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

boolybooly said:
Purely FYI, I have heard of practices which claim to be able to treat ligament laxity for sports injuries under the name of "prolotherapy".
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I have not seen any mention of the use of prolotherapy for CCI. In this 2019 paper by Henderson, he mentions that CCI surgery is only indicated after conservative measures have failed. These are the conservative measures he lists:
physical therapy, activity modification, pain medications, neck brace, and in some circumstances, chiropractic, electrical stimulation, massage
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Prolotherapy does not appear to be mentioned.



As an aside: I was looking at prolotherapy to see if it might fix a yoga injury I sustained to my pelvis 20 years ago: I managed to stretch all the ligaments in the joint between my right pelvis and my spine (sacroiliac joint), such that my right pelvis feels loose. (But now with ME/CFS, this injury seems minor and irrelevant, so I did not pursue it).

There's now also prolozone, which has similar effects to prolotherapy.
 
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Dear @Hip I have watched those videos but so far I can see no reason to think they are relevant to PWME. We have so far not a single medically or scientifically trained person suggesting there is a relation between ME and CCI as far as I know. We simply have some personal stories from patients and their speculations. As far as I know Dr Hendreson has not been involved in any ME cases.

Considering the serious risks involved in this procedure and the stress put on vulnerable people who may consider asking for surgery and who may be offered surgery by surgeons for the wrong reasons I think this whole business should be put on the back burner until we actually have a doctor or scientist endorsing the idea that any of this makes any sense at all.

As someone trained in neurology and having looked after people with CCI, I say again that I cannot make anything meaningful out of what has been suggested to us. I am seriously concerned that there will be unnecessary deaths. From what I hear there may even have been one already.
 
debored13 said:
Well, for one, did the people who said they experienced remission from the LP track any objective markers for activity like steps per day, etc?
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The point is not whether the remission of Jen or the LP patients is real. They're both very real. LP patients certainly had metrics like "I couldn't get out of bed; now I'm working." The point is how we interpret that remission. And the answer at this point is simply it is unknown how Jen or the LP patients got better. While it may be understandable to want to interpret her remission as caused by the surgery given her improvement directly afterward, what @Jonathan Edwards is saying is that at this point that interpretation cannot explain it based on what we know of human physiology. That does not preclude it explaining it in the future if we, say, imaged hundreds of ME/CFS patients and they all unambiguously showed signs of CCI and new explanatory information about compression on the brainstem were found. Just as @Sid 's explanation above about the role neurobiology may prove to be explanatory for why the LP cures some patients. But at this time, both CCI and glucocorticoids are just speculation, not explanation. And both treatments come with considerable risk -- CCI surgery being orders of magnitude more risk with death or paralysis.
 
A key point still is that Jeff and Jen ended up developing symptoms that are quite atypical of ME or CFS. I don't see why it is controversial to believe that their symptoms were due to CCI and that surgery was the cause of the remission. Perhaps they had rare atypical presentations of CCI - given the non-specific nature of potential neuronal damage, I don't see why it is unreasonable to expect patients to have a range of presentations until their illness becomes very severe.

Over analysing a few words like PEM stopped straight after surgery is mostly meaningless, it is the long term remission that we actually care about.

But it is important to also realise that unless ME patients also develop those atypical symptoms more characteristic of CCI, it means it is unlikely that many or most ME patients actually have CCI as the cause of their illness.
 
Snow Leopard said:
A key point still is that Jeff and Jen ended up developing symptoms that are quite atypical of ME or CFS. I don't see why it is controversial to believe that their symptoms were due to CCI and that surgery was the cause of the remission. Perhaps they had rare atypical presentations of CCI - given the non-specific nature of potential neuronal damage, I don't see why it is unreasonable to expect patients to have a range of presentations until their illness becomes very severe.

Over analysing a few words like PEM stopped straight after surgery is mostly meaningless, it is the long term remission that we actually care about.

But it is important to also realise that unless ME patients also develop those atypical symptoms more characteristic of CCI, it means it is unlikely that many or most ME patients actually have CCI as the cause of their illness.
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Yes, but that’s not the message that’s getting “out there” to people too sick to research and/or without science background.

I read a comment recently on a Facebook mecfs group in response to someone having POTS-like symptoms, which said ‘if you are diagnosed with POTS check to see if you have CCI. It’s very treatable’

I don’t equate dangerous surgery with very treatable.

I’ve been thinking about this though. It’s not just that people are desperate (which they are). It’s also that many MECFS patients are distrustful of doctors due to having been diagnosed with conversion disorders.

This happened to me, so on the one hand I think to myself that I’ve had full neurologic exams, and nothing abnormal was found. And then, on the other hand, I don’t necessarily trust those doctors since they clearly had decided quickly to write my physical symptoms off as psychological.
 
