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

I can also do this ... but only if I'm standing a couple of steps down from the top of the stairs!

 

I also started being able to touch my toes after many years of ME but it felt as if I did not have the muscle tone to stop my body bending.

 

Love the reference to leg-warmers and leotards! Been there done that. FWIW I just tried touching my toes and can easily, but not hands flat on floor though, no way. I think I have always been able to touch toes though. I was good at gymnastics when I was wee, but not hypermobile AFAIK.

 

Hello Dr. Edwards, @Jonathan Edwards

I thought you maybe want to comment on this?

Thank you.


Stretch-associated Injury in Cervical Spondylotic Myelopathy: New Concept and Review
Fraser C. Henderson, M.D.1
Department of Neurosurgery, Georgetown University, Washington, District of Columbia

01 May 2005
Abstract
THE SIMPLE PATHOANATOMIC
concept that a narrowed spinal canal causes compression of the enclosed cord, leading to local tissue ischemia, injury, and neurological impairment, fails to explain the entire spectrum of clinical findings observed in cervical spondylotic myelopathy.
A growing body of evidence indicates that spondylotic narrowing of the spinal canal and abnormal or excessive motion of the cervical spine results in increased strain and shear forces that cause localized axonal injury within the spinal cord.

During normal motion, significant axial strains occur in the cervical spinal cord.
At the cervicothoracic junction, where flexion is greatest, the spinal cord stretches 24% of its length. This causes local spinal cord strain. In the presence of pathological displacement, strain can exceed the material properties of the spinal cord and cause transient or permanent neurological injury.

Stretch-associated injury is now widely accepted as the principal etiological factor of myelopathy in experimental models of neural injury, tethered cord syndrome, and diffuse axonal injury.
Axonal injury reproducibly occurs at sites of maximal tensile loading in a well-defined sequence of intracellular events: myelin stretch injury, altered axolemmal permeability, calcium entry, cytoskeletal collapse, compaction of neurofilaments and microtubules, disruption of anterograde axonal transport, accumulation of organelles, axon retraction bulb formation, and secondary axotomy.
Stretch and shear forces generated within the spinal cord seem to be important factors in the pathogenesis of cervical spondylotic myelopathy.

 

I don't think it is saying anything particularly unexpected or surprising. Cord damage is likely to be a mixture of pressure and tension. That does not change the way we understand the clinical picture. Also he is talking about cervical myelopathy from narrowing in the lower cervical region which is a different problem from CCI.

This looks like an abstract presented at a meeting? So it sounds like a talk intended to put across a new view. It does not seem to be linked to any new data. Seems a bit like re-inventing a wheel.

 

Well, how would you test for a hypermobility of the ligamentous structures of the spine that allows „unphysiological“ movement as in so far that it „stretches“ the cord?

The little understanding of biomechanics that I have makes me wonder whether seemingly little hypermobilities in between vertebrae could cause „exponential“ stretch of the cord?


That is what is so unbelievably puzzling to me, why would someone (or the whole medical community) think that this is of no potential interest to look into more precisely:

A stretch of the cord results in damage, YES, nothing new you say.

A spine that allows for too much movement due to lax ligaments that could result in stretch and therfore damage is for whatever reason still completely unheard of or not looked into, one could make the argument that this is a potential blind spot.

If you ask me (nobody does) it is statistically IMPOSSIBLE that there are no folks with such instabilities that cause stretch injuries of the spinal cord due to this „weakness“.

(Instability is actually a bed term I think)

When we assume that length/distance X is the maximal length the spinal cord can stretch without injury and your ligamentous and spine structure allow for length/distance Y (X+1mm), how would injury be visible for the physician?

My personal educated but not professional guess is that it would not be more than a slightly visible (if at all) hyperintensity on a MRI that radiologists would not even comment on?

How would you test for such hypermobility in relation to „healthy mobility“? Maximal flexion and extension on a xray?

So many questions.

(these issues could also only present as segmental instability elsewhere and not just in the cervical region I would say)

Thank you.

 

I think you are confusing two issues. Henderson is talking about the situation where there is pressure on the cord from disc herniation or osteophytes. that traps the cord at certain points. In this context normal movement of the spine may pull at particular points and cause shear. Everyone in medicine recognises that.

I think you are talking about a situation where the spine is just very mobile. As far as we know this causes no problems at all. Circus contortionists do all sorts of strange things with their spines and do not suffer as far as we know. If there was a problem Olympic gymnastics would be banned.

