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

Some people are worried about the safety of the community. Some others don't see a reason for it. And some don't care.

 

I was stating a fact. Members who would like to contribute to this thread are being prevented from doing so because they feel uncomfortable with all the labels flying around.

Yep, that's what I'm talking about. Whatever dog piling is.

It's all very well people calling for politeness and using labels like dog piling, aggressive and hostile in the same post. We need to be clear who it is who is closing down the conversation and preventing others from posting here.

 

When we figure out the physiopathology. I'm guessing it won't be from an persistent pathogen. Even Ron Davis ruled this out, unless he's found new evidence to show otherwise?

 

Does this include people with viral infections vs ME patients?

 

If carried on long enough, a debate can push people with opposing beliefs to a deeper level of understanding. This thread has helped me understand the different views of people here. I appreciate and value the differences of opinion. JenB’s comments have been helpful as they clarify her position. The majority of the questions and comments have been interesting and helpful. What I don’t find helpful is people accusing others of this and that because the negative labelling of behaviour feels like the debate is being shut down.

 

That's fair enough, I shouldn't have said that. I don't know what dog piling is either but I think it means everyone piling up on one person. What I should have said is that the majority of posts in my feed in all CCI related threads are critical of JenB whereas the posts that are positive or speculating on potential mechanisms are few and far between. It is understandable why this creates an unpleasant atmosphere for some people.

 

There’s an old mantra in medicine that reminds doctors not to grasp for exotic diagnoses: “When you hear hoofbeats, think of horses, not zebras.”

"Though surgery wasn’t needed to save her life, there were procedures that could improve it".

"Swedish called Delashaw a “world-renowned” surgeon sought by patients from across the country. And fusions were a routine part of his care — records show he did at least 140 of them in 2014".

 

Phew!

 

This is just an observation but Jen shared on twitter a while back after mold avoidance and Valcyte in 2014 her mental stamina and cognition were much improved and one tweet described herself as for the most part by then not suffering cognitive PEM or rather have greater than average cognitive stamina. She had said for much of the last few years - presume this may have not been possible in the period after her thyroid surgery last year when she got worse again until her CCI surgery shortly after - she has been able to work equivalent to a full time working week from home*. Yet until her CCI surgery her walking ability was very limited and she struggled with standing due to POTS. @JenB, please correct me if I have misrepresented this in any way.

*edited to add - I am starting to doubt I did read Jen use the words she worked a a full time working week. I remember her using the word workaholic. I googled today and found this tweet. She explains the context was she was safer being a workaholic than doing fun things as she didn’t monitor herself so well when doing a brief fun activity so could crash. However, I can’t today find anything with her specifically talking about doing a full working week from home. I will wait for Jen to clarify and apologies if I got this wrong. I did find the tweet where she said she had better than average cognitive pem and for the most part didn’t have it in the last few years after certain treatments whilst her walking ability remained very limited and she struggled with standing due to POTS.

 

Sorry @Hip i seem to have missed your post.

I think @Trish replied pretty much as I would.

I would also like to say though that I have worked for quite a few years in academic research and product development/innovation, the latter of which required all of the things you suggest. I am more than familiar with brainstorming. However is brainstorming without limits that useful?

I never used “brainstorming” in research....rather we had peer to peer expert discussions, challenging each other’s ideas in an open way to stress test a hypothesis...this would often be done quite casually over a coffee going back and forth. The key thing for this to work is for the originator of the idea not to be precious about challenging their own thoughts and take value from their peers/experts.

In product development I occasionally used ‘brainstorming” but quickly found that brainstorming without structure or facts pretty much led nowhere other than a good team building exercise. I’ve seen it used by others to try and bring teams together to “get engagement” for a fixed idea that is seeded in. I find seeding rather manipulative though. I use it occasionally, mainly when I want to drive engagement, team building and focus the team on an objective. To make it work well though you need to be quite structured and provide stimulus material etc etc.