Michelle said:
The point is not whether the remission of Jen or the LP patients is real. They're both very real. LP patients certainly had metrics like "I couldn't get out of bed; now I'm working." The point is how we interpret that remission. And the answer at this point is simply it is unknown how Jen or the LP patients got better. While it may be understandable to want to interpret her remission as caused by the surgery given her improvement directly afterward, what @Jonathan Edwards is saying is that at this point that interpretation cannot explain it based on what we know of human physiology. That does not preclude it explaining it in the future if we, say, imaged hundreds of ME/CFS patients and they all unambiguously showed signs of CCI and new explanatory information about compression on the brainstem were found. Just as @Sid 's explanation above about the role neurobiology may prove to be explanatory for why the LP cures some patients. But at this time, both CCI and glucocorticoids are just speculation, not explanation. And both treatments come with considerable risk -- CCI surgery being orders of magnitude more risk with death or paralysis.
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This is a good point and for sure we cannot fully rule out all the various possibilities of how these recoveries were achieved. But if we take a closer look for example at the story of Jeff which is documented on his website, it mentions specifically how mounting a halo brace helped his severe OI symptoms. More remarkably, when he pushed his halo vest upwards, thus increasing traction, it would have an immediate effect of improving his OI and decreasing his heart rate further.

If we go by what was reported (and I see no reason to believe the improvements after surgery, but not believe the improvements experienced from wearing the halo), I think the halo part of the story is maybe more significant. It's subject to less other potential explanations than recovery following a complicated surgery.

Edit: There was just a new blog post published by Jen that describes a very similar experience with cervical traction.
 
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JES said:
it mentions specifically how mounting a halo brace helped his severe OI symptoms. More remarkably, when he pushed his halo vest upwards, thus increasing traction, it would have an immediate effect of improving his OI and decreasing his heart rate further.
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But you are interpreting this without actually knowing the neuroanatomy, or the experience of neurologists. From my knowledge of CCI there would be no prediction that these symptoms would change in this way. The anatomy is not like that. The brain stem cannot be 'lifted' off the cervical spine. This is why I keep saying that as a trained neurologist this story is impossible to interpret. If anything the story points well away from the symptoms being due to CCI.
 
Jonathan Edwards said:
But you are interpreting this without actually knowing the neuroanatomy, or the experience of neurologists. From my knowledge of CCI there would be no prediction that these symptoms would change in this way. The anatomy is not like that. The brain stem cannot be 'lifted' off the cervical spine. This is why I keep saying that as a trained neurologist this story is impossible to interpret. If anything the story points well away from the symptoms being due to CCI.
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@Jonathan Edwards What do you think the story points to? I am concerned that people are starting to think POTS is a sign of CCI, and if you search for CCI symptoms, POTS and OI are listed, but I note that they were not on your list of most important physical signs of CCI.
 
vsou said:
@Jonathan Edwards What do you think the story points to?
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I have made some suggestions earlier in the thread. I would prefer not to keep going over issues that have implications for individuals.

I have never heard of POTS being linked to CCI. This sounds suspiciously like gossip to me. The clinical picture of CCI has been known for decades and POTS is a relatively new controversial concept that is not as far as I know in any way a reliable indicator of CCI and seems less and less to be relevant to ME (see the thread on the recent OI paper from baraniuk).
 
Michelle said:
The point is not whether the remission of Jen or the LP patients is real. They're both very real. LP patients certainly had metrics like "I couldn't get out of bed; now I'm working."
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I actually think you’re wrong, the point is always still worth it to scrutinize recovery stories. Did the people involved have ME. Did they improve on any objective measures (sustained activity being one)... etc etc
 
Jonathan Edwards said:
I have never heard of POTS being linked to CCI. This sounds suspiciously like gossip to me.
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Yes, well I am just saying that when I did a google search for CCI symptoms POTS issues were mentioned on several sites. I was confused initially also, because I didn't recall they were related. I just went back to search now to see exactly what the wording was. The pain relief foundation lists "Dysautonomia" "tachycardia" and "orthostatic intolerance" under symptoms of CCI. Then the zebra network uses that list, crediting the pain relief foundation. I am not saying these are the best sources, just that they came up at the top of my google search.

Also, as I mentioned above, I read a comment recently on a Facebook me/cfs group in response to someone having POTS-like symptoms, which said ‘if you are diagnosed with POTS check to see if you have CCI. It’s very treatable’.

I belong to several facebook groups for ME/CFS and also for EDS, and CCI has been mentioned in them all recently, with comments indicating that many people are not fully informed on the issue, and that many people are in the process of trying to get testing for CCI done.

I share concerns expressed here, and appreciate the efforts made here to share important information on this issue.
 
