The Nightingale definition of ME - why was it never used?

[Hip]

There's no disease that has a brain stem hypoperfusion .... only post polio patients.

Possibly that's right, but according to this article, other brain areas also suffer from hypoperfusion in ME/CFS:

In this regard, brain scans have been of enormous interest to the CFS/ME community because they provide concrete proof of neurological impairment. Dr. Ismael Mena and Dr. Jay Goldstein pioneered the use of SPECT (Single-photon Emission Computed Tomography) to document brain abnormalities in CFS/ME patients. SPECT scans measure blood flow in the brain, as opposed to MRIs, which show structure. Studies in the 1990s by Mena, Goldstein, Richardson, and Costa showed brainstem hypoperfusion (low blood flow) in a high percentage of CFS/ME patients.

In 1998 the late John Richardson conducted SPECT scans on some of his patients suffering from ME. The scans showed hypoperfusion in 90% of the patients in several areas. These included the brainstem (62%), the caudate nuclei in the basal ganglia (51%), temporal lobes (62%), parietal lobes (31%), and frontal lobes (23%).

A group of Australian researchers led by R. Casse also found a deficit in regional cerebral blood flow in similar areas: the brainstem, left medial temporal lobe, right medial temporal lobe, frontal lobe, and anterior cingulate gyrus. These are the areas of the brain responsible for auditory processing, attention, autonomic nervous system regulation, memory, sleep and pain.

The most recent studies to show brain hypoperfusion in CFS/ME have not used SPECT scans, but a xenon-CT. This type of scan measures the uptake of xenon gas by the brain. (When the gas is inhaled, it is distributed through the brain via the bloodstream.) Using this technique, Yoshiuchi et al found that patients with CFS/ME have reduced absolute cortical blood flow in broad areas when compared with healthy controls.

 

[Jesse2233]

The million dollar question is... can these areas of brain hypoporfusion be corrected by removing any ongoing triggers and restoring normal metabolism? Or is abnormal metabolism the result of these brain injuries with or without an ongoing trigger? And is it simply a case of poor blood flow or permanent brain damage, or something in between? And if a central CNS cause is the most basic driver of dysfunction then why does healthy serum make the cells normal? Can cellular metabolism correct itself while cognitive symptoms remain?

One could argue that RTX, Ampligen and other recoveries point to an ongoing trigger being removed and the brain naturally healing (over 3-9 months aka the first year in spontaneous remission / post viral fatigue / acute ME).

But then what to make of instant recoveries or full temporary remissions like Dr Goldstein brought about and others have experienced through experimentation? Compensatory brain pathways suddenly activated? Restored blood flow? A chemical correction or blocking of maladaptive pathways? Downstream corrections of metabolism? Specific idiosyncratic cases where CNS injury was not the primary driver of symptoms?

 

[JollyRoger]

Its like a never ending circle.

The brain stem is important for the autonomic function.
A few weeks ago I read " cfs unravelled" and he explained that everything can be explained with the autonomic dysfunction although his opinion is a wrong conditioning of the autonomic system; even the mitochondrial dysfunction.
High stress leads to th1->th2 shift and suppresses nk cell function......
But a malfunction of the autonomic system is also caused by dysfunction of the brain stem. (Enterovirus or postviral????)


https://www.ncbi.nlm.nih.gov/pubmed/8542261

This study claims that hypoperfusion of the stem is caused by hypocapnia (often caused by hyperventilation; metabolic acidosis).
So the hypoperfusion can also be caused by the mitochondrial dysfunction and on going lactat production.

It's a vicious circle and to find the cause is a brain twister.

Many had a remission with ampligen or interferon but at the end they relapsed so maybe we have to treat various stages of the circle.... killing enteros, restoring mitochondrial dysfunction and lowering oxidative stress.

In my case I had polyathritis with 17, afterwards i had raynaud, between 22-26 I had recurrent pericarditis and/or myocarditis and now for about 8 months I have ME after 4 months of a chronic sore throat.
I think in my case its a chronic entero infection which wanders through the body but I have no official diagnosis BUT I think you can tame this beast because I always had a remission after the other diseases.

 

[JollyRoger]

It would be interesting to find patients who developed ME with hypoperfusion of the brain stem with a pathogen that is not entero.
Does it also happens in a case after vaccination or mold exposure?

If so we could exclude the brain stem infection theory....

 

[Dechi]

Yeah....but in cfs there's a unique pattern of hypoperfusion ... in the brain stem.
There's no disease that has a brain stem hypoperfusion .... only post polio patients.


Two studies using SPECT have documented that decreased
brain stem metabolism, and by inference decreased activity of RAS
neurons, was the only physiological finding differentiating subjects
with CFS from healthy controls and subjects with depression or
neurological disease

@JollyRoger That's very interesting. Would you have the links to these studies ? I also had Raynaud after being infected. Didn't seem to last though, I think it's gone now.

 

[JollyRoger]

https://www.ncbi.nlm.nih.gov/pubmed/8542261

Its a unique pattern....i also find this:

Decreased energy metabolism in brain stem during central respiratory depression in response to hypoxia


https://www.ncbi.nlm.nih.gov/pubmed/8904598

Maybe this for into this pattern

 

[JollyRoger]

I also found a reader letter (or something like this) about this study.


