Senior Member
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5,679
Location
Alberta
The paper's description and history of ME should probably be required reading for doctors ... and politicians, and it wouldn't hurt if everyone else read it too.

Vascular cuffing probably fits my theories of ME. Maybe the astrocyte feet are clenched too tightly because something elsewhere in our immune systems is sending that signal. Astrocytes release their grip during deep sleep, allowing nutrients and toxins to cross the BBB, so it's plausible for the same mechanism to malfunction.
 

Wishful

Senior Member
Messages
5,679
Location
Alberta
Cerebral vascular hypoperfusion is also found in MS patients, and I assume, other neurological disorders, so qEEG testing may not be a suitable biomarker for ME. This paper discusses the MS version: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4640326/

Items that caught my interest:

- "Astrocytes are the cells that actively regulate cerebral blood supply to match regional neuronal glucose and oxygen needs,"

- "Enhanced blood levels of the potent vasoconstrictive peptide endothelin-1 (ET-1) were found in peripheral venous blood and cerebrospinal fluid of patients with MS.43, 44 This has been associated with reduced extra-ocular blood flow velocities. ... After the administration of the ET-1 receptor antagonist bosentan, CBF in the MS patients significantly increased in all brain regions to reach values obtained in the controls. ... Under normal circumstances, ET-1 can be found in some type of neurons but not in glial cells. Very little is known about ET-1 in astrocytes, although a few studies have found increased levels in reactive astrocytes in various brain pathologies, such as acute ischemic stroke, Alzheimer's disease, viral infections, and traumatic injury. ... The above data suggest that reduced CBF in MS is mediated by elevated levels of ET-1, which are likely released in the cerebral circulation from reactive astrocytes in MS plaques to induce arteriolar vasoconstriction."

- "Animal models demonstrate that chronic brain hypoperfusion induces mitochondrial dysfunction and production of free radicals, resulting in neuronal damage.51 In human MS cortex, evidence exists of significant reductions in gene products specific for the mitochondrial electron transport chain and that cortical mitochondria have a diminished capacity to exchange electrons in respiratory chain complex I and III.40 The mitochondrial electron transport chain ionic cascade has been unequivocally documented as the cause of myelinated axonal degeneration in experimental models of central nervous system white matter hypoxia and ischemia"

- "Reduced CBF in patients with MS is not the result of loss of axonal integrity but appears to be mediated by elevated levels of ET-1, likely released in the cerebral circulation by reactive astrocytes, and, moreover, can be reversed by the non-selective ET-1 receptor antagonist bosentan."

Bosentan sounds fairly nasty, causing liver damage, and is a restricted prescription. If it was readily available, I'd probably try a dose or two and see if it affected my symptoms. Maybe one of the very severe victims might qualify for an experimental prescription. Green tea is supposed to reduce damage from cerebral hypoperfusion, but at really high dosages (green tea polyphenols 400 mg/kg per day: what's that in cups of tea?).
 

Wishful

Senior Member
Messages
5,679
Location
Alberta
From: https://www.nature.com/articles/s41467-019-13956-y

- "Astroglial populations that are intermingled with the respiratory and cardiovascular control neuronal networks are well positioned to orchestrate adaptive changes in breathing, heart rate and arterial blood pressure in conditions of increased metabolic demand. Failure of these mechanisms may augment metabolic deficit, precipitate neuronal damage, contribute to the development of neurological and neurodegenerative disease and reduce brain longevity."

Calcium signalling is part of this control process, which may interest those whose ME responds to calcium supplements or other things that affect calcium levels.
 

Wishful

Senior Member
Messages
5,679
Location
Alberta
This study, from 2011 seems similar: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3146818/ It seemed like a good potential tool for diagnosing ME, but it's obviously not being used to diagnose ME today. Did it prove ineffective, or did it just fail to get funding? It's too bad that papers like this don't get tagged with later information, such as "Independent testing by <group> showed much lower correlation", or "We're still applying for funding, and keep getting rejections".
 

Pyrrhus

Senior Member
Messages
4,172
Location
U.S., Earth
This study, from 2011 seems similar: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3146818/ It seemed like a good potential tool for diagnosing ME, but it's obviously not being used to diagnose ME today. Did it prove ineffective, or did it just fail to get funding? It's too bad that papers like this don't get tagged with later information, such as "Independent testing by <group> showed much lower correlation", or "We're still applying for funding, and keep getting rejections".

Or no one bothered to even try a replication. Novel research is always scientifically "sexier" than replication work. But we do need replication work.

For those who are curious about the paper that @Wishful mentioned, here is an excerpt:
Duffy et al. 2011 said:
EEG spectral coherence data distinguish chronic fatigue syndrome patients from healthy controls and depressed patients-A case control study

Background: Previous studies suggest central nervous system involvement in chronic fatigue syndrome (CFS), yet there are no established diagnostic criteria. CFS may be difficult to differentiate from clinical depression. The study's objective was to determine if spectral coherence, a computational derivative of spectral analysis of the electroencephalogram (EEG), could distinguish patients with CFS from healthy control subjects and not erroneously classify depressed patients as having CFS.

[...]

Conclusions: EEG spectral coherence analysis identified unmedicated patients with CFS and healthy control subjects without misclassifying depressed patients as CFS, providing evidence that CFS patients demonstrate brain physiology that is not observed in healthy normals or patients with major depression. Studies of new CFS patients and comparison groups are required to determine the possible clinical utility of this test. The results concur with other studies finding neurological abnormalities in CFS, and implicate temporal lobe involvement in CFS pathophysiology.
 

Wishful

Senior Member
Messages
5,679
Location
Alberta
Novel research is always scientifically "sexier" than replication work.

That's sort of what I meant by lack of funding. If funding for replication was available, it would be done. I came across mention of a similar study--and result--from 1990. Here's a potential diagnostic tool for ME, duplicated if not identically replicated, at least three times in the past 30 years, and no one is making an effort to make it available. If someone publishes a new study about an effective test for ME, whether involving blood or MRI scans or whatever, will that too go unreplicated and lost? Would an actual treatment for ME, proven in a small study, also go unreplicated and lost, because it's not as sexy or self-beneficial for a researcher? This is really depressing. :(