Just to clarify, my only point was that when discussing the remissions from CCI surgery, the improvement following traction described in both cases seems highly relevant. Both Jen and Jeff experienced a massive and instant remission of their symptoms following cervical traction performed in a hospital, in Jen's case only after 30 pounds of traction was added. Whatever the underlying cause of their symptoms were, CCI or something else, it improved with traction. This almost certainly rules out some of the alternative explanations for the remission that were suggested, e.g. the anesthesia or the stress from the surgery pushing the patient into remission. The latest blog post of Jen actually describes some objective measurements obtained during the traction procedure:
On my fluoroscopy, the Basion Dens Interval (BDI), a measure of the vertical distance between the skull and the spine, was very clearly abnormal. Under traction, a normal person will have very little to no change in this measurement. If traction is able to lift the skull, this shows the skull was too “low” on the spine to begin with and that it is hypermobile. Anyone with a change of 2mm or greater is considered a candidate for surgery. My measurement was 4.8mm. This indicated that my skull was moving more than it should, as a result of ligament laxity. This craniocervical instability was causing cranial settling — my skull was sinking on my spine, crushing my brain stem and likely also causing problems with cerebrospinal fluid and blood flow (which could cause or contribute to intracranial hypertension).

The radical change in my symptoms I experienced while under traction amazed me, but this is something that my surgeon sees all the time in people who have CCI.
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I was unfamiliar with the terms used and just looked up for information (see link below). My interest was piqued by Jen describing a 2 mm difference as significant. This must be a very small tolerance for bones I thought (not knowing anything about it). Looking up the term Basion Dens interval my link said this:

Normal values are <12 mm on plain radiographs and <8.5 mm on CT 1.
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So now I’m really confused ...a change of 2mm is quite small right? In the context of normal being <8.5, 2mm is a big percentage, and Jen refers to differences of hers being 4.8 ...is this difference in readings on different days or difference when the head is angled/moved. What’s classed as a normal range in the general population before surgery is required? And what’s the prevalence of the range of differences? Once it’s changed does it ever change back on its own without the need for surgery?

I find it difficult to understand the context of the measurements described when I have so many clarifying questions (mainly due to ignorance).

https://radiopaedia.org/articles/basion-dens-interval?lang=gb
JES said:
Just to clarify, my only point was that when discussing the remissions from CCI surgery, the improvement following traction described in both cases seems highly relevant. Both Jen and Jeff experienced a massive and instant remission of their symptoms following cervical traction performed in a hospital, in Jen's case only after 30 pounds of traction was added. Whatever the underlying cause of their symptoms were, CCI or something else, it improved with traction. This almost certainly rules out some of the alternative explanations for the remission that were suggested, e.g. the anesthesia or the stress from the surgery pushing the patient into remission. The latest blog post of Jen actually describes some objective measurements obtained during the traction procedure:
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vsou said:
I belong to several facebook groups for ME/CFS and also for EDS, and CCI has been mentioned in them all recently, with comments indicating that many people are not fully informed on the issue, and that many people are in the process of trying to get testing for CCI done.

I share concerns expressed here, and appreciate the efforts made here to share important information on this issue.
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Thanks for the info. It looks to me as if there is a 'meme' going around not only social media but also some of the support charities. I am trying to contact people who really know about all this and am hopeful that I may have found someone who may be able to help provide some solid information.
 
JES said:
Just to clarify, my only point was that when discussing the remissions from CCI surgery, the improvement following traction described in both cases seems highly relevant.
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I feel very uncomfortable about discussing individuals case histories without any official medical input. So I am not going to make further comments except to say that what I have heard so far is still impossible for me to make anything of, and the reasons are complex.
 
Snow Leopard said:
A key point still is that Jeff and Jen ended up developing symptoms that are quite atypical of ME or CFS. I don't see why it is controversial to believe that their symptoms were due to CCI and that surgery was the cause of the remission. Perhaps they had rare atypical presentations of CCI - given the non-specific nature of potential neuronal damage, I don't see why it is unreasonable to expect patients to have a range of presentations until their illness becomes very severe.

Over analysing a few words like PEM stopped straight after surgery is mostly meaningless, it is the long term remission that we actually care about.

But it is important to also realise that unless ME patients also develop those atypical symptoms more characteristic of CCI, it means it is unlikely that many or most ME patients actually have CCI as the cause of their illness.
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Exactly.
 
arewenearlythereyet said:
So now I’m really confused ...a change of 2mm is quite small right? In the context of normal being <8.5, 2mm is a big percentage, and Jen refers to differences of hers being 4.8 ...is this difference in readings on different days or difference when the head is angled/moved. What’s classed as a normal range in the general population before surgery is required? And what’s the prevalence of the range of differences? Once it’s changed does it ever change back on its own without the need for surgery?
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This article seems to be the one used as reference for radiopaedia and it indeed mentions a BDI of <8.5 or <12 mm in 95% of the population. It also references to a study where the mean BDI was measured as 4.7 mm. Jen's numbers don't make much sense to me either when compared to the referenced ones, but I'll have to read the full article when I'm less brain fogged. Curiously the same article mentions an ADI of <2 mm was observed in 95% of the population, but from the images it looks like ADI is not the relevant measurement here and not the one Jen was referring to.
 
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