Question to those with neck issues/CCI/AAI etc

[Hip]

Couple more key questions -- I asked him whether Chronic Fatigue (in his opinion) comes first or CCI/AAI. He responds that based on the subset of patients he has seen which complain about both, they later develop CCI/AAI after getting ME/CFS.

That's very interesting, @gm286.

Out of the 20+ ME/CFS patients on this forum who have now been tested for CCI/AAI, it was found that 90% have CCI/AAI.

So that obviously leads to the question: is CCI/AAI a cause or a consequence of ME/CFS?

If CCI/AAI is a cause, then fixing the CCI/AAI with surgery might well cure ME/CFS. But if CCI/AAI is a consequence, then perhaps surgery will not help much.

But it seems from Dr Gilete's observations in Barcelona that CCI/AAI may be more a consequence of having ME/CFS.


So does that mean surgery will not help reduce ME/CFS symptoms? Well, it seems to me that even if CCI/AAI were a consequence of having ME/CFS (and the viral or Borrelia infections associated with ME/CFS), it's possible that the CCI/AAI once it appears could further worsen ME/CFS symptoms.

In other words, when you first get ME/CFS, the CCI/AAI may not be there; but a few years down the line with ME/CFS, perhaps a CCI/AAI slowly manifests, and this manifestation and the brainstem compression it may cause might conceivably then act to further worsen ME/CFS symptoms.

This might even help explain why ME/CFS often progresses to a worsened state over the first few years of illness.

 

[gm286]

I'll try to write down what I've been thinking throughout the day and make something coherent of it. Then I'll have to crash for the night.

First. One thing was pretty clear for me after seeing Dr Gilete. I am not a candidate for surgery right now. He said that I seemed functional. "You look fine. Well, you appear to be fine" or something to that near effect. How do I build on this...? If I'm not a candidate for surgery, then CCI/AAI is not the 'first order of business'. This is a form of simplification.

I have had a slouched neck for the longest time. Well before full on ME/CFS. Perhaps CCI is co-morbid with CFS. @Hip "manifestation" is a good word choice for CCI/AAI (i.e. ligaments / connective tissue 'become' worse). It is a procedural, iterative thing.

At what point did my CCI/AAI 'become' worse? For me, it was several years after my CFS. A kind of crystallization the way I see it -- if you look at Dr Gilete's syndrome list for CCI (and yes they may be generic symptoms but at least they defer right back to the notion of ANS / brainstem compression) I can say that I'm familiar with most of them.

Take the last one on the list "weakness in arms, hands or legs." This is one that I've experienced more frequently and consistently later rather than earlier in the timeline of issues. Same thing with numbness in arms or legs. These are latter day symptoms for me.

Take the very first symptom on the list, headaches, a benchmark symptom for manifest or overt CCI/AAI if you will. Dr Gilete asked if I get them. I said yes. He asks "where?" as in point to the area on the head... This is a frequent and consistent thing for me as a latter day symptom.

In my case, headaches were never a real, noticeable problem around the time of getting badly ill (sudden-onset illness). Even vertigo, or dizziness, which I've experienced more frequently around my late twenties (seven years at least from the time of getting really ill).

Other observation. If CCI/AAI may be posited to worsen CFS/ME, then why couldn't CFS/ME be posited to worsen CCI/AAI? CCI is monolithic. It is a specific mechanism. CFS/ME is thought to be a nexus of illness.

It is always worth asking both sides of the question: at one point does one get better, at what point does one get worse? Consider patients with CCI who also have EDS. My state may not be as compromised (or as clear cut) as a person with EDS, who may also have CCI, who may also have autonomic nervous dysfunction.

A person with EDS has a well understood variation which establishes a probability, 1 in 15, that they will go on to develop CCI due to lax ligaments. Never mind the website's use of the future tense in that statistic -- EDS is a clear genetic expression of hyperflexbility implying direct causality with CCI (without indicating necessity).

This is why I think (I believe) that CFS is worth being understood as many have attempted to understand it previously, as a nexus to better preventing, or even restoring, damaged ligaments (or otherwise).

What was certainly very clear to me (as if it happened yesterday): joint pain (not CCI and well before my neck got worse) right after I got severely ill. A kind of hip pain ensued right after recovering from my illness (2-3 days in bed to recover, passed out for most of it). As far as I am concerned, there has to be some correlation with when I got sick.

