The science of craniocervical instability and other spinal issues and their possible connection with ME/CFS - discussion thread

These cases are so rare and the description so limited that I am not sure they tell us much.
The only mechanism I can think of is bone or ligament erosion from sepsis - the bone loss might appear after infection has been treated with antibiotic. That seems to be the implied mechanism in the case reports.

That sort of bone erosion would be very obvious on plain x-ray or MRI/CT as an erosion of the odontoid peg or an increase in anterior atlanto-odontoid distance on neck flexion (should be no more than about 2mm. As far as I am aware there is no suggestion that anyone with ME has had these findings on imaging.

So I don't think this situation is of any relevance.

Thank you @Jonathan Edwards.
 
I have been wondering about this for a while and am now trying to get some hard information.

I have been asking around the UK research community. I do not have any specific information so far but the implication of the one specific comment I have had is that none of a large cohort of PWME have an EDS diagnosis. So I will try and get some facts.
For many getting any kind of referral from a GP is difficult. That alone may skew things.
If it is not something that has an association then who will look for it?
 
If it is not something that has an association then who will look for it?

If EDS is not associated with ME then the process of diagnosing EDS is the same for everybody - picked up by its clinical features.

In terms of looking for whether there is an association, I think the depends on using cohorts without expectation bias and that is really the main thrust of building a genetic research programme in the UK - which is being put to the MRC.
 
New thread on PR about Grisel Syndrome, a condition involving atlantoaxial subluxation as a result of an inflammatory process of the head and neck, typically an upper respiratory tract infection.

This makes me wonder whether the (presumed) inflammation driving the chronic sore throat in ME/CFS might be responsible for creating atlantoaxial and craniocervical effects. Plus some ME/CFS patients report an inflammatory feeling at the back of the head, around the nape of the neck, so that's another head/neck location where there may be ongoing inflammation.
 
This makes me wonder whether the (presumed) inflammation driving the chronic sore throat in ME/CFS might be responsible for creating atlantoaxial and craniocervical effects.

If it did then it would show on x-ray and it doesn't.

It is a bit like suggesting that PWME have trouble walking because they have broken legs. They don't.
 
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If ME is an abnormal metastable signalling system state then maybe in some forms it can be knocked out of its 'well' and the signalling system return to normal.
This is what I was sort of asking:
So if the stresses of surgery could push cells from their healthy state to just past the neutrally stable point, so they flick over to their unhealthy state, could it be that in some cases further surgery could push them back to their neutrally stable state, and perhaps this sometimes allows them to then flick back to a healthy stable state?

Just musing. Any thoughts @Jonathan Edwards?
https://www.s4me.info/threads/conce...ty-surgery-in-me-cfs.9638/page-12#post-171874
 
It seems that the blog would have been the work of one Courtney Gunter. It would be interesting to know whether and by whom it was signed off.
Wow, the Jackson Labs "Advances in ME/CFS" blog has posted about this without additional comment, therefore, arguably, endorsing it unreservedly, https://jaxmecfs.com/2019/06/04/jennifer-breas-me-cfs-is-in-remission/

Perhaps not a surprise as ME Action is part of the patient advocacy Steering Committee for this research collaborative.
 
When @Barry mentioned upthread the idea of stress from surgery pushing patients back into remission, my first thought was, didn't Suzanne Vernon suggest something like that a decade ago? And since it's been brought back up, I decided to just see if I could find it via Google and it, thankfully, didn't take more than a minute. Hers is based on cortisol, which seems rather dubious at this point, but have a look. Nancy Klimas has been doing system reset both in Gulf War Illness and now ME/CFS but with etanercept and mifepristone, which is what I think she's talking about in this video? In watching that video, she talks about using a computer animal model that appears to reset neuroinflammation and other markers to normal, which is why they are doing this trial. Yet we don't even know that is what is causing function to be impaired in ME/CFS. I suppose if the trial works, it might be more suggestive, but it does seem to make a huge logical inference without enough evidence.

And I appreciate what you've said @Sid about the ways stress and its neurobiology may theoretically induce remission for some people who go through Lightening Process. Throughout this thread I keep thinking of people who have gone through the LP and been cured. Some of them have been genuinely very ill and appear to have genuine recoveries/remissions. I didn't know how to ask how @JenB 's case was different without sounding like I'm invalidating her experience (for which I'm genuinely very pleased!). The question, in my mind, is not whether Jen or @Jeff_w had "real" ME or are really better but what made them better. The interpretation that Jen had surgery and woke up in remission does not necessarily mean it was the surgery that is what made her better -- as tempting and understandable a conclusion as that may be to come to. The only thing we can say with certainty is that we don't know. Which is deeply unsatisfying. Humans like patterns and eschew lacuna too much.
 
