Opposite white matter abnormalities in post-infectious vs. gradual onset chronic fatigue syndrome revealed by diffusion MRI, 2024, Yu et al

[Utsikt]

For one HHV-6B is listed on some official list of empirically validated ME/CFS triggers. I don't remember where I saw it. But I will let you know if I see it again.

I think any infection can be followed by the onset of ME/CFS, but that doesn’t make ME/CFS contagious in the normal sense of the word, because there is clearly something more needed for ME/CFS to occur. ME/CFS seems to be a reaction to infections (that by themselves are contagious).

If EBV is required for MS, that doesn’t make MS contagious.

I base the idea that ME can be infectious on my own experience and the observation that there are many families and couples where several who are all ill.

Those observations can also be explained by shared genetic and/or environmental factors.

There are a couple of threads where this is discussed, and we should probably continue the discussion there to not clog this thread.

https://www.s4me.info/threads/is-there-any-research-into-whether-me-cfs-is-contagious.16484/

Or

https://www.s4me.info/threads/evidence-that-m-e-isn%E2%80%99t-contagious.29980/

 

[PageofME]

Those observations can also be explained by shared genetic and/or environmental factors.

Well, these observations are not my argument. My argument is inspired by these observations.

But yes, let's stop discussing HHV-6B hypothesis and possible ME contagiousness here.

 

[Yann04]

the observation that there are many families and couples where several who are all ill.

Couldn’t that be explainable through genetics and shared trigger?

For example both my mum and I got sick after the same COVID infection.

I assume we both shared genetic susceptibility and we also both got an infection that for one reason or another was particularly prone to causing post-viral illness.

If you have a situation of ongoing distress, an illness or an infection as far as I understand it your HHV-6B will always go up a little bit because your immune system is a little bit compromised at controlling reactivation. See here where it is suggested that HHV-6B loads in saliva can be used as a predicter for athletic fitness to be used in training plans for sports medicine.

One could also interpret this the other way around. That the bodily stress of ME makes HHV6 more likely to reactivate. And so it’s more a consequence than a cause.

Obviously none of us can be sure we’re right as we just don’t have the data for now.

 

[PageofME]

Couldn’t that be explainable through genetics and shared trigger?

For example both my mum and I got sick after the same COVID infection.

I assume we both shared genetic susceptibility and we also both got an infection that for one reason or another was particularly prone to causing post-viral illness.

One could also interpret this the other way around. That the bodily stress of ME makes HHV6 more likely to reactivate. And so it’s more a consequence than a cause.

Obviously none of us can be sure we’re right as we just don’t have the data for now.

I think they are all good explanations. But none of them is a proof that it is impossible that some patients might have caught ME directly from an acute ME patient - like I think was the case for me.

 

[Jonathan Edwards]

I think they are all good explanations. But none of them is a proof that it is impossible that some patients might have caught ME directly from an acute ME patient - like I think was the case for me.

I don't understand what this means. If we know infections trigger ME/CFS then you can presumably get ME/CFS from catching the infection from someone else. I am not sure it helps to call that 'catching ME directly'. What more would that mean?

 

[SNT Gatchaman]

I must say that, as a person with gradual onset ME and a lot of cognitive issues (indeed, I would characterize my symptoms as primarily cognitive), this is pretty damn discouraging, especially as reading about the sort of damage associated with low axial diffusivity seems to match up pretty damn well for me.

Except it may not be damage. (In the same way T cell subset exhaustion markers do not mean globally tired T-cells.)

The changes in diffusivity might not indicate neuroinflammation or cell damage. It could relate to myelin maintenance and even be compensatory, ie increased or decreased to preserve conduction velocities for signalling between brain regions that rely on simultaneous time-of-flight for effective neurological performance. (Perhaps this process might be deficient in FND.) See —

Change of conduction velocity by regional myelination yields constant latency irrespective of distance between thalamus and cortex (2003)

Spoiler: Abstract

The widely spanning sensory cortex receives inputs from the disproportionately smaller nucleus of the thalamus, which results in a wide variety of travelling distance among thalamic afferents. Yet, latency from the thalamus to a cortical cell is remarkably constant across the cortex (typically, ≈2 ms).

