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

Kitty said:
According to Wikipedia (not the most reliable source, I agree, and not necessarily even up-to-date), none of the multiple lawsuits against Dr. Bolognese has been resolved. I don't know how common it is for surgeons in the US to face lawsuits, though – it might be anything on the scale from exceptional to routine.
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That’s an astonishingly long time. Must be awful for the people bringing these cases to have to wait so long for resolution. If the claims are found to be true then that’s also an awful lot of new patients that are being seen in the meantime.
 
According to this article, 19% of neurosurgeons have to deal with one malpractice claim each year. It says that "the vast majority of these claims are resolved in favor of the surgeon".
 
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Minnie said:
I have wondered about this too, if perhaps Jen deep down was not entirely convinced she had ME and wanted reassurance/confirmation.
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It would be unwise for anyone to be convinced that they have ME/CFS, especially in the early years with the disease, when you are trying to figure out what illness you might have.

Many conditions can mimic ME/CFS symptoms, and a diligent patient will consider and get tested for the most common conditions that can produce ME/CFS-like symptoms — conditions which include hypothyroidism, anemia, lupus, hepatitis B and C, celiac disease, growth hormone deficiency, vitamin D deficiency, macrophagic myofasciitis, multiple sclerosis, and numerous others.

There was a case on Phoenix Rising of a patient who thought she had ME/CFS for 10 years, but eventually tests revealed she had growth hormone deficiency, and she was fully cured within a month of starting growth hormone replacement therapy.
 
3A58919D-09F0-49B1-883D-AAA67819B18A.jpeg And among neurosurgeons, spine surgeons are most likely to get sued.

“Elective spinal surgery cases constitute the majority of litigation.” https://thejns.org/view/journals/j-neurosurg/106/6/article-p1108.xml

That of course doesn’t tell you anything about these particular cases, just that lawsuits are not uncommon. You can look up the number of malpractice judgments any doctor has by going to their state licensing board. I actually did this a while back and found Henderson had one judgment, Bologense one, the other surgeons on Jeff’s site, zero (at least in the last ten years).

I imagine it’s very difficult to win one of these cases, though, especially given all the disclaimers you sign, etc. I imagine most people settle...

The attached graph is probably a reason to try very hard not to have neurosurgery unless you really, really need it!
 
I'm not sure looking at the number of lawsuits, or the number of won lawsuits, is that helpful. If we judged the BPS brigade on the number of lawsuits brought and won against them by dissatisfied patients, we'd all be queuing up for CBT and GET. The interesting thing about these reports of law suits against Bolognese isn't necessarily the outcome, but the frequency, and the perspectives from colleagues and dissatisfied patients that they contain.

Those promoting a consideration of CCI surgery etc seem to place a lot of emphasis on patients' anecdotes and perspectives. Well, we can't just look at the positive ones. Here are some more to consider.
 
TiredSam said:
I'm not sure looking at the number of lawsuits, or the number of won lawsuits, is that helpful. If we judged the BPS brigade on the number of lawsuits brought and won against them by dissatisfied patients, we'd all be queuing up for CBT and GET. The interesting thing about these reports of law suits against Bolognese isn't necessarily the outcome, but the frequency, and the perspectives from colleagues and dissatisfied patients that they contain.

Those promoting a consideration of CCI surgery etc seem to place a lot of emphasis on patients' anecdotes and perspectives. Well, we can't just look at the positive ones. Here are some more to consider.
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Agreed. And this is likely the tip of the iceberg. What is unusual about these cases is how visible they are. I imagine very few lawsuits actually wind up in the press. We don’t know the frequency of lawsuits brought against any of these surgeons. We know very little even about these public cases, and nothing about the ones we can’t observe. I’m sure people who did settle had to sign NDAs.

I do think there’s a lot more information contained in the word-of-mouth discussions, most of which are on Facebook. The majority of patients who are dissatisfied or have bad outcomes never sue at all. However, many of them do talk. Their stories are important. Before I had surgery, I was able to read pretty deep in the archives of some of these groups which stretch back many many years, and it gave me a very good picture of what could go wrong and what the consequences of that might be. Anyone considering surgery should do this.

It’s also worth noting that these surgeons all use different techniques (and have modified them over the years), so when you look at these archives, the types of complications or long-run difficulties people develop tend to follow distinct patterns. Conditional on having surgery, there are better and worse ways of doing it but no one knows what those are. Surgery (at least in the US) is not regulated the way that, say, a drug is regulated. It cannot be mass-produced. It’s an artisanal product. And so surgeons have a lot more latitude to offer you *their* technique. I have no idea how a patient is supposed to assess whose technique, or medical device, or pair of hands is “best.”
 
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Elestar said:
I have concerns about one of the main surgeons involved in these surgeries (Dr Bolognese),

https://www.google.co.uk/amp/s/www....nese-milhorat-article-1.172605?outputType=amp
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Trish said:
Hi @Elestar. I can't access the article you have linked. Can you clarify when the article was published, and by what publication, and whether it gives any links to other sources.

The content you have posted is very concerning.
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This is the direct link to the article (Aug 09, 2009)
https://www.nydailynews.com/news/ca...osurgeons-bolognese-milhorat-article-1.172605

And the Web Archive version
http://web.archive.org/web/20160427...osurgeons-bolognese-milhorat-article-1.172605
 
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Jonathan Edwards said:
Which picture looks the safest position? I think it has to be the sitting position because in this position the odontoid peg is directly underneath the lip of skull bone and so cannot move up and press on the brainstem. On the other hand in the supine (lying face up) and traction positions the odontoid is further back and if it moved up it might slide up behind the bony lip and press on the brainstem. The brainstem is in the black space to the right of the bony lip on the first picture.

So it looks as if fixation in a traction position is a bad idea. This is something that used to worry me twenty years ago when patients came back from surgery apparently fixed in a worse position than before.

Traction will pull the neck straight and reduce kyphosis due to slippage at lower levels (not shown here) and it will pull the head back from the maximum flexion position that would be most dangerous (and associated with the smallest clivo-axial angle) but unfortunately it also seems to pull the head away from the truly safe position of normal sitting bringing it a little bit further forward.
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Are you saying that the smaller the bdi is, the safer, because the smaller position allows for less horizontal movement, and therefore less retroflexion of the odontoid?

Because the paper we are discussing found that the cxa was more acute (kyphotic) when upright and the BDI was also smaller , in the same group of patients, on average.

So it seems like a smaller BDI is correlated with a more acute cxa. And a more acute cxa leads to kyphosis. So is this indication that a sufficiently small BDI would mean the skull is sