Autopsy findings: Summary of discussions

Pyrrhus

Senior Member
Messages
4,172
Location
U.S., Earth
I thought I would start a thread to summarize any and all autopsy findings from ME patients. Please feel free to share any relevant case reports, anecdotes, and studies. I'll start this thread with one of the earliest reports of autopsies in ME patients:

Autopsies from the 1955 Royal Free Outbreak (Crowley et al., 1957)
From:
Epidemiological aspects of an outbreak of encephalomyelitis at the Royal Free in the summer of 1955.
Crowley N, Nelson M, Stouin S., J Hygiene. 1957;55:116.
https://www.ncbi.nlm.nih.gov/labs/pmc/articles/PMC2217874/pdf/jhyg00143-0110.pdf
Post-mortem tissue was examined from two further cases, both of whom had died from other causes several months after an attack of the epidemic disease. One of these fatal cases showed an ovarian carcinoma with multiple metastases and a terminal clostridial peritonitis and septicaemia. Microscopic examination of the brain, spinal cord and peripheral nerves showed no abnormality except for that attributable to either the septicaemia or carcinomatosis.

The second fatality, due to acute carbrital poisoning, occurred in a woman, aged 32, who had the epidemic disease 7 months before death and who had had definite clinical evidence of organic disease of the central nervous system for the last 7 months of her life. Post-mortem examination revealed small, circumscribed, grey or yellowish plaques in the white matter of the cerebral hemispheres, mainly para-ventricular in distribution, in the brain stem and in the spinal cord, particularly in the cervical segment.

Microscopic examination showed multiple, small, well, or fairly well, demarcated areas of demyelination with associated microglial and astrocytic proliferation and a variable degree of gliosis. There was no evidence of primary neuronal damage and no viral cell-inclusions were seen. Occasional cellular foci composed of lymphocytes and cerebral histiocytes, mainly perivascular in distribution, were present in the leptomeninges overlying the brain, but this was not a marked feature except in one section taken from the hypothalamus which showed intense perivascular cuffing.
 

Pyrrhus

Senior Member
Messages
4,172
Location
U.S., Earth
Pathology of Chronic Fatigue Syndrome: Pilot Study of Four Autopsy Cases (O'Donovan et al., 2010)
(as published in the Journal of Neurological Sciences) from the UK post mortem research group:

Pathology of Chronic Fatigue Syndrome: Pilot Study of Four Autopsy Cases
DG O’Donovan1, 2, T Harrower3, S Cader2, LJ Findley2, C Shepherd4, A Chaudhuri2
1Addenbrooke’s Hospital Cambridge UK
2Queen’s Hospital Romford Essex UK
3Royal Devon & Exeter Hospitals UK
4Honorary Medical Advisor to ME Association UK

"Chronic Fatigue Syndrome / Myalgic Encephalomyelitis is a disorder characterised by chronic exercise induced fatigue, cognitive dysfunction, sensory disturbances and often pain. The aetiology and pathogenesis are not understood.

We report the post mortem pathology of four cases of CFS diagnosed by specialists.

The causes of death were all unnatural and included: suicidal overdose, renal failure due to lack of food and water, assisted suicide and probable poisoning.

Selected portions of tissue were made available by the various Coroners in the UK and with the assent of the persons in a qualifying relationship.

The cases were 1 male, and 3 female. Ages (years) M32, F32, F43 & F31.

One case showed a vast excess of corpora amylacea in spinal cord and brain of unknown significance but Polyglucosan Body Disease was not supported by clinicopathologial review. No ganglionitis was identified.
One case showed a marked dorsal root ganglionitis and two other cases showed mild excess of lymphocytes with nodules of nageotte in the dorsal root ganglia.

This raises the hypothesis that dysfunction of the sensory and probably also the autonomic nervous system may lead to abnormal neural activity eg hyperalgesia & allodynia rather than anaesthesia and may explain some of the symptoms of CFS / ME such as pain, hypotension, hyperacusis and photophobia. However, the syndrome may be heterogeneous.

Nevertheless, the precise relationship of fatigue, which may be either peripheral or central, to abnormalities in the peripheral nervous system (PNS) needs to be studied.

The differential diagnosis of ganglionitis should be investigated in CFS / ME patients hence Varicella Zoster, Lyme disease, HIV, Sjogren’s disease, paraneoplastic sensory ganglionopathy should be excluded by appropriate history and tests.