Hypermobility in itself, as far as I can discover from the literature, does not cause any problems unless there is frank distortion of the anatomy as in a dislocation.

 

The circus and bendy people made me wonder too, I do believe this could be different from what I am talking though, not sure.

These people are not required per se to bring their spine in a position that is automatically unphysiological, that for sure is a misconception. Also I do not have any numbers but there seem to be quite a lot of people who were former ballet dancers with me/cfs (or whatever this could be connected to) issues

I also do not believe there is data of health outcomes for circus gymnasts, maybe for classical gymnasts but I doubt it.

Pursuing Boxing or American Football are not exactly a good idea to become a rocket scientist later in life either, still nobody would come up with the idea to ban it due to its inherent health risks, therefor the „argument“ that it would be banned is definitely not a good one in that case.

Most of what I say is pure speculation, I wish someone would try to prove me right or wrong, someone who is unbiased by his potential income increase after the „hypothesis“ is proven correct.


Thank you for your thoughts!

 

I agree that our main problem is lack of evidence, so everything is speculation.

But we are seeing people speculate without knowing basic anatomy and clinical neurology and saying things that are entirely implausible

I am completely unbiased because I am on a pension and have no financial interest in any of this. I just find ME interesting and I do not like to see people being misled by those who do have a financial interest. I also have the advantage of having worked alongside many of the professionals who figure in the story. I worked with the surgeon who trained Henderson. I worked with the physician who trained Hakim (as well as myself).

 

Thank you.

I am not sure you alluding to me when talking about these people.

It would be a fair statement when it comes to „advanced neurology“ but not so fair when it comes to anatomy in my case.

In any case, it would be interesting to know if you see a potential problem in the cord being potentially stretched in hypermobile people, I am kindly asking for your personal opinion, not proven facts.

Thank you.

 

I thought this might be interesting:

 

No, only the people who are putting out hypothesis about ME as if they were medically knowledgeable.

I see no reason to think the cord would suffer with stretching alone in the context of a hyper mobile spine. As Henderson implies, you need also to have some sort of entrapment at a particular point like C6 or the craniocervical junction. Below about L2 only roots would be entrapped so lumbar discs probably would not do it.

 

I tried to find out exactly what that meeting was. Nothing comes up in association with Royal Society of Medicine itself. It appears to be a meeting run by a syringomyelia and Chiari foundation and the UK EDS organisation. It may be that they have used RSM facilities for a private meeting.

Henderson has an association with the syringomyelia and Chiari group.

 

Just read that Naviaux agrees that CCI fits with his cell danger response theory and plans to meet with Dr Kaufman in 2 weeks to discuss intersection of mecfs, CCI and cell danger. This was reported on a me Facebook group and attributed to Naviaux’ clinical study coordinator.

Can someone who is smarter and less ill than I help me to understand what this means?

 

I am not sure it means anything much. It does not make any sense to me. If a problem is due to brainstem compression it is not due to a metabolic defect and vice versa.

 

I think that the most prudent way to move forward with CCI hypothesis would be to conduct research from random patients meeting the CCC.

i get worried when scientists start making assumptions based on anecdotal experiences. This is simply not how science is supposed to work.

 

Just dropping this Twitter thread here:

https://twitter.com/user/status/1189967356568563712



https://twitter.com/user/status/1189980463156387840

 

Observation and the history of the lived experience is where all good science starts from. No good having a model that works in the lab but does not translate in reality.

We have to be careful here as cooking up a storm of dismissing people who have lived experience, is what we are all fighting against?

Jen is right and from past history we know things get missed. So many of our children get dismissed as CFS/ME and NICE now are funnelling children into overlap of Functional Neurological Disorder or Cognitive functional disorder - where no scans are offered and actively discouraged. Those children with obvious hEDS because of the genetic component/autoimmunity and the obvious overlap with fatigue are getting missed and many children are suffering years of medical abuse because of this.

Is hEDS/EDS separate to ME? or is the result of infection ongoing inflammation caused by mast cell? Or are they all part of ME? Do we want to shove those children down a rabbit hole or under a bus because they don't fit someones idea of ME?

We need advocates to show their concerns and nudge doctors into thinking and questioning. Does it matter that they are posing a question and get taken down? I think it does for 101 reasons mostly it silences other to ask important questions or pose points that need to be raised.