I would say that most of my innovation work required very little brainstorming. Brainstorming without boundaries or targets is pretty pointless unless you move on to feasibility. Nowadays it’s fallen out of fashion ...it’s more about using data, facts and hunches to drive insight (which is similar to how I started off in research interestingly).

I don’t think anyone has poured cold water on ideas here, rather this is a normal process in the world where I’m from anyway.

I agree though that if people come with a fixed idea and are unwilling to take criticism or act defensively to protect their pet theory this could ‘feel’ intimidating. To not expect a critique though is definitely not scientific ...more like trying to set up a belief system?

I’m sorry if anyone feels like this is suppressing discussion ...it seems like a long thread with a lot of participants to make that claim though?

 

Yes unfortunately hurt feelings are sometimes an unavoidable consequence of a rigorous skeptical investigation into a scientific hypothesis or empirical study. And certainly eventually all science needs to be scrutinized under a skeptical light.

However, when a new scientific or observation idea emerges, and has not yet found its feet, it really needs to be given a chance to blossom in people's minds, so that we can better understand the significance of it. You need to make those lateral connections in your mind, and this is best done when the tone of discussion is positive, enthusiastic and creative.

By lateral connections, I mean for example: how does the CCI/AAI brainstem compression relate to all the other stuff we know about the brainstem in ME/CFS? How does autonomic dysfunction due to this compression relate to all the other info we have about the autonomic nervous system in ME/CFS? And so forth. I'm still trying to make these connections in my mind.

Skepticism is important too, but because it inevitably carries a negative tone, it can kill the creative thinking process. And it can make people close up, or make them stop communicating. I'm not knocking skeptical analysis per se, I just suggesting that at this embryonic stage, heaping on too much criticism too early is not conducive to the scientific process.

Those are certainly legitimate concerns. But perhaps we should also look at this from another perspective:

Worldwide we can estimate there will be around 22,000 ME/CFS patient suicides each year, as a result of the sheer hell that ME/CFS can be. (One study showed the suicide rate in ME/CFS is 6 times that of the general population, so from that you can work out this 22K figure).

Thus we are not in a neutral situation; for every year of delay in finding a cure for ME/CFS, 22,000 more die.

Now it's possible that if more ME/CFS patients start exploring CCI/AAI surgery, there inevitably will be some cases of negative outcomes, and perhaps even the occasional death due to post-surgery complications. That's to be expected from any major medical treatment. But that thought has to be balanced against all these annual deaths from suicide, not to mention the misery of millions more who don't kill themselves, but nevertheless live for decades with this horrible disease.

 

I agree, eventually you have to examine each idea proposed during the brainstorming mode in the cold light of day, when you are in a more down-to-Earth and critical mood.

I remember reading about a theoretical physicist with bipolar: during the manic stage of his condition, when had the dopamine high of mania, he'd come up with dozens and dozens of creative, lateral thinking scientific ideas. Dopamine is the neurotransmitter of creativity and lateral thinking, so he used his bipolar dopamine boost to good purpose.

But then during his down periods, where he felt depressed and low, he'd examine his own ideas in a very sober and skeptical mood, which would enable him to separate the wheat from the chaff.

 

Sorry, I missed your post here. Please move my two above posts to that thread if you think it's appropriate. Though I think those comments are also pertinent to this thread too.

 

What I mean is any mechanism (which may not be the same thing as cause) which results in the symptoms described, for example, in the International Consenus Criteria and would be likely to result in a diagnosis of ME, based on those criteria.

It is likely that spinal fluid leaks and cervical stenosis can cause these symptoms (a la Peter Rowe’s work). It is likely CCI can as well, given the now four remission and one improvement stories (I believe there are more). So can Chiari. It’s unclear to me whether intracranial hypertension can cause these symptoms but it has been implicated in “CFS” and can certainly cause some of the symptoms, as can MCAS. All of these conditions are also associated with hypermobile Ehlers-Danlos Syndrome, and many of them are diagnosed by super specialists, further complicating the picture. (E.g., Ian Carroll at Stanford and Scvienk at Cedars Sinai focus on spinal fluid leaks.) However, none of these conditions require PEM nor is PEM likely to be a part of the clinical picture in all cases.