Thorough histopathological study of cases coming to autopsy may help to confirm or refute the hypothesis, that CFS is a disease process, and whether the symptomatology may be explained by inflammation of the sensory and autonomic divisions of the PNS."
NB: These autopsies included the case of Sophia Mirza and likely included the case of Lynn Gilderdale.


Related discussion:
The Naked Scientists...............including autopsy reports on ME (2012)
https://forums.phoenixrising.me/threads/the-naked-scientists-including-autopsy-reports-on-me.17463/

Interview with Dr. Abhijit Chaudhuri, Queen's Hospital and with Professor Hugh Perry, Southampton University

Louise - Think back to the last time you had the flu. You probably had some muscle pain and a bad headache, felt completely exhausted, and you might even have had trouble thinking straight. Most people get over the flu and other viral infections including glandular fever in a few weeks or so. But for a few people, those symptoms continue for months and years afterwards, becoming chronic fatigue syndrome. Not everyone with chronic fatigue syndrome has a viral infection before they develop the disease, but many patients do, and it is often the flu or glandular fever. And although chronic fatigue syndrome was first defined in 1988, we still don't know how, or why, these viral infections seem to be able to trigger the condition. And in fact, we have very little idea of what's happening in patients’ bodies to cause their symptoms. Post mortem studies are one of the best places to start. Now, a team including Dr. Dominic O'Donovan from Addenbrooke’s Hospital in Cambridge and Dr. Abhijit Chaudhuri from Queen’s Hospital in Romford has looked at the nervous systems of four patients who suffered from chronic fatigue syndrome. Here’s what Dr. Chaudhuri has to say.

Abhijit Chaudhuri - It is quite clear that there is an abnormality that is directed towards specific parts of nervous system.

Louise - So, what abnormalities did they find? In the first patient Dr. O'Donovan examined, he found large numbers of deposits called corpora amylacea spread throughout the brain and spinal cord. Professor Perry is the professor of experimental neuropathology at Southampton University and although he wasn’t involved in the study, he has given us his opinion of the findings.

Hugh Perry - Corpora amylacea are little deposits that are seen in the brain of quite a lot of people who have different types of neurodegenerative disease. Precisely what their significance is, I think is really unclear, except that they are usually associated with tissue degeneration. So they could be the deposits if you like, evidence of a degeneration process.

Louise - This finding suggests that nerve cells in the patient’s brain and spinal cord were being damaged or destroyed while he was still alive. But it tells us nothing about what was causing that damage. The next patient the team looked at might provide the answer. There was inflammation in the dorsal root ganglia. These are structures near where the sensory nerves enter the spinal cord and normally, they only contain nerve cells and a few supporting structures. But Dr. O'Donovan found immune cells infiltrating these ganglia and these immune cells, which are called cytotoxic T cells, normally kill other cells in the body in order to control viral infections or to remove damaged cells. Previous work has shown that patients with chronic fatigue syndrome often have more of these T cells in their blood. But what does it mean if they're infiltrating the dorsal root ganglia? Professor Perry again...

Hugh Perry - The dorsal root ganglia are the neurons that convey sensory information into the spinal cord and that sensory information includes pain, temperature, pressure, and so forth, where possibly pain information is the most important of all in this context, as we know that there are many people with CFS who complain of pain in their extremities. So, to then find around those neurons evidence of inflammation, which is what the T cells are telling us, is there's some sort of inflammatory response, is of itself very interesting.

Louise - Both Professor Perry and Dr. O'Donovan agree that this inflammation could be causing referred pain - meaning the muscle and joint pain people with chronic fatigue syndrome often experience could actually be the result of their own immune systems attacking these nerves in the dorsal root ganglia. And when Dr. O'Donovan stained the dorsal root ganglia of two other patients to detect T cells, he found the same inflammation, although milder. So, all the chronic fatigue patients included in this study had either active inflammation in their peripheral nervous system or signs of a degenerative process in their spinal cord and brain. But it’s not clear how, or if, the inflammation is related to the degeneration found in that first patient, particularly as they’re affecting different parts of the nervous system. And with only four patients, this is a very small study and much more work is needed before we can be sure what these preliminary findings might mean. In particular, it is very important that we compare patients with chronic fatigue syndrome with people who do not have the disease. But this part of the nervous system is not normally examined in detail during a post mortem. Nonetheless, these results could be an interesting starting point for future research as Dr. Chaudhuri points out...

