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

Jonathan Edwards said:
So eating bananas might cause ME/CFS in one in 10,000?
You need to have some rational basis for bothering to speculate about something.
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You think suspecting intracranial pressure making neurology/neuroimmunology hypersensitive in some people is about same as suspecting eating bananas? Doesn't certain headache make some people light-sensitive?

Jonathan Edwards said:
If people want to speculate, that is fine, but why pick something peddled by fringe surgeons and all over social media? Why not something original?
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I'd rather keep my eyes on the prize rather than getting distracted by unscrupulous people.
 
We had yet another discussion of this topic earier this year when Jeff Wood, who makes money out of promoting this surgery, published a preprint which claimed successes, but even after several years the only 'case studies' they included where himself and Jen Brea. @poetinsf, you raised all the same points on that thread as you are raising again here. As far as I can see the preprint is just a sales pitch, not a scientific paper.
https://www.s4me.info/threads/hypot...vid-2025-jeff-wood-kaufman-et-al.44557/page-3

There seems little point pursuing discussion based on speculation until and unless the surgeons involved publish a decent study of all the cases they have treated on the basis of the so called ME/CFS connection. The fact that they have published nothing, not even a case series, tells me they have nothing new to report that supports using CCI surgery unless people have classic CCI symptoms, signs and imaging.
 
poetinsf said:
implicates vagus nerve, which can be compressed by CCI, as the nexus for the communication between peripheral inflammation and the brain.
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As I pointed out earlier, the vagus nerve goes nowhere near the cervical canal so this is just anatomically wrong.

poetinsf said:
Doesn't certain headache make some people light-sensitive?
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Meningitis does but that is not CCI. All I hear are attempts to make connections that are based on lack of basic knowledge of neurology.

Maybe it's a cultural thing but I find it hard to understand how anyone can take this sort of bogus medicine seriously.
 
Trish said:
We had yet another discussion of this topic earier this year when Jeff Wood, who makes money out of promoting this surgery, published a preprint which claimed successes,
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I'm not interested in what Jeff Wood says. I'm only interested in the recovery cases. But I sense that there is a strong push-back in this forum on anything that is attached to his name.

Trish said:
you raised all the same points on that thread as you are raising again here.
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Actually, it got kicked up from the thread on peripheral inflammation to brain communication. I raised a new possibility of CCI effecting vagus nerve implicated in that paper. There are several texts that says that CCI can compress or irritate vagus nerves that are next to C1/C2. But I'll accept @Jonathan Edwards claim for now, since I'm not an expert on the topic, that that is not anatomically possible.

Jonathan Edwards said:
As I pointed out earlier, the vagus nerve goes nowhere near the cervical canal so this is just anatomically wrong.
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They are not in cervical canal, but they are near C1/C2 that are effected by CCI. But I'll take your word for it since I have no expertise on this matter.
 
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poetinsf said:
There are several texts that says that CCI can compress or irritate vagus nerves that are next to C1/C2. But I'll accept @Jonathan Edwards claim for now, since I'm not an expert on the topic, that that is not anatomically possible.
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Can we see those texts? It would be useful to know what is being argued.
 
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Jonathan Edwards said:
Can we see those texts? It would be useful to know what is being argued.
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Several will pop up if you google "can CCI compress vagus nerve?". Here are couple:

www.chronicpainpartners.com

Cervical Spine Instability: Patient Guide

This patient guide helps people with Ehlers-Danlos syndrome get diagnosed with cervical spine instability and find treatment options.
www.chronicpainpartners.com www.chronicpainpartners.com
caringmedical.com

Vagus nerve compression in the neck: Symptoms and treatments

Ross Hauser, MD The vagus nerve plays a key role in regulating many of our body’s functions. Its name best describes its physical characteristics: Vagus is Latin for “fugitive,” or “wanderer.” It is the longest and most widely extended of the nerves of the body. The vagus nerves keep us alive by...
caringmedical.com caringmedical.com
 
poetinsf said:
Several will pop up if you google "can CCI compress vagus nerve?". Here are couple:
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One is a sales pitch for a private clinic and the other an information sheet from an advocacy group for a condition where misinformation is rife?

Why are we supposed to take these seriously?

