Have you ruled out Chiari or Craniocervical Instability (CCI) as a cause of your CFS

[sb4]

I have been trying to figure out how an infection can trigger cervical spine problems and then CFS. It's a long shot but apparently bacteria like Lyme consume hyaluronic acid and leads to connective tissue problems. This, of course, combined with EDS / whiplash etc could then lead to CCI.

Anyone smarter than me know if this is worth chasing down? @jeff_w @Hip

I know some (Klinghardt) believe that Lyme is much more prevalent than currently thought, and even if not Lyme, perhaps similar virus/bacteria consume connective tissue which leads to CCI/etc.

 

[Lisa108]

I never thought about an infection as a trigger/cause for a cervical spine problem (and then leading to ME or CFS).
In my view, the cervical spine problem would come first (inherited or whiplash injury). But who knows?

 

[Hip]

if not Lyme, perhaps similar virus/bacteria consume connective tissue which leads to CCI/etc

I know coxsackievirus B infection results in increased levels of matrix metalloproteinases (MMPs), which are enzymes that break down connective tissue. CVB infection can increase MMP-2, MMP-3, MMP-8, MMP-9 and MMP-12.

Indeed, as soon as I caught the Coxsackie B4 virus which appeared to trigger my ME/CFS, I developed sudden onset receding gums (periodontitis), which is linked to elevated MMPs. One of the treatments for periodontitis is low dose doxycycline 20 mg (Periostat®) daily, which inhibits various MMPs.

 

[tornerose]

Throat infection is listed in the literature as a possible cause of CCI/AAI, and as a trigger of CCI/AAI in groups that are prone to developing instability (like people with Down’s syndrome). My understanding is that this is believed to occur through inflammation, and not via direct pathogen damage. Is that what you are saying @Hip? (That stuff is way too difficult for me...)

I’ve been wondering if also mast cell activation could cause inflammation and damage to the connective tissue... Though I haven’t found any literature supporting that theory. Anyone know?

 

[Hip]

My understanding is that this is believed to occur through inflammation, and not via direct pathogen damage. Is that what you are saying @Hip?

Yes, these MMPs can be secreted by the immune system in response to infection. This study for example found that coxsackievirus B4 infection triggers MMP-9 release, with the MMP-9 mainly originating from macrophages and neutrophils (which are immune system cells).

These various MMPs can degrade connective tissues such as collagen and elastin.


MMP-9 incidentally features in Dr Ritchie Shoemaker's treatment protocol for mold illness. If you have elevated MMP-9, Shoemaker-trained doctors may recommend you follow a no-amylose diet, to help bring MMP-9 down.

 

[sb4]

Very interesting, perhaps when we look we will find that infections other than coxsackie + Lyme cause connective tissue problems.

Interesting that you mentioned receding gums. I remember looking in the mirror one day a few weeks after starting this illness and I was legitimately worried my teeth where going to fall out. In a few weeks I went from normal gum line to significantly receded.

Also throat infection (tonsilitis) is what triggered this off for me. It's interesting that this is shown in literature to be a potential cause of CCI.

 

[Sidny]

I never thought about an infection as a trigger/cause for a cervical spine problem (and then leading to ME or CFS).
In my view, the cervical spine problem would come first (inherited or whiplash injury). But who knows?

Interestingly since acquiring multiple infections I have experienced a progressive loss of connective tissue. I've also recently felt much spinal instability much of it around my neck and base of skull as if it's hard for me to hold my head upright. Would be interesting if chiari itself is the result of the infectious process and maybe why in me/cfs the symptoms worsen overtime for many.

 

[sb4]

I recently came across this ( http://www.theilcfoundation.org/wp-content/uploads/2012/04/Driscoll_Theory_EDS_-_Online3.pdf ) theory that links into CCI and Chiari.

Basically it's saying that EDS is causing the vessels that hold and filtrate CSF to become lax causing lack of CSF outflow and increased pressure in the brain. This causes downward pressure on the brain, brain stem, etc which can lead to chiari and, I assume, CCI, which of course can lead to dysautonomia/POTS and CFS.

It also says that a virus can cause the tipping point of this disease by entering through the blood brain barrier due to EDS causing more permeable BBB. The virus then damages the arachnoid villi (by degrading connective tissue?) which of course makes the Idiopathic Intracranial Hypertension worse.

Interestingly enough I don't have many headache or head pressure symptoms, just POTS. Apparently some people have had some success using Acetazolamide but there doesn't seem to be much mention of it on these forums.

@jeff_w @kangaSue @pattismith

 

[kangaSue]

@sb4 Your link also mentions CCSVI (Chronic Cerebospinal Venous Insufficiency), there is another little known aspect that can play a part in this which also causes autonomic dysfunction (POTS at it's worst), left renal vein compression (Nutcracker Syndrome - NCS).

Interestingly, NCS is somewhat prevalent in those with EDS and in MS.

The theory with CCSVI is that veins bringing blood from the brain and spine back to the heart become too narrow, causing some of that blood to leak into the brain tissue.

Dr Sal Sclafani, a Vascular Surgeon with an interest in MS, presented at the the 2017 International Society of Neurovascular Diseases Annual Scientific Meeting.