Abhijit Chaudhuri - The fact that we are seeing an abnormality should persuade us to undertake more focused research into the neuroimmunological aspects of the disease.

Louise - And could the fact that T cells are involved in controlling viral infection such as glandular fever be the link between these infections and chronic fatigue syndrome? We’ll just have to wait and see.
 

Pyrrhus

Senior Member
Messages
4,172
Location
U.S., Earth
Evidence of enterovirus at autopsy by Mcgarry, Gow, and Behan (1994)
https://pubmed.ncbi.nlm.nih.gov/8172448/
Enterovirus in the Chronic Fatigue Syndrome

To the Editor: The chronic fatigue syndrome is a recurring illness of unknown cause characterized by incapacitating fatigue and a range of symptoms and laboratory findings suggestive of hypothalamic dysfunction (1-3). Rare patients who have died from other acute causes have had cellular infiltrates in the hypothalamus (4). The syndrome usually follows a flu-like illness, and circumstantial evidence has implicated enteroviruses (1). We therefore examined the central nervous system of a woman with the syndrome who died from suicide for the presence of enterovirus.

In June 1992, a 30-year-old woman who had met all criteria for the syndrome for 5 years was brought to the hospital after attempted suicide and died of complications. Immediately after death, tissue was removed from the brain, heart, skeletal muscle, lungs, and spleen and was stored at -8 0 °C. The brain samples were from the frontal, temporal, parietal, and occipital cortices and from the mid-brain, hypothalamus, and brain stem. Control samples were obtained from four patients who died of cerebrovascular diseases and from four age- and sexmatched patients who had committed suicide during severe depression over the next 2 months.

Ribonucleic acid (RNA) from the tissues was prepared for analysis by polymerase chain reaction (PCR). The RNA samples were prepared and amplified using oligonucleotide primers.

No enteroviral sequences were detected in any of the control tissues. Positive PCR sequences were detected in the muscle, heart, and brain samples from the hypothalamus and brain stem region of our patient with the syndrome (Figure 1). Sequence analyses on the PCR products were compatible with exogenous virus and not with contamination. The results showed an enterovirus with an 83% similarity to Coxsackievirus B3. Although the findings may represent chance occurrence, they further support the possibility that hypothalamic dysfunction exists in the pathogenesis of the syndrome. Also, they suggest that the chronic fatigue syndrome may be mediated by enterovirus infection and that persistent symptoms may reflect selective persistence in affected organs.

Frances McGarry, BSc John Gow, PhD Peter O. Behan, MD
Southern General Hospital Glasgow G51 4TF Scotland

References
1. Bakheit AM, Behan PO, Watson WS, Morton JJ. Abnormal argininevasopressin secretion and water metabolism in patients with postviral fatigue syndrome. Acta Neurol Scand. 1993;87:234-8.
2. Bakheit AM, Behan PO, Dinan TG, Gray CE, O'Keane V. Possible upregulation of hypothalamic 5-HT receptors in patients with the postviral fatigue syndrome. Br Med J. 1992;304:1010-2.
3. Demitrak MA, Dale JK, Straus SE. Evidence for impaired activation of the hypothalamic-pituitary-adrenal axis in patients with chronic fatigue syndrome. J Clin Endocrinol Metab. 1991;73:1224-34.
4. Crowley N, Nelson M, Stouin S. Epidemiological aspects of an outbreak of encephalomyelitis at the Royal Free in the summer of 1955. J Hygiene. 1957;55:116.



Evidence of enterovirus at autopsy by Dr John Richardson (2001):
Viral Isolation from Brain in Myalgic Encephalomyelitis (Richardson, 2001)
Description of enterovirus detected in the brain during autopsy.
https://forums.phoenixrising.me/thr...rom-brain-in-myalgic-encephalomyelitis.10780/
(Please note that this article is only viewable to Phoenix Rising members with at least 100 posts.)
Paraffin section from cerebral cortex; Immunoperoxidase staining with monoclonal D8-1 against enteroviral VPI protein:
There is staining of cytoplasm of fibroblasts around small vessels. In addition there is patchy distribution of stain in isolated glial cells throughout the section. Only a small fraction of all the glial cells are stained. Specificity confirmed by absence of staining of glial cells or perivascular fibroblasts with either normal mouse serum or a control mouse monoclonal antibody to dengue virus.

