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

I am one of maybe no more than a score of musculoskeletal physicians worldwide who have made connective tissue structure, pathology and biomechanics a special interest. I used to write the chapters in textbooks on connective tissue physiology. I still sometimes get things wrong but the situation here is pretty clearcut I think.

Along the length of a ligament the maximum stretch is set by the collagen fibres - like a rope. Just like a rope you cannot lengthen it without damaging so many fibres that it tears. So we can discount inflammatory or enzymatic effects leading to ligament lengthening without snapping along their length.

The place where a ligament gets longer during growth, and yes, @Skycloud, during pregnancy a bit, is at its attachment or enthesis. There is a transition zone of cells that are neither bone cells nor ligament cells but sort of 'superglue cells'. In inflammatory diseases like rheumatoid arthritis this area can undergo change so that the bone at point of attachment is eroded away and the ligament may possibly lengthen. I say possibly because the normal mechanism for ligaments getting lax in inflammatory conditions like RA is something quite different. It is that the bearing surface of joints and discs are eroded away, making them loose in the way that a worn axle gets loose - the ligaments are actually unchanged.

The long and the short of this is that for basic physics reasons ligaments can only get laxer if bone or cartilage is removed either at the attachment or a bearing surface. (During growth the situation is different because the attachment is growing - paying out new ligament on demand. So during childhood ligaments can become lax through growth.)

Removal of bone or cartilage shows easily on an x-ray if it is enough to allow laxity. In RA and pregnancy we see the bone dissolved. In EDS as far as I know there has never been any suggestion of this. There would be no reason because the genetic basis is in defects in the structure laid down during growth. There is no suggestion of a genetic tendency to inflammation.

I do not know how to interpret a sense of increased laxity after an acute illness. The only thing I can think of is that if one loses weight the mobility of certain joints increases because they are naturally limited by muscle or other tissues (elbow flexion for instance).

I would be very surprised if real EDS specialists thought this could occur. But then I would distinguish EDS specialists in the sense of clinical geneticists, who by and large do not see hEDS because there is no gene, and the 'EDS specialists' who diagnose all hypermobility as 'hEDS' and associate it with widespread pain and fatigue. I have reason to think the latter mostly do not know anything much about connective tissues.

 

Interesting, thanks @Jonathan Edwards.

 

Very interesting, thank you!

What is the actual mechanism in ballet dancers when they do become more flexible due to stretching?

I will add this study, they are partly geneticists, if they are „the real thing“ is absolutely not for me to decide, after all, I am a baker.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6335943/

I do absolutely trust your expertise insofar that what you say has merit, but I definitely trust my own experience and those of other patients more, why is that?

It is relatively clear cut, if your hands could not touch the floor at all and your joints did not subluxate before a certain factor like mentioned above and afterwards they did and you miracoulously are bendy like a yogi and this happened on 3 separate instances and many other people report the same, than it is more than just a coincidence. (not definitely but likely)

50 so called specialists told me that it is impossible to get sicker by moving my body and that there is no cfs, 99% these of all specialists would tell me the same thing at this point in time after being bedbound for 2 years.

I do not believe that you must have a genetic disease for having EDS like symptoms and pathology and that secondary factors could lead you there.

Also having talked to THE TOP EDS GENETECISTS, the picture is not as clear as many present it, there are reported cases with only heterogeneous mutations in any given EDS identified variant that still have the full picture of the disease! Interesting isn‘t it?

I am grateful for your input. ty.

 

A very good friend of mine was once a soloist at the Royal Ballet. She and my wife go to open days at the ballet school to spot new talent. To have any chance of success ballet dancers have to start as children, often quite young. As far as I am aware all the flexibility they show is a combination of genetics (mobile children find ballet easy, non-mobile children give up early) and training the tissues during growth. I do not know of any data but it is likely that ligament lengthening during growth depends on use. We see excessive laxity into certain positions in some cases of infantile paralysis for instance.

Most ballet dancers that will go on to be professionals are identified for their talent by age about 12 and certainly age 15. I do not think there is any need to suggest that they get more flexible after that, once they have stopped growing.

I think there may be a confusion here. In hypermobile people, some of whom are classified as hEDS, there is every reason to think the mobility is genetic (unless they have been to ballet school maybe). They do not have single gene mutations of a dominant type as in classical EDS. But that just means that their mobility is determined by several genes making a small contribution, with different ones contributing different amounts in different individuals. That is still genetic but not Mendelian genetic.

 

Ok so following on from my previous post here

And now having caught up with what you said earlier @Barry & @Jonathan Edwards too....
here

Barry responds to JE...

I wonder... Do people think - & I ask this mainly of @Jonathan Edwards since he is likely to be the one answering most of the questions if we did it, if it would be worth having a kind of brainstorming thread along the lines of 'what else could be causing the "CCI" remission"?'
I know it'd be unlikely for laymen to come up with the answer, but sometimes the less expert can spot something that's so obvious to the expert that they don't even notice it.