He defines CCSVI as a clinical syndrome caused by inhibition of cerebrospinal venous hemodynamics. Sclafani stated that there are several causes of spinal venous congestion and numerous radial veins, which are valveless, until the vertebral veins. His focus is on renal vein compression (Nutcracker Syndrome) where the left renal vein transverses over the aorta. Dr Sclafani believes that many neurological symptoms are associated with Nutcracker Syndrome and said in his experience of treating 100 patients with MS, 60% have a greater than 50% stenosis of the renal vein.

Depending on the route taken by the blood being returned to circulation from the left kidney, it can increase venous pressures in the spinal tract as well as in the abdomen and pelvis and surgical resolution of left renal vein compression reduces venous pressures and can also resolve POTS symptoms.

 

[kangaSue]

By the way, having a 50% narrowing of the left renal vein in imaging is likely to be considered just a natural variant of the vein and unless you have stenosis somewhere around the 80% mark, it likely won't get a mention in any report either. Also, if you don't have a clued up sonographer or technician, it's not uncommon for a significant stenosis to be completely missed if it's not something specifically being looked for.

 

[sb4]

@kangaSue Very interesting, thanks. The question is how do they all relate to each other, and which syndrome/disease is causing the others. You could say that it's the lax vessels in the CSF that cause high intracranial pressure; This then causes blood to become to difficult to pump into the brain causing CCSVI; this means less blood is coming out of the brain causing left renal vein to contract (???). Or you could start at any other point and say that that's the starting point. Perhaps it's all these things at once since they all relate to EDS and some people seem to achieve remission from treating any one of the causes.

Do you have any opinion on the drug Acetazolamide? Suppose to reduce intracranial pressure.

 

[kangaSue]

@sb4 Being a connective tissue disorder, those with EDS tend to have stretchy veins that are more easily subject to compression by stronger arteries or other organs and structures.

Left renal vein stenosis is a physical vascular compression abnormality in most cases. The angle at the junction of superior mesentery artery is seen to be at a much reduced angle to normal and compressing the renal vein so this is relatively simple to identify with a Doppler Ultrasound or CT scan.

I don't identify as having EDS and haven't had cause to try acetazolamide so don't have an opinion on it other than to say that, from reading in different forums, it looks to be a patient specific thing that either helps or it doesn't.

 

[jeff_w]

Hi Everyone,

I've been away from here for about a month. A lot of good things have happened with me. I've also been learning a lot more information about these neurosurgical issues, and I will share everything here.

There are so many replies to get to. I'll catch up with everyone's private messages, tags, and posts over the next few days.

 

[alkt]

we all certainly hope a lot of good things happen for you. you have worked hard for a better future for yourself . and it is nice to hear good things.

 

[lafarfelue]

So glad you're doing so well! Very very veryyy happy for you

I've also been learning a lot more information about these neurosurgical issues, and I will share everything here.

Thanks so much for continuing to post and share info with us all. Looking forward to this info. Will you share this info in a separate post/thread or in this thread (or both?)? Just wondering in terms of getting the information out to as many eyes as possible

 

[Jackdaw]

I am interested in this topic. I have had ME for 14 years. I have PEM and it often is accompanied by a swollen feeling in the top of my spine. Also a sore throat. I have had a severe relapse and am bedbound. Being upright always been difficult. My joints are the opposite of mobile. Always stiff. Is this condition a possibility for me? Very ignorant, apologies.

 

[MichaelK]

Hi @jeff_w ... great to hear that you are constantly improving and also thanks for your incredible effort to share your knowledge. You have already been linked in another Thread. In that thread I am writing for @MartinDH who is in a very severe condition (100% bedbound, no communication possible anymore). Currently there is no chance to do the whole procedure with MRI (...).
But we are thinking about doing the Trendelenburg-Position, Traction Test and buying a neck brace/neck stretching device. What would you suggest to do first? Has the Traction Test to be done by an expert (which one?) or can I do it? Which neck device did you use first to get out of the severe condition?

Thank you so much in advance.

Best regards
Michael

 

[lafarfelue]

Tagging @JenB here in case you get notifications for the forum. I saw you mention on Twitter wanting more positive CCI stories and this is one of them (even if it's titled Chiari)!

 

[Rufous McKinney]

Did any of you see the Episode of 20/20? In which this doctor was widening the skull opening in patients with CFS/FM. this episode was around 2001 perhaps see link here: I remember watching this and it really resonated as I feel that this SQUEEZE in the base of my skull/spine is like where all this pain and inflammation is radiating from. Both chiari and spinal stenosis are new to me: I will be looking into this further.

https://abcnews.go.com/2020/story?id=123951&page=1

 

[Rufous McKinney]

At any rate, my craniocervical problem is entirely correctable with neurosurgery. I'm scheduled for surgery at the end of the month. But for now, I'm in a halo vest that's keeping my head from sinking onto my spine.

In the halo, I no longer have POTS. I no longer have PEM. My ME/CFS might have been, all along, a neurosurgical/structural problem.

Will your medical insurance cover this surgery? Curious