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

High hydroxyproline levels would be an effect of collagen breakdown, not a cause.

But in any case it makes no sense to relate collagen breakdown to ligamentous laxity. This is where people are simply not understanding the anatomy. Ligaments are like elasticated cords. The collagen provides the non-elastic base that has the tensile strength. If you dissolve away an elastic cord it does not become lax. It remains intact until finally it snaps. Nobody with ME has ligaments that have snapped. In EDS the ligament is built during growth as a lax structure, it does not stretch. There is simply no mechanical way for collagen dissolution to produce ligamentous instability of the sort seen in EDS.

 

I worry about that too. There are plenty of examples with this disease alone. And it makes me wonder what the pathology will explain and what it won’t explain. Hypotheses sometimes fly as high as kites...

 

Yes, PEM is characteristically delayed, the feeling of being slammed into ground the next day, after exertion, and it is an all over exacerbation of symptoms. But I‘d like to make two further points. It is not, in my experience, ‘after a period of being okay’, I never feel okay. And also I experience what I call a microPEM where my muscles can often burn on trivial exertion, washing hair, brushing teeth, lifting kettle. It is my ‘normal’. I think this is what Ramsay meant by muscle fatigability.

 

I meant OK in the sense of being able to manage - better than, as you say, you can when 'slammed into the ground the next day'. This is what people repeatedly tell me occurs.

 

Yes, there are different things happening and if it was better understood it could give clues to where the dysfunction causing ME exists.

There is a background lack of function which could be said to be where we are mild, moderate or severe. Then we try to do extra and get a flare of PEM which makes us feel sicker and more limited.

At other times I try to do what I usually manage but come to a stop mid action; a minute or so later I can continue. This type of stop is why my usual life is limited it is just further till it happens. If I am full of adrenalin, reacting to an emergency say, I can do much more than I expect but this is always followed by a crash.

The final strange thing is when I do something and feel normal at the time then three days later I can't get out of bed and realise it was actually beyond my limit.

It is not just prolonged recovery from exertion as many papers assert it is delayed start of the problem then an out of proportion and abnormal reaction - mental effort can cause physical problems and vice versa.

 

The US ME/CFS Clinician Coalition: Guideline - Diagnosing and Treating ME/CFS, discussed here, https://www.s4me.info/threads/us-me...ne-diagnosing-and-treating-me-cfs-2019.11080/, includes CCI as a differential diagnosis (under neurologic disorders).

 

I think that is what happens when you get a collection of 'experts' round a table and chuck in everything they suggest, including some stuff that probably should not be there.

 

I am (still) trying to come back in a few more days with a longer post as of why I think that many syndromes and disease states are indistinguishable from each other and will probably (unfortunately) be for a long time and many of them are now diagnosed as ME/CFS.

From my humble perspective, the only thing that could literally prove this wrong (and I really do hope for it to be wrong!) is a unifying mechanism for PEM, which I highly doubt exists.

It is somewhat likely at this point that ME/CFS is a cake from which other disease states that have been identified will be cut out, given a long enough time axis, there will be nothing left of it or people will fight for what it REALLY is (happening already), which is totally insane.

The main issue of people that want to unify this syndrome and put in a box is clear, they want a trajectory for a biomarker and a treatment, the problem being that this is impossible to happen if you do not define your patients into clear subsets that have emerged from clinical observation in the last 3 decades.

The disease criteria are NOT ENOUGH, it does not matter which ones.

That is why, CCI is not part of me/cfs while at the same time being part (it does not matter if primary or secondary at this point) of me/cfs until proven otherwise.

How can I say that? That is very easy to answer:

Because there ALREADY have been people diagnosed with me/cfs by the best in our field and got better or recovered after fusion surgery!

What does that tell you?

At this point it is impossible for me or you or anyone else to say what is what.

The lack of science for any given theory is no proof for it being wrong, to use that argument (no matter how long the time axis and how sure one is that „we should have found that already if being true“) selectively is deeply unscientific and the actual reason for why me/cfs has not been looked into for decades!

Apart from that some comments here are worrying because they are incorrect (mortality rate of fusion surgery for example, there is meta data) and I will follow with science to show that.