DNA probe report:
Enterovirus-specific cDNA probes labelled with biotin and hybridized in situ on formalin fixed and paraffin-embedded 5 micron sections of autopsy material from cerebral hemispheres.

Results:
Positive hybridization signals were observed in the form of dense brown staining of glial cells and fibroblasts in the adventitia of small blood vessels. No hybridization was observed in control adjacent sections hybridized with a control biotin labelled vector plasmid clone.

Conclusion:
Enterovirus specific genomic sequences were detected in this specimen, indicating active infection of these cells.


Related discussion:
Two previous ME/CFS brain autopsies are detailed in this post (along with Dr Chia's autopsy); in the Mcgarry, Gow and Behan brain autopsy of one deceased ME/CFS patient, they also tested the brains of 8 controls, and all these 8 were found to be enterovirus negative.
 

Pyrrhus

Senior Member
Messages
4,172
Location
U.S., Earth
BMJ: CNS findings in CFS Autopsy and a neuropathological case report (Ferrero et al., 2017)
https://forums.phoenixrising.me/thr...sy-and-a-neuropathological-case-report.76626/


CNS findings in chronic fatigue syndrome and a neuropathological case report

  1. Kimberly Ferrero1,
  2. Mitchell Silver1,
  3. Alan Cocchetto2,
  4. Eliezer Masliah3,
  5. Dianne Langford1
Chronic fatigue syndrome (CFS) is characterized as a persistent, debilitating complex disorder of unknown etiology, whereby patients suffer from extreme fatigue, which often presents with symptoms that include chronic pain, depression, weakness, mood disturbances, and neuropsychological impairment.

In this mini review and case report, we address central nervous system (CNS) involvement of CFS and present neuropathological autopsy findings from a patient who died with a prior diagnosis of CFS.

Among the most remarkable pathological features of the case are focal areas of white matter loss, neurite beading, and neuritic pathology of axons in the white matter with axonal spheroids. Atypical neurons displaying aberrant sprouting processes in response to injury are observed throughout cortical gray and white matter. Abundant amyloid deposits identical to AD plaques with accompanying intracellular granular structures are observed as well. Neurofibrillary tangles are also present in the white matter of the frontal cortex, thalamus and basal ganglia.

Taken together, these neuropathological findings warrant further studies into CNS disease associated with CFS.


medical record:

"In 1975, she participated in a golf tournament
but could not remember the event or how she got
home. The patient then continued to decline and suffered
from malaise, headache, joint and muscle pain, swollen
lymph nodes and ‘brain fog’ that persisted for over
6 months. Rest did not alleviate these problems. Other significant
medical history included a diagnosis of CFS made
in 1987, fibromyalgia, celiac disease and hypothyroidism.
The diagnosis of CFS was made according to the Holmes
criteria,73 whereby the patient met both major clinical criteria
1 and 2, and 6 or more of the 11 symptom criteria and
2 or more of the 3 physical criteria, or 8 or more of the 11
symptom criteria.73 Criterion 1 is defined as “new onset of
persistent or relapsing, debilitating fatigue in a person who
has no previous history of similar symptoms that does not
resolve with bed rest, and that is severe enough to reduce or
impair average daily activity below 50% of the patient’s premorbid
activity level for a period of at least 6 months.”73
Criterion 2 is the exclusion of other clinical conditions that
may produce similar symptoms."

histology finding discussion:

"First of all, AD-like pathology and vascular
changes were observed. However, unlike AD, this case does
not show typical dystrophic neurites. On the other hand,
the tauopathy observed may not necessarily explain the
mechanisms of cellular dysfunction but rather serves as a
useful (pathological or phenotypic) marker for CFS. Taken
together, holistic analysis of the neuropathological findings
from this case point to severe neuronal dysfunction with
hallmarks characteristic of neurodegeneration. This being
the first neuropathological report of a CFS case points to
the need for more extensive large-scale investigations into
the neuropathologies associated with CFS in order to establish
a consistent rubric for identification, diagnosis and
scoring of the syndrome as part of a greater class of CNS
diseases with similar clinical presentation."
 