As I said before, we used to send patients to have their vagus nerves cut completely through for stomach ulcers and nobody got ME/CFS. Isn't that a fairly conclusive piece of evidence against tickling the vagus making people bedbound?

Edit: and of course if it has to be ticking rather than impairing then there are published studies of stimulation of the vagus nerve, which people thought might cure arthritis, and nothing much happened at all.
 
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Wouldn't it be just as likely that these rare remission responses are due to the long anaesthetic rather than the surgery? These procedures are 4-5 hours duration.

In order to switch off conscious brain function, general anaesthesia suppresses glutamate receptor excitatory activity, alongside increasing inhibitory GABA-ergic transmission. It works as a combination of lipid membrane fluidity and ion channel modulation. (It's not known precisely how these anaesthetic agents work with respect to lipid membrane fluidity and phospholipid configuration to achieve this, but as I understand things it disturbs the receptor/lipid raft configuration.)

DecodeME highlights multiple genes potentially related to post-synaptic glutamatergic receptors and excitatory signalling (see ME/CFS Science Blog's summary article here: section "Zooming in on the signal") and there is recent PET/MR evidence of significant increase in their density in LC (needing replication, confirmation in ME etc).

Maybe things can line up just so and break a feed-forward loop. There could be all sorts of other factors, for example the metabolic (sphingolipids?) response to acute fasting, the range of peri-operative drugs. Having two long anaesthetics for CCI and then cord de-tethering would double the rare chance of a positive outcome.
 
SNT Gatchaman said:
Wouldn't it be just as likely that these rare remission responses are due to the long anaesthetic rather than the surgery? These procedures are 4-5 hours duration.
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Yes. But, we don't even have really solid evidence that these remission responses actually occurred following the surgery. That seems to me to be the first couple of dots that aren't connecting up in any sort of a solid way. i.e. was there a remission, and, if so, did it follow the surgery?


I looked into this a bit yesterday as I have no medical background with which to assess the conflicting claims about cervical instability affecting vagal nerve function and resulting in ME/CFS symptoms.

Ross Hauser and Caring Medical were the names that kept coming up in the search - they seemed to be a key primary source of this idea. I couldn't find a reliable (unconflicted) source supporting the idea.

I'm not clear on whether the idea is that there is an abnormal stretching of the nerve or a compression of the nerve.

If a compression, then the vagus nerve seems to be bundled up with other squishy things - major blood vessels to and from the brain, all wrapped with a tough protective membrane, with other squishy things around it. As far as I could see, the location of that bundle seems to be well away from the cervical spine. There doesn't seem to be a 'rock and a hard place' location where things wouldn't just move to accommodate any misalignment heading towards the vagus nerve unless there was really some catastrophic misalignment that would surely be incredibly visible on imaging. I don't know, is there anywhere where compression of the vagus nerve could occur against the cervical spine?

(Edit: Jonathan mentioned up thread the jugular foramen, an opening at the base of the skull,
"The vagus enters through the jugular foramen. Someone I know has recently had a fracture of the jugular foramen with compression of the vagus nerve. They cannot speak or cough properly because it supplies the larynx.")

If an abnormal stretching, then is the damage supposed to be permanent? In which case, how would surgery to realign the spine fix it? If it's just a temporary stretching, wouldn't the body have a lot of scope to accommodate that given we are moving all the time?
 
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Hutan said:
Yes. But, we don't even have really solid evidence that these remission responses actually occurred following the surgery. That seems to me to be the first couple of dots that aren't connecting up in any sort of a solid way. i.e. was there a remission, and, if so, did it follow the surgery?
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I'm also not quite sure how this would be argued as positive evidence for anaesthesia when the exact same argument that is used as negative evidence elsewhere also applies. From what I've seen what people are saying is there have been only very few operations with subsequent remissions and numerous that haven't and this has sensibly been used as negative evidence. Surely the same argument would apply to anaesthesia. And of course you have much more negative evidence here because there's also far more people that receive anesthesia for other reasons.
 
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Sure, but whereas mechanical compression doesn't really work as a good explanation, as highlighted above by Jo, anaesthetic agents are specifically modulating some of the prominent identified targets from DecodeME. And there is other evidence for deranged glutamate metabolism/function.