 

Why does it seem highly unlikely?

 

This logic seems obvious to me yet so often gets lost.

Yup.

People have also started to re-contextualize facts in a way that a find super interesting as social psychology but also quite frustrating as the human living this. I’ve said a million times I had an acute viral onset. Now I have to constantly correct people when they describe my case as traumatic or “structural, not viral.” Similarly, I have people saying I don’t have ME because the “folks at Stanford say it’s mitochondrial” even though I’ve had numerous abnormal metabolomics testing that comport with findings in the literature or clinical practice. There is a human bias/tendency to alter or discard facts that don’t fit one’s paradigm. I think it’s far better to let things that don’t fit or don’t make sense continue to float there, not making sense, rather than rush to judgment or closure. Eventually, new information or a better explanation will come along, if we are willing to sit with the mess and discomfort. Saying I never had ME or rejecting our stories as implausible/doesn’t make sense/doesn’t fit with what I think I know allows for a very quick return to the status quo, but I think the even greater opportunity lies in trying to truly grapple with and understand why all this is happening.

Here is Karen, a British PwME who recently had surgery in Spain. If I were standing outside of all this, I would be deeply skeptical and these stories would worry me for all the reasons people have pointed to here. I have always hated recovery stories. Now I am one. Here is another. There will be more. I hope “they” can figure out something constructive to do with all of this soon, whether that’s proving, disproving, subsetting, caveating, etc.

https://twitter.com/user/status/1134165235210870784

I think PEM is a form of dysautonomia, or at least it was in my case. The folks at the Workwell Foundation who do the 2-day CPET think this, too. The brain is inappropriately telling your cells to go into anaerobic metabolism (possibly via the system that tells cells when the body is in the state of hypoxia). It has analogies to other forms of dysautonomia such as POTS (inappropriate sensing and signaling around HR, BP, vasodilation), sleep disturbances, and central apnea. My experience with the latter is what helped me get to this place. After my traction and ICP bolt tests I literally woke up and thought, “Oh my God. PEM is a form of dysautonomia!” Then Workwell came out with their “chronotropic intolerance” review article a few weeks alter where they flat out said this and also said we have to stop looking at downstream stuff in the blood and need to focus on the brain. Anyway, it’s still very speculative theory but (and at the risk of reinforcing the idea that I have a secret media campaign strategy ), this is something I also plan to write about further. I don’t know if this is true for me or more generally, but it is certainly in line with my diagnosis and surgery experience and would explain in a very parsimonious way nearly all aspects of my case.

 

So I appreciate the likes but really am honestly asking these questions, not being rhetorical. I am severely ill. I was able to read posts on this thread from bed for several days but was too sick to sit up or formulate my questions. Took great effort yesterday to sit up, join this group, and write my post, and I paid for the effort. I would be most appreciate if anyone could answer.

The post about the surgery in Seattle increases my concerns.

Thanks.

 

Then it is equally possible that all of us are misdiagnosed and that neither our criteria, nor our experts, nor any of our research/lab findings to date is up to the task, in which case we truly do know nothing and cannot ever know if any of us actually has ME.

ME is a clinical criteria. I met the criteria. *In addition* I have a whole lot of labs. If I was misdiagnosed, then CCI is such a twin sister wife disease to ME, capable of causing the same symptoms and labs as ME after an identical onset, that we should all be studying it right quick.

 

Hi, Jen, Is it okay on this forum to embed Karen’s video/tweet without her permission? I thought that was frowned upon wrt to forum rules. Also, I understood Karen was misdiagnosed with ME but has EDS.