Pyrrhus

Senior Member
Messages
4,172
Location
U.S., Earth
Autopsy of Merryn Crofts 2018 (Siddle, 2018)
From:
Inquest Ruling: Young drama student Merryn Crofts killed by M.E. | 18 May 2018
https://forums.phoenixrising.me/thr...th-me-with-inflammation-of-the-ganglia.59363/
(https://meassociation.org.uk/2018/0...dent-merryn-crofts-killed-by-m-e-18-may-2018/)
Pathologist Daniel DuPlessis said that a post-mortem showed low-grade inflammation of nerve roots. It was suggested that this inflammation could have made her bowel hypersensitive to processing nutrients. Dr DuPlessis pointed out that Merryn had inflammation of the [dorsal root] ganglia – gatekeepers to sensations in the brain.


Autopsy case report from Dr. Matthew P. Anderson 2021
(in process of publication)
This autopsy of an ME patient finds evidence of inflammation along the dorsal root ganglia of the spinal cord, involving cytotoxic T cells and macrophages.
 

Pyrrhus

Senior Member
Messages
4,172
Location
U.S., Earth
Autopsy evidence of chronic EV infection by Dr John Chia (Chia, 2015)
https://forums.phoenixrising.me/thr...-chronic-ev-infection-dr-chia-oct-2016.47710/

Autopsy Evidence of Chronic EV Infection in ME Patient Presented by Dr. John Chia at IACFSME Conference October 2016

Poster 13
Chronic enterovirus (EV) infection in a patient with myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) – Clinical, Virologic and Pathological Analysis

John Chia, David Wang, Andrew Chia, Rabiha El-Habbal. EV Med Research. Lomita, CA
Objectives: A 23 y/o Caucasian male developed prolonged, recurrent gastrointestinal symptoms, followed by onset of severe ME/CFS (CDC criteria, ICC).

At initial evaluation, Echovirus 11 antibody titer was >1:640 (normal <1:10); IgG and IgM antibody for EBV and HHV6 were negative, CMV IgG was positive. He failed to respond to combination of alpha and gamma interferon; and debilitating symptoms of the stomach and central nervous system were minimally alleviated by SSRI, benzodiazepine and acid-suppressant.

Repeated MRI scans of brain and spinal cords showed normal results. The patient committed suicide 6 years after the onset of symptoms. Brain was harvested and frozen within 24 hours of death for evaluation of chronic viral infection.

Method:
Using EV- and dsRNA-specific monoclonal antibody (5D8/1 and J2 mAb), stomach and colon biopsies obtained 5 months after onset of illness were stained for viral capsid protein (VP1) and dsRNA by immunoperoxidase technique. Blood drawn in Paxgene tube 3 years after illness was screened for enterovirus RNA by RT-PCR. ~1 cm3 sample was taken from the ponto-medullary junction (PM), medial temporal lobe (MT), frontal lobe (FL), occipital lobe (OL), cerebellum (CL) and midbrain / hypothalamus area (MB) of brain.
The brain samples were homogenized in 10 ml of serum-free medium. Aliquots were processed for viral cultures. Trizol-LS reagent was used for RNA and protein extraction, as well as other lysis agents.
'
Tris-Glycine and MES gels, wet and semi-dry transfer, then western blot was performed with Ibind (Life technology) using EV-, CMV- and HHV6-specific mAbs, patient’s own serum and control serum samples. Viral culture was performed in WI-38 and BGMK-DAF cell lines. RT-PCR for conserved highly-conserved sequences of 5’ end and 3D polymerase sequence were performed on extracted RNA.

Results:
Stomach and colon biopsies stained positive for EV VP1 soon after initial infection documenting the initial viral infection; dsRNA was detected in the stomach biopsies. EV RNA was not detected in blood 3 years after illness.
Initial culture of brain samples did not grow virus; 5’ EV RNA sequence was not detected by RT-PCR. Using 5 D8/1 mAb, western blot revealed 37-42K and 46K protein bands in the brain samples, which corresponded to viral protein and creatine kinase b extracted from infected stomach biopsies, but not in brain biopsy samples taking from patients with brain tuberculoma and lymphoma. 3D pol gene was amplified from the DNase-treated RNA extracted from PM, MT and FL. 5’ RNA sequence was in one of the FL specimens.
'
Conclusion:
The analysis of the second brain specimen taken from ME/CFS patient replicated the British findings published in 1994 (Ann. IM). The finding of viral protein and RNA in the brain specimens 6 years after documented acute enterovirus infection of the gastrointestinal tract is consistent with a chronic, persistent infection of the brain causing debilitating symptoms.

'EV is clearly one of the causes of ME/CFS, and antiviral therapy should be developed for chronic EV infection.
 