I'm not suggesting we'd all be cured just with an anaesthetic, but it is reasonable to explore the possibility of an effect on neural function: both centrally and peripherally. Apart from being, on the face of things, a good explanation for neuro-hypersensitivities if not brain fog, these excitatory receptors are also important in autonomic and pain transmission in the periphery. We have recent papers showing these nerve fibres behaving pathologically, so maybe there's a story to be built.

In relation to lots of negative evidence, most anaesthetics are for surgical procedures that are <60 minutes. And it's probably true that people with ME/CFS simply don't pursue surgical and medical interventions to the same degree due to the potential extreme negatives associated with hospitalisation (or even simply in-clinic care). Laparoscopic cholecystectomy might be relatively common but isn't a particularly long duration procedure. Barriers to being offered a hip or knee replacement might be higher for someone who already has limited mobility and "complaining of pain everywhere anyway." Complicated endometriosis surgery would be a candidate for long duration I suspect.

Out of interest I've made a poll on anaesthetic duration experience.
 
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Hutan said:
But, we don't even have really solid evidence that these remission responses actually occurred following the surgery. That seems to me to be the first couple of dots that aren't connecting up in any sort of a solid way. i.e. was there a remission, and, if so, did it follow the surgery?
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I am happy to believe at least one person who said they were much better following surgery. It is maybe more a question of how one interprets that in the context of people feeling much better after various implausible things.
Hutan said:
If an abnormal stretching, then is the damage supposed to be permanent? In which case, how would surgery to realign the spine fix it? If it's just a temporary stretching, wouldn't the body have a lot of scope to accommodate that given we are moving all the time?
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I think your post gives a good analysis of how none of this adds up.
The other thing, which would certainly apply to vagus nerves, as well as the cord itself, is that there doesn't seem to be any need for surgery when you can perfectly well prevent any mechanical issues from neck movement with a high spec collar. If anyone takes this seriously why has there not been a trial of wearing custom fitted collars for 6 months? There was some story about needing traction to get the effect, which makes no sense unless there is upward migration of the C2 peg even for the cord and would be irrelevant to the vagus.

The reality is that the story keeps changing like a game of whack-a mole. Spines too stiif, spines too bendy, pressure on cord, no, brainstem, no vagus, no not pressure, stretching, no....
There comes a time when enough is enough when nobody ever found a relevant neurological sign.
 
SNT Gatchaman said:
I'm not suggesting we'd all be cured just with an anaesthetic, but it is reasonable to explore the possibility of an effect on neural function: both centrally and peripherally.
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I agree. Chris Ponting asked the question whether the brain genes and the immune genes should be seen as part of one story or two separate stories. I think that is an important question but the answer may be both. There are different dynamic patterns over time with ME/CFS in different people and a question that has been around forever is whether the process keeps going because of a persistent immune cycle or whether you end up left with just a brain cycle (to oversimplify). Some people's illness may continue to feed off an immune cycle, for others not so much. It is entirely conceivable that there is a small subgroup that just needs a brain cycle to be switched off. It is also possible that the effect might last for months followed by a relapse because even for them the immune cycle can re-engage.

I am constantly reminded of the analogy with depressive illness and my wife's psychosis due to malarone. That responded to switching her brain off with ECT but only a small proportion of people with that sort of illness are even considered for ECT and not all respond by any means. It is just that when they do, it is like a miracle.
 
SNT Gatchaman said:
Having two long anaesthetics for CCI and then cord de-tethering would double the rare chance of a positive outcome.
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In this framing, would the impacts of this remission wear off down the road? Or is the suggestion that the anaesthesia-induced changes would actually be long-lasting? Seems like it might useful to review whether non-CCI ME/CFS patients who have had general anaesthesia for other reasons had similar responses?
 
dave30th said:
In this framing, would the impacts of this remission wear off down the road? Or is the suggestion that the anaesthesia-induced changes would actually be long-lasting?
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From a theoretical perspective it could be either and both, as I think I suggested above.
Going by the ECT experience it is either but the rationale is based on the chance of long term remission.

It is purely a guess but I think it quite likely that as few as 10% or less of ME/CFS cases might be amenable to this approach on its own. And not that many of those will have had five hour operations.
 
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