Do I personally believe CCI is me/cfs or is an issue in a significant part of the me/cfs population?

No, but I do not know, neither do you!

I do have (very) severe me/cfs, eds, pots, mcad, sfnp, cci, aai. I have unofficial information that 50% of the very severe subset of me/cfs patients in the Stanford Group have EDS, and some probably CCI. To me this seems a little too high for a random comorbidity, at least in the most severe.

Keep it open! ty!


PS: I consider myself as a „Ramsay ME“ patient, just to make it more complicated.

PPS: I do not believe fusion surgery (no matter who does it) is a good idea for patients like myself but if you stop breathing and have issues swallowing, what is one to do?

 

You have expressed some interesting points @butter.

Just two points in reply.

We have discussed here in the past the fact that although people have improved in terms of symptoms dramatically after cervical fusion that does not necessarily tell us there was anything wrong with the neck prior to fusion or that ME symptoms were due to a neck abnormality. The situation is extremely complex. There are other explanations.

So there is no reason to include CCI as part of ME/CFS. There is no similarity in the clinical picture.

You may be referring to previous comments of mine that the mortality rate for cervical fusion in RA in the 1980-2000 period was about 50%. It was, but that was because we mostly operated on people who were in a dire state and we were dealing with a progressive disease that continued despite surgery. Nobody has suggested that the mortality rate for operating on people with minimal abnormalities in their necks would be that high. (From the images I have seen some people may be getting surgery with normal necks.) But there are likely to be a few deaths. And the real concern, as mentioned in the Liverpool based review, is that the restriction of movement due to surgery at the skull base is likely to cause secondary damage to the lower neck that may generate serious problems over a period of 50 years.

 

That is a great concern of mine as well
I don't think people are enough aware of that.

When I was still dancing if I locked up my neck I could be sure that my back would follow and visa versa. The surgery must have a similar effect and on the long term possibly devistating effects.

 

Can somebody point me to this Liverpool based review, I seem to have missed it sorry!

Thanks in advance,

 

https://www.ncbi.nlm.nih.gov/pubmed/28961036

It has been quoted earlier on this thread or another, not sure which. I have access to full text but not sure if someone has found open access.

 

Thanks. It seems I was confused because the paper is just a short editorial. By the words 'Liverpool review' I thought there might be an extensive review of the best use of methods and treatment recommendations on this.

Perhaps such a review by experts would be indicated, given how prevalent CCI diagnoses and theories are in the ME/CFS and EDS patient communities and the potential harm it can cause.

 

thank you!

Was not aware of this paper, unfortunately have no access, can someone post the text here maybe?

 

https://twitter.com/user/status/1170917646209957888

 

We probably should not post the whole thing for copyright reasons. For me it would be against College rules. But somewhere a few days back pretty much all the relevant paragraphs were pasted in to a thread here. Sorry not sure exactly where. It really does not say much other than that.

 

This should be it:

https://sci-hub.se/https://www.ncbi.nlm.nih.gov/pubmed/28961036

 

Thank you!

Dr. Edwards, you mentioned that ligaments more or less (I am paraphrasing here) either snap or are the way they are predestined by your genetics and that you doubt that that an inflammatory process could increase the laxity of this type of tissue.

I have to say I that my own experience (and that of a hundred patients with EDS that I spoke too, not exaggerating here) says otherwise, but I can absolutely not prove it, I also do not know if that process that changed my ligaments and or joint mobility is of an inflammatory nature, but I do know the process exists, such as there is a sudden worsening in my and other patients joint laxity after „crisis“ like infection and/or antibiotic use.

This is an observation that many EDS clinicians also made.

I have nothing to back it up, just the observation.

There is a very interesting study though that most people are not aware of, it postulates the hypotheses that heds could be an inflammatory disorder:

 

This has been niggling at me - I thought that hormonal changes in pregnancy (and perhaps the menopause?) could affect ligaments. Maybe that’s an old wives tale, but it was told to me by midwives in an antenatal class and by a GP back in the early nineties. I’m not able to research this myself - is anyone able to confirm one way or the other?