Judee

Psalm 46:1-3
Messages
4,584
Location
Great Lakes
I read though most of these posts...though probably not with your better level of scientific understanding, @Pyrrhus. :)

Thanks for posting them. Though they're autopsies trying to find out what's going on with this disease they also make me feel sad for the lives that were lost that didn't need to be. :(
 

junkcrap50

Senior Member
Messages
1,382
Thanks for linking and centralizing all autopsy discussions. I think autopsy studies is very important for ME/CFS research and there's so little of it. So much research is inconclusive because it's in the wrong tissue or not looking for intracellular infections. With an autopsy, you'd think you could search every part of the body and map every virus, infection, inflammation, tissue destruction, etc.

It is essential a autopsy and tissue bank is created, as well as a organization to collect donations from passed ME/CFS patients donating their bodies to science. Something like https://braindonorproject.org/ or https://www.autismbrainnet.org but for CFS specifically and not limited to the brain but the whole body.

It's a delicate subject as so many desperate patients consider suicide, and a project like could possible incentivize them, which would be very unfortunate. Yet, there is so much potential to learn from autopsies.

Hopefully some studies on the bodies of Long Covid patients will occur and be fruitfull.
 

Pyrrhus

Senior Member
Messages
4,172
Location
U.S., Earth
It is essential a autopsy and tissue bank is created, as well as a organization to collect donations from passed ME/CFS patients donating their bodies to science.

I'm not sure about the current specifics, but I believe that Solve ME has something like that set up in the U.S.:
https://forums.phoenixrising.me/threads/us-brain-donation-brain-donor-project.51999/

And I believe that the U.K. ME Association might have something similar:
https://forums.phoenixrising.me/threads/autopsy-options.35647/page-2#post-842493
If you live in the UK you can use our 'Statement of Intent' form on the MEA website to register your permission for body parts and tissues to be used for post mortem research into ME/CFS:

http://www.meassociation.org.uk/wp-content/uploads/MEA-RRF-Statement-of-Intent-2015.pdf


Related discussion:
Autopsy Options
https://forums.phoenixrising.me/threads/autopsy-options.35647/
 
Last edited:

Diwi9

Administrator
Messages
1,780
Location
USA
And I have to admit that I find it quite shocking that there is permanent damage! I always thought we could completely recover. But now I think it might be an explanation why I often can’t remember names or don’t find the right words to express myself
Even with my improvements in other aspects of functioning, I find that working memory, memory consolidation, and retrieval remain problematic. I am 44, so young to be having such difficulties. Cognitive problems are not a required component to the current IOM diagnostic criteria. I think this is one diagnostic defining line between illness subtypes. Autopsies are not going to be helpful unless they are paired with clinical symptomatic profiles. ME/CFS remains a large diagnostic umbrella.
 

Martin aka paused||M.E.

Senior Member
Messages
2,291
Even with my improvements in other aspects of functioning, I find that working memory, memory consolidation, and retrieval remain problematic. I am 44, so young to be having such difficulties. Cognitive problems are not a required component to the current IOM diagnostic criteria. I think this is one diagnostic defining line between illness subtypes. Autopsies are not going to be helpful unless they are paired with clinical symptomatic profiles. ME/CFS remains a large diagnostic umbrella.
10000% agreed!!!
 

lenora

Senior Member
Messages
5,011
Very interesting. It's not often that one is able to read autopsy reports relating to our illness. It's particularly good that the first study was done by British researchers only.

What a shame that the young man committed suicide six years after diagnosis. I find it sad to read of this outcome, but it's good that so many other researchers went ahead with their work.

I went back to the beginning and was rewarded with an addition of a total of 4 victims of ME. Sadly, all were so young and suicide was the cause of death.

Pyrrhus, once again thanks for putting this info on the Forum, it was most informative. Something came out of it and that's good for the young people of today and for the thinking that seems to be so prevalent in the U.K. L.
 

Pyrrhus

Senior Member
Messages
4,172
Location
U.S., Earth
I find interesting the inflammation in the dorsal root ganglia. I wonder what can cause that?

One important thing to keep in mind is that the dorsal root ganglia are technically part of the peripheral nervous system, not the central nervous system.

The central nervous system consists of the brain and spinal cord, and is protected by the blood-brain-barrier, so blood-borne immune cells generally can't enter the central nervous system, preventing classical Greco-Roman inflammation. But tissue-resident immune cells that normally live in the central nervous system can indeed be activated, resulting in neuroinflammation.