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I would be against an isolated Hoffman. It is positive randomly in a small proportion of normal people. A Hoffman test should be done as part of a complete neurological examination and for me is never worth doing unless the major reflexes are equivocal. So I would agree with the NIH group there.

But of course someone presenting with symptoms of ME should have a full neurological examination.
What constitutes a full neurological examination.
Our diagnosis ( default CFS) was by paediatrician - i can' anythingt recall remotely neurological in her examination

Eta read post explaining. Don' t think as full an exam.as suggested was done. Deteriorated since then anyway.
 
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If it did then it would show on x-ray and it doesn't.

I don't think the inflammation in chronic coxsackievirus B myocarditis shows up on X-ray.

Nevertheless, there are several studies which demonstrate coxsackievirus B myocarditis leads to connective tissue remodeling as a result of increased secretion of matrix metalloproteinases, which degrade connective tissue.

Thus you might expect similar connective tissue remodeling in the head/neck if there were an ongoing coxsackievirus B infection there.
 
I don't think the inflammation in chronic coxsackievirus B myocarditis shows up on X-ray.

That is because it is not remodelling bone and it is bone that shows on an x-ray!

If inflammation remodels bone it will show on an x-ray.

Acquired CCI due to inflammation has to work through remodelling of bone or ligament. If the remodelling is purely ligament then it will only lead to instability if there is rupture. Rupture of the transverse atlantal ligament shows on x-ray as movement of the odontoid peg on plain x-ray - it is obvious. I do not see how the ligaments stabilising the occipital-atlantal articulation can rupture. They may be lax developmentally but that is a different issue.
 
Acquired CCI due to inflammation has to work through remodelling of bone or ligament. If the remodelling is purely ligament then it will only lead to instability if there is rupture.

On the YouTube presentations of Dr Fraser Henderson and Dr Paolo Bolognese (the two leading CCI surgeons in the US), they talk about ligamentous laxity being the cause of the CCI cases they see.

From the "student notes" I made from these videos, in this 2012 video at 13:12, Dr Henderson says says there are three components to diagnosing craniocervical instability:

1 — Clinical: the presence of cervical medullary syndrome (symptoms: headache, neck pain, visual changes, photosensitivity, hearing loss, tinnitus, hyperacusis, dizziness, vertigo, imbalance, dysarthria, word finding difficulties, dysphagia, choking, dyspnea, disordered CO2 regulation, sleep apnea, disordered sleep architecture, loss of REM sleep, gastric reflux, nausea, vomiting, IBS, weakness, spasticity, tremors, jerking, clinic movements and dystonia, sensory loss, hypersensitivity, RSD, Raynaud's, memory and cognitive issues).

2 — Radiological (MRI scan): metrics of instability, pannus, syringomyelia, spina bifida.

3 — Etiological: a reasonable explanation for ligamentous instability (such as inflammation, rheumatoid arthritis, lupus, infection, etc).​

So they think infection or inflammation can cause the lax ligaments that lead to CCI/AAI.
 
Purely FYI, I have heard of practices which claim to be able to treat ligament laxity for sports injuries etc under the name of "prolotherapy".

How effective this treatment is I dont know, just thought I would mention it as I only came across it quite recently, not sure what to make of it.
 
In this 2018 video by Dr Henderson at 7:47, he addresses the question of "When does ligamentous laxity at the craniocervical junction become pathological".

He details the metrics used to measure craniocervical instability on MRI scans. There are over 20 metrics available, and in the early days, researchers and surgeons used many of these. But nowadays (as a result of an international conference in 2013) they narrowed it down to three basic metrics:

Clivo-axial angle
Grabb-Oakes method
Harris method

These are all described in the video.



It's also interesting to look at what happens if you do stretch or compress a part of the brain or nervous system: in this 2014 video at 10:42, Dr Fraser Henderson explains that if you stretch a mouse optic nerve just 20% of its length, you see axon retraction balls, and then later you get apoptosis of the neurons. So this is the basis of the neurological damage done when neurons are stretched.
 
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