My hip pain was probably as consistently evident as Jennifer Brea's neck issues were when she moved or tilted in certain directions and felt that something was undeniably different.

Maybe CCI predisposition + virus = CFS + fibromyalgia (if one wants to look at it the other way around, and wants to include fibro and pain in the equation)..

 

[wholepartthings]

If the muscles in the arms/legs are weak (due to lack of energy), then probably all muscles are affected, even those which should hold the head correctly.

By the way, I got my "CFS" diagnosis about 2 years before an arm operation in which my neck was overstretched (visible in upright MRI).
However, the doctor said during the discussion of the MRI that no operation was necessary, but correct muscle building and he knows the visible scarring of many Lyme patients.

So if there is no direct cause of CCI/AAI (no accident and no problems at birth etc.) I would say that this is simply a result of muscular weakness.

translated with the help of deepl.
Translated with www.DeepL.com/Translator

Very interesting article from Dr. Kurt Müller
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3751012/

Damage of Collagen and Elastic Fibres by Borrelia Burgdorferi – Known and New Clinical and Histopathological Aspects
...
Dysfunction of the Atlaido-occipital Joint
The atlaido-occiopital joint has been reported to be another common and clinically significant site for symptoms [71]. The structural change of the ligaments which fix the atlas to the base of the skull [alar ligaments] or stabilise the dens axis [transverse atlantis liagments], have special significance owing to their complex effects on cranio-mandibular function, vegetative control through sympathetic and parasympathetic nerves, the function of various centres of the brain stem, the induction of increased nitrogen oxide and peroxynitrite formation [72, 73], increased production of pro-inflammatory cytokines and cyclooxygenases [74], and finally also due to dislocation of vertebrae and intervertebral discs and accompanying myopathies [72].

Dysfunction of the atlaido-occipital joint without traumatic damage but correlated to chronic Lb has been described inducing a variety of symptoms [71]. 12 [18,8%] of the 64 patients reported had positive IgG antibodies in ELISA and 17 [26,6%] in immunoblot. IgM antibodies had not been found in any of the cases. In 57 (89,1%) patients the stimulation index (SI) in lymphocyte transformation test (LTT) was pathologically increased (SI > 3,0) in one of the four antigens investigated (B. burgdorferi, B. afzelii, B. garinii, Ospc). A functional magnetic resonance imagin (MRI) scan was carried out on 28 (49,1 %) of the 57 patients with pathological SI in LTT. Structural damage has been described to the alar ligament, the transverse axis ligament included involvement of the spinal cord medulla with mechanically triggered myelopathy as it has been reported in cases following traumatic damage [75]. As published before [76], the number of CD57+ natural killer cells (NK-cells) was determined. 36 (78,3 %) of the examined 46 patients showed significant reduction of this cell type.

Collagen and elastic fibres are essential structural elements of tendons and ligaments.

@gm286

 

[gm286]

@wholepartthings thanks for the article. I definitely think that whether or not CFS or CCI comes first in people with both, the role of viruses is perhaps quasi-undeniable.

This is why moving ahead, I will look for the viral titer testing labs and try to get the case straight on any possible low-level infections. There are a handful of viruses thought to be involved with CFS. And there are only a handful of labs who will test in a sensitive enough way to yield definite answers.

Although PCR tests are considered unreliable (e.g. a standard blood test), I was tested negative for Lyme (multiple times). However, there is ambiguous evidence on my PCR tests for possible EBV and other herpes viruses.

 

[wonderoushope]

I don't know much about CCI/AAI. I just wanted to chime in and I do get neck pain and when it flares up enough I get headaches and migraines from it. I've always had very tense muscles around that area since a teenager.

I used to go to a few osteopaths, but I had to make them not do any manipulation. Even just massaging I would always come away with a headache. I think even just lying down with my head down on those beds plus touching sensitive areas near my neck and shoulders just brings on a headache.

My pain does seem to improve dramatically with diet. I think gluten is an issue for me.

 

[gm286]

@wonderoushope consider getting checked for CCI in the future.

Diet is certainly important. I'm not sure if I have a gluten intolerance, but I had done a relatively expensive intolerance test on multiple foods and a lot of dairy (cow's milk) came back as reactive for me. I am considering going vegetarian actually. EDIT: I checked for gluten on my intolerance list and it was not an intolerance food for me.