For more information on the difference between classical inflammation and neuroinflammation, see this post:
https://forums.phoenixrising.me/thr...n-in-me-subcortical-brain.80923/#post-2289868

The peripheral nervous system, on the other hand, has no blood-brain-barrier, so blood-borne immune cells are free to attack the peripheral nervous system, resulting in classical Greco-Roman inflammation.

So the fact that classical inflammation was seen on autopsy in the dorsal root ganglia, which are part of the peripheral nervous system, raises the following question: does this mean that neuroinflammation is also occurring in the central nervous system?

And I have to admit that I find it quite shocking that there is permanent damage!

Remember that inflammation does not mean permanent damage. If inflammation can be resolved, the tissue can often recover on its own.

Even amyloid deposits, and other types of deposits, can be cleaned up by the tissue-resident immune cells of the brain once one resolves the disease process that is generating the deposits.

There may be some loss of nervous tissue evident in these autopsies, but that doesn't mean that ME itself is irreversible or permanent.
 
I tried to summarize the first two studies for myself and anyone else it'd be helpful for as they're complex:

Dr. Chaudhuri Study

"found large numbers of deposits called corpora amylacea [neurodegeneration marker] spread throughout the brain and spinal cord"

"There was inflammation in the dorsal root ganglia [convey sensory information like pain, temperature, pressure, etc. into the spinal cord, aka] structures near where the sensory nerves enter the spinal cord."

"and normally, they only contain nerve cells and a few supporting structures. But Dr. O'Donovan found immune cells infiltrating these ganglia and these immunecells, which are called cytotoxic T cells, normally kill other cells in the body in order to control viral infections or to remove damaged cells."

"And could the fact that T cells are involved in controlling viral infection such as glandular fever be the link between these infections and chronic fatigue syndrome? We’ll just have to wait and see."

Dr. Chia's study

"Initial culture of brain samples did not grow virus; 5’ EV RNA sequence was not detected by RT-PCR. Using 5 D8/1 mAb, western blot revealed 37-42K and 46K protein bands in the brain samples, which corresponded to viral protein and creatine kinase b extracted from infected stomach biopsies"

So I think the first two studies summarized are telling us:

(1) the virus is getting into the brain (confirmed with EV), and
(2) the virus or body's response is causing some sort of damage to the spinal cord and brain (per presence of corpora amylacea), and
(3) the virus or body's response is causing inflammation where the sensory nerves enter the spinal cord (dorsal root ganglia).

Then next we need to confirm:

(1) are glandular fever, coxsackie, and COVID also traceable in the brain of pwME/Long-COVID?
(2) when and why are corpora amylacea created?
(3) what is causing inflammation in the dorsal root ganglia? Are cytotoxic T cells present in this area during the initial infection, and how could we test this? Could we later treat and lessen the inflammation here?

Any others I'm (probably) missing? And how can we get researchers to look into this? I think it's very promising.
 

YippeeKi YOW !!

Senior Member
Messages
16,075
Location
Second star to the right ...
I tried to summarize the first two studies for myself and anyone else it'd be helpful for as they're complex:
Thank you so much for doing this @TinaYesen .... I'm currently revisiting a place I've escaped repeatedly, and neither my focus nor processing portals seem to be open and functionig.

So until they're back to some sort of functionality, this is a HUUUUUGE help, and I'm very grateful to you for both the effort and the thoughtfulness of posting this ....
 

godlovesatrier

Senior Member
Messages
2,609
Location
United Kingdom
Very interesting.

I've been trying to grapple with the reasons why some people can ultimately get sicker through treatment not better. As Joshua's protocol is entirely experimental.

Interestingly I have resolved all of my spinal and cranial cervical inflamation. I still don't really know if this was from spinal attack or tissue swelling or brain based infection. But based on what you said about it sounds more like tissue based swelling from viral attack.

My question now really is how far can beta glucan and triterpene treatment take anyone in terms of viral clearance. Moreso if they've got an entereoviral infection.

But the main thing that bothers me and it's why I'm replying is that my core symptom of dizziness which is currently worse (even in the absence of an immune response) could be some sort of aberrant immune activation. Which might be made simply worse through treatment not better.

Really interesting studies these. It's nice to know the tissues can self heal. But the potential brain based infection might be flogging a dead horse. E.g. if you can't clear it from the brain then no treatment will truly work for full remission?

Thanks for others for explaining the studies.
 
Back