Here, we found a mechanism that produces invariability of latency among thalamocortical afferents, irrespective of the variability of travelling distances. The conduction velocity (CV) was calculated from excitatory postsynaptic currents recorded from layer IV cells in mouse thalamocortical slices by stimulating the ventrobasal nucleus of the thalamus (VB) and white matter (WM).

In adults, the obtained CV for VB to WM (CVVB-WM; 3.28 ± 0.11 m/s) was ≈10 times faster than that of WM to layer IV cells (CVWM-IV; 0.33 ± 0.05 m/s). The CVVB-WM was confirmed by recording antidromic single-unit responses from VB cells by stimulating WM. Exclusion of synaptic delay from CVWM-IV did not account for the 10-fold difference of CV.

By histochemical staining, it was revealed that VB to WM was heavily myelinated, whereas in the cortex staining became substantially weaker. We also found that such morphological and physiological characteristics developed in parallel and were accomplished around postnatal week 4. Considering that VB to WM is longer and more variable in length among afferents than is the intracortical region, such an enormous difference of CV makes conduction time heavily dependent on the length of intracortical region, which is relatively constant.

Our finding may well provide a general strategy of connecting multiple sites irrespective of distances in the brain.

Web | PDF | Proceedings of the National Academy of Sciences | Open Access

Myelination and isochronicity in neural networks (2009)

Spoiler: Abstract

Our brain contains a multiplicity of neuronal networks. In many of these, information sent from presynaptic neurons travels through a variety of pathways of different distances, yet arrives at the postsynaptic cells at the same time. Such isochronicity is achieved either by changes in the conduction velocity of axons or by lengthening the axonal path to compensate for fast conduction.

To regulate the conduction velocity, a change in the extent of myelination has recently been proposed in thalamocortical and other pathways. This is in addition to a change in the axonal diameter, a previously identified, more accepted mechanism.

Thus, myelination is not a simple means of insulation or acceleration of impulse conduction, but it is rather an exquisite way of actively regulating the timing of communication among various neuronal connections with different length.

Web | PDF | Frontiers in Neuroanatomy | Open Access

 

[DHagen]

Except it may not be damage. (In the same way T cell subset exhaustion markers do not mean globally tired T-cells.)

The changes in diffusivity might not indicate neuroinflammation or cell damage. It could relate to myelin maintenance and even be compensatory, ie increased or decreased to preserve conduction velocities for signalling between brain regions that rely on simultaneous time-of-flight for effective neurological performance.

This is certainly important to keep in mind (and I think the authors at least allude to this). My dismay (which I understand is likely premature) was more in response to the statement that, in contrast to PI-ME/CFS sufferers, GO-ME/CFS patients would be left with nothing but "strategies focused on neuroprotection, mitochondrial support, or cognitive rehabilitation" in place of, say, an actual treatment. Obviously, more work is needed, and I am certainly hoping they are wrong about this particular part of the equation.

 

[SNT Gatchaman]

The distinct WM impairments between the PI-ME/CFS and GO-ME/CFS groups highlight the heterogeneity of ME/CFS. Interestingly, conventional clinical measures (SF-36, HADS, PSQI and BDS) did not differentiate between the two groups. This discrepancy calls into question the effectiveness of current clinical assessment tools for distinguishing ME/CFS subgroups and highlights the need for more sensitive instruments.

 

[Hutan]

For one HHV-6B is listed on some official list of empirically validated ME/CFS triggers. I don't remember where I saw it. But I will let you know if I see it again.

I wrote the following as part of a review of an UNREST education resource (a video):

0.53 I think this may be the source, or at least a source, of what I think is the misleading idea that HHV6 is a trigger of ME/CFS. Given that most people get HHV6 when they are a child, it doesn't seem likely that an HHV6 infection is a trigger of ME/CFS. It's possible that it reactivates around the time of ME/CFS onset, due to the person being immunocompromised, in the same way that HSV also often reactivates. Maybe it's even that cause of ME/CFS. But, I don't think it's accurate to say that we know it is a trigger in the same way that EBV or SARS-CoV-2 are.

I don't think we have any evidence that people are getting ME/CFS as a result of a late primary HHV-6 infection i.e. after say age 5, although it would be interesting if we did.