Differences of opinion uncover opportunities for
research, and so I do not regret my inability to
accept the letter from Dr Costa and his colleagues
as an answer to my comments.
I agree that mild and moderate hyperventilation
can produce vasoconstriction, whereas severe and
prolonged hypocapnia does not. Lum has given the
reason: in minor respiratory alkalosis the neurone is
stimulated, but in major and prolonged hypocapnia
the accumulation of lactic acid reduces neuronal
activity even to the point of extinction.1
As Costa ef al. point out, people exposed to high
altitudes for 3-5 days have higher cerebral blood
flow than at sea level, but this is the period required
for acclimatization, and its unsurprising that the
processes of adaptation can be generous.
Rosen and I have already commented on the tests
that purport to tell us whether important acts of
hyperventilation have occurred: as yet without
agreement.2
"
5
On the other hand, it is possible to diagnose gross
depletion of the body's alkaline buffering systems by
identifying the respiratory response to the anaerobic
threshold using capnography during rapidly
incremental exercise.5
This buffer depletion is usually
due to overbreathing in response to effort and
distress, and its symptoms are indistinguishable from
ME/CFS.5
Finally, the Costa team argue that reduction of
cerebral blood flow in hyperventilation, in contrast
to their findings in CFS, is global or generalized, and
assert 'there is, so far, no evidence to suggest that
regional differences are likely to exist'. This is a bold
claim when Wyke has already demonstrated them,6
and Terada ef al. have reported that Tc-99 HMPAO
brain SPECT studies of hyperventilation 'have greatly
contributed to the quantitative evaluation of focal
perfusion decrease'.7
I hope that others will investigate deletion of the
alkaline buffering systems before concluding that
there is no known cause of MF7CFS symptoms. I
shall continue to rely on Wyke and Terada's work,
because their findings provide an explanation for the
repeated focal and transient ischaemic attacks that
can be found in exhaustion and hyperventilation
where there is no evidence of organic arterial disease
or embolism.

 

[Gingergrrl]

Jesse, Roger, Hip & all, couldn't someone also have autonomic dysfunction from autoantibodies attacking the beta adrenergic and other receptors vs. enterovirus (in some people, not in all of course).

 

[Hip]

The brain stem is important for the autonomic function.

It is possible the brainstem dysfunction in ME/CFS may (in part or in whole) be causing autonomic function, but as @Gingergrrl points out, evidence suggests that POTS and orthostatic hypotension (OH) may be due to autoantibodies binding to the adrenergic receptors (as well as the muscarinic receptors in the case of OH) of the autonomic nervous system.


However, a very important function of the brainstem is the regulation of consciousness (conscious awareness). I tend to view brain fog as a deficit of consciousness: something like meditation is considered a consciousness expanding practice, but the brain fog of ME/CFS seems to me to be a consciousness contracting condition.

With brain fog, your mental radar of awareness seems to become much diminished. I think this reduction of consciousness in ME/CFS may be due to the brainstem dysfunction, since the brainstem is responsible for regulating consciousness — specifically it is the reticular activating system in the brainstem that regulates consciousness.

The brainstem is also one of the areas involved in sensory gating (the processes of filtering out irrelevant environmental stimuli), and so a dysfunction in the brainstem may give rise to sensory gating problems, and I think the sound sensitivity of ME/CFS may be a sensory gating issue that arises from brainstem dysfunction.

More info in this post.



Dr Chia points out that an enterovirus infection in the gut can travel to the brain along the vagus nerve itself in matter of just 3 days. The vagus nerve runs from the gut to the brain, and so enterovirus can just hitch a ride along this nerve route. The vagus nerve terminates in the brainstem area of the brain, so the brainstem may be where enterovirus enters the brain.

More info here.

 

[JollyRoger]

http://studylib.net/doc/9068893/brainstem-perfusion-impaired-in-chronic-fatigue-syndrome

I think the autonomic dysfunction and the brainstem are the main culprit:
Everything from the hormone imbalance to the mitochondrial dysfunction can be explained with it.
In burnout syndrome and overtraining also happened a autonomic dysfunction. If you remove the stress it works.
Mitochondrial dysfunction and neuroinflammation also happens in major depression- this can not be the cause.

But if the cause of the mitochondrial dysfunction is a damaged brain stem is it irreversible?

Some had a full remission, some go to 50 or 70% and some stay on 10% for 20,30 years despite treatment.
Th mean that one part was an (auto)inflammation (@Gingergrrl) or virus and the remaining part is damage.

It would be the same pattern as in myocarditis despite the fact that you can't get a brain stem transplant in the worst case.
Myocarditis can be autoimmune, viral even toxic.
Some have a remission or get to certain level with or without treatment and other people die.
And it is important to rest to heal the heart because every effort damages the heart.

I would be really interested in what the experts like prof.edwards would say about this.
Is it a unique pattern or can it be explained as a symptome ?
Could it be a diagnostic marker?

 

[Gingergrrl]

It is possible the brainstem dysfunction in ME/CFS may (in part or in whole) be causing autonomic function, but as @Gingergrrl points out, evidence suggests that POTS and orthostatic hypotension (OH) may be due to autoantibodies binding to the adrenergic receptors (as well as the muscarinic receptors in the case of OH) of the autonomic nervous system.

I used to think that brainstem damage was the mechanism behind POTS and OI (and all dysautonomia) but now I believe that autoantibodies and autoimmune POTS is much more common than we ever knew.