I dunno it's just a thought.

ETA I'm sorry I appear to have gotten confused & posted this in the wrong thread, we appear to be having almost the same conversation on 2 diff thread & i cant work out whats from where now.... it's the follow on from the thread about Jen's blog on medium I think, but i'm so sorry I am too fried & exhaust to work out how to move it all now it took agaes making all the quotes follow on properly I think I've mistakenly quoted from 2 threads at same time. I'm so sorry for the confusion, if any mod has time to move the whole post for me i'd be most grateful

 

I am not sure I have a lot more useful to say on this. Too many unknowns.

 

No worries it was prossibly a daft idea. Clutching at straws.

 

I started at a quite young age but was rather on the stiff side. I'm more of a pirouette turner and high jumper. The dancers that are flexible fit more the hEDS picture. Actually many of my former colleagues do. It also makes me wonder where to draw the line between hEDS and healthy Über flexible dancers.

My hamstrings were always very short. I could only touch the floor with my hands if I was very warmed up but even then barely and only occasionally. They did get a bit more flexible at a later age but that felt more from training my big muscles rather than the tendons or ligaments. A bit the same way as beefing up but then in flexibility if that makes any sense. My tendons and or ligaments/joints however felt stiffer as I got older. So ligaments/joints wise I think Jonathan is correct!

 

As a student I found touching my toes nigh on impossible. I was fit, healthy and did all that ‘80s Aerobics stuff complete with leotard and leg warmers. I once decided that I “needed” to be able to touch my toes. It took me 6 weeks of daily stretching and effort to finally manage it. As soon as I stopped this I lost that ability.

Yet now in my 50’s after having ME for 7 years, I have found that I can touch my toes! (Okay I can only just touch them, but even trying to dab down on a sort of bounce I could never get even close before now.)

Why is that?

Is it that inactivity loosens ligaments etc? I certainly am much less active than previously, and my strength is much reduced too. Did those 3 years when I was walking only 500 daily steps have an effect? I would have thought that would have made me MORE inflexible, not less!

??

 

A very interesting question.

So to answer it we want to know what limits toe-touching.

Toe-touching, or more than that, palm to floor touching, is one of the criteria for hypermobility and is usually assumed to be a sign of lax ligaments. But toe or floor touching is, I suspect, almost entirely dependent on maximum hip flexion. Knee extension beyond straight ('swayback') would not help much. Spine flexion would help a bit but to really get down to the floor you really need your whole spine vertically downwards - i.e. to have more or less 180 degrees of hip flexion.

Now hip flexion is not determined by ligaments because the hip has no surrounding stabilising ligaments because it is a ball and socket. Its range is entirely limited by how much the muscles on the outer side of a movement can be stretched or how much muscles on the inner side get in the way. That may be why we can improve toe-touching with exercises but we cannot, for instance, increase knee or elbow extension (fortunately).

Spinal ligament range probably does play a part but I am pretty sure that being able to touch toes when one has been doing a bit of gym work has nothing to do with ligaments. And maybe if muscles are not trained mobility can actually increase because they do not get in the way so much.

 

It makes sense to me that the ability to put one's palms flat on the floor comes from the hips. I have always been able to do it easily. After a hip replacement less than a year ago and the other one probably not too far off, and quite advanced spinal degeneration, that hasn't changed.

I was an aerobics fanatic for years and for long periods have done no exercise at all. It never changed my palms on the floor party trick. Don't ask me to sit cross-legged though. Never could.

 

I could always touch my palms to the floor but have never been very flexible otherwise. Puzzling. Long legs and arms but comparatively short back.

 

Wow that is interesting. I've always had difficulty touching my toes. As a kid, after doing daily stretching, I could only touch them for a split second at a bounce! I tick every other box in the hEDS criteria for hypermobility plus hernia/prolapses/gut issues/slow healing sores and bruises/stretchy skin etc... I've never bothered to get a diagnosis as I don't think there are any local specialists educated in it and they'll just tell me to see a physiotherapist, who were the ones that suspect I have it in the first place.

I just tried to touch my toes on the off-chance I could touch them now, but nope! Although, I was surprised at how far I could go considering my tight hamstrings and sore back. I've had ME for 6 years, maybe I should try again in 12 months

But seriously, I find it really fascinating that you can now touch your toes Keela. And with the recent research mentioning collagen degradation, there might be something to it.

 

I’ve had ME for over 25 years, I still can’t touch my toes.

 

Before I fell ill I could touch my toes. Now it is imposseble.

 

This is why I’m staying sceptical about all this stuff.

 

I have always been able to put my palms on the floor with ease.

 

Normally the test is without bending your knees.

(this was intended as a joke)

 

@Michiel Tack I meant without bending my knees