Dr Gilete asked me not to have anyone manipulate or massage anywhere close to my neck... He was pretty firm about it. I noticed massage therapists tell me over the years that I had incredibly stiff neck muscles, one of them even saying they were the most stiff they'd ever massaged.

Now I know that it is related to CCI. Either fibroblasts in the tissue or muscle are depleted/worn or the muscles are working to compensate for weak ligaments.

 

[Hip]

Now I know that it is related to CCI. Either fibroblasts in the tissue or muscle are depleted/worn or the muscles are working to compensate for weak ligaments.

Did Dr Gilete say anything about the general relationship between neck muscle stiffness and CCI/AAI?

I've often tended to have taught neck muscles; too much tense muscle tone in the neck and shoulder muscles.

 

[gm286]

@Hip I can't recall who exactly said that muscles work double time to compensate for weak ligaments. It was either his secretary (I am pretty sure she did mention that muscles eventually work harder when ligaments are weak), pulled out of my own presumptions (less likely!), or said by Dr Gilete.

The secretary used a building analogy to explain things to me before I saw the dr. She said the structure of your head and neck becomes unsound or compromised if one of the three building blocks (bone, connective tissue, or muscle) become compromised.

I wish I could tell you straight up if neck tension was mentioned by him. I actually recorded the entire conversation with him (my partner was with me and did this for me). I will consider re-listening to the file, maybe sharing it at some point, etc.

 

[Hip]

Update: I’m currently investigating stem cell / PRP therapy with a neurosurgeon who now deals exclusively with regenerative medicine in Belgium. I had a Skype consultation and he recommended 20 PRP injections up the neck to see if it improves instability
...
The treatment cos is €3,000 and done under local anesthetic. He said 50% of people experience 80-90% recovery and the others are mixed, and try further treatments etc.
I’m trying to avoid fusion surgery if I can.
...
He said 50% of people experience 80-90% recovery

Just responding to your comment in this thread, so as not to take the other thread off track.

This 50% of patients experiencing near full recovery: do you know if this 50% figure is referring specifically to ME/CFS patients treated by Dr Gilete with platelet-rich plasma therapy (PRP), or does it refer to a broader category of Dr Gilete's patients, who have various symptoms resulting from CCI/AAI (but not necessarily ME/CFS symptoms).

It is certainly very interesting to have this non-surgical option to try first.

 

[Pyrrhus]

Did Dr Gilete say anything about the general relationship between neck muscle stiffness and CCI/AAI?

I've often tended to have taught neck muscles; too much tense muscle tone in the neck and shoulder muscles.

In neurology, neck stiffness is a classic sign of encephalitis or meningitis.
It feels just like taught neck muscles, but it actually has little to do with the neck muscles.
For what it’s worth...

 

[Gingergrrl]

In neurology, neck stiffness is a classic sign of encephalitis or meningitis. It feels just like taught neck muscles, but it actually has little to do with the neck muscles. For what it’s worth...

That is interesting, and also for what it’s worth, one of the classic side effects from IVIG is neck stiffness (even worse if you have aseptic meningitis).

 

[Strawberry]

@jeff_w said this:

This is the perfect example! Thank you! I think this thread will be a great example of things to do and NOT TO DO during the investigation. I did recover, but it took a few weeks. And honestly I think I'm still more bobblehead than normal. I made a huge mistake doing this, but it was informative.

Lots of good information and experiences coming out lately.

Also, welcome to @gm286

 

[brando]

Just responding to your comment in this thread, so as not to take the other thread off track.

This 50% of patients experiencing near full recovery: do you know if this 50% figure is referring specifically to ME/CFS patients treated by Dr Gilete with platelet-rich plasma therapy (PRP), or does it refer to a broader category of Dr Gilete's patients, who have various symptoms resulting from CCI/AAI (but not necessarily ME/CFS symptoms).

It is certainly very interesting to have this non-surgical option to try first.

This quote was from Dr J in Belgium (the neurosurgeon now using exclusively regenerative treatments) talking about PRP's effect on instability, not people ME/CFS specifically

 

[Capecodder]

I know this thread is inactive, but I got substantially worse after first, my PT doing manual traction, then recently, using a hard cervical collar. Prior to the collar the back of my neck hurt. After using the collar, my scalenes in the front of my neck are spasming, as well as my pecs.
I have EDS. Had an upright MRI, but was only read by local Neuro.
My issues started w Chiro adjustment. Had no idea I had EDS then.
Next steps? Should I consider prolotherapy?