I spend my time trying to get things in the open and I am fuming that this is happening. Just this week we have many new threats of mothers with children with complex and multisystem conditions that cannot go to their doctors because there legitimate concerns are dismissed and belittled.

One mother with a child with Lymes and signs of autoimmune/mast cell that needs to use an Epipen, has to question every time she needs to take her child to the A&E because she is said to Fabricate or Induce skin reactions and enjoys the power of using the Epipen. She herself has to wear a collar due to instability in her neck, which also brings into question her motives. She cannot get looked at by a doctor because of the dismissive nature of the medical profession, and then what do I see when I get on here? Dismissing concerns!

Lymes has just come out as having an impact on the brain and yet still we do not understand the impact on the body even after treatment https://www.sciencedaily.com/releases/2019/02/190205090533.htm


More than 1 in 10 people successfully treated with antibiotics for Lyme disease go on to develop chronic, sometimes debilitating, and poorly understood symptoms of fatigue and brain fog that may last for years after their initial infection has cleared up. Now, in a small study, Johns Hopkins Medicine researchers report they have used an advanced form of brain scan to show that 12 people with documented post-treatment Lyme disease syndrome (PTLDS) all show elevation of a chemical marker of widespread brain inflammation, compared with 19 healthy controls.


and this also effects connective tissue. My vet is well aware of this but my doctor not so much. Vets have found that different limbs can go lame at different times, yet humans are blamed as FND with CFS/ME when clear signs of Lymes are there. The primate research shows us a lot of information and yet we belittle due to someone being diagnosed with ME and latter found that they had different yet comorbid problems?

Sometimes we as mothers know more than the doctors and yet you want to dismiss our understanding, our questions and yet again put us in the firing line? You dismiss one, you dismiss us all.

NO ONE HAS THE ANSWERS BUT SOME QUESTIONS IN THE RIGHT PLACES MAY HELP OUR CHILDREN. How many have cranial instability ? More than you think! Yet they are silenced due to this behaviour.

We know Lymes is being investigated for being used as warfare in the USA and we know birds and other animals carry the ticks. We also know that Lymes has been hidden and lacks diagnostic ability in the UK, with Doctors even with the bulls eye rash seen, children are dismissed. We know the UK tests come up with a false negative. Is Lymes really part of ME?

We also know these marks are the same as hEDS or mast cell dismissing stretch marks is now beyond a joke and is very harmful and again the problem is that there is not enough research

Why does this matter because there are hundreds of children suffering and their lives in danger with these skin and joint problems and it does not matter what you call the disease or how it starts, they are suffering and it is about time we look at the whole picture and not just a small piece of history we want to cling onto.

LET SCIENCE FIND THE ANSWERS BY US ASKING THE QUESTIONS AND LIVED EXPERIENCE SHOWING US THE JOURNEY.

We need doctors to look at the links and possibilities while research looks for the biomarkers and tests and we should stop verbally beating up advocates and doctors who are looking beyond blaming the patient and putting it down to beliefs and support looking at the connections and how they fit together, because what ever ME is, it is bigger than just one impact and it will have a different or many names, when research does its job.

Lymes, flaccid paralysis, EDS hEDS, Mast cell the list is endless are all being put under CFS/ME and patient blame along with demonising mothers, this has to stop and protecting children has to happen.

Scans should be encouraged and advocates supported, all conditions looked for and symptoms explored to what is the cause. The starting point when flue has lasted more that 6 weeks or fatigue is suspected is CFS and then if PEM present it should sound alarm-bells for ME and it needs to be recognised as imperative to understand what could happen if CFS is not taken seriously in the first instance.

This sort of behaviour on Twitter is putting children like Bethany, Daniel, Gigi and Angus and 25,000 other children in danger, when diagnosed with CFS. We need to see the syndrome and break it down into the components of symptoms. At the moment CFS is seen as a no name illness and braking families up with the mother blame that comes with denying the lived experience of those with symptoms that mimic, what some demand ME is.

We should all be working together not enjoying putting advocates down, because for the last 30 years, that is what has held research back, harmed patients and let others die awful deaths.

 

I don't see anyone putting JB down. She has every right to share her own personal experiences, but she is not the authority on M.E. and needs to be called out when she crosses the line.

 

There are definitely instances of people putting JB down, but you may not have seen them depending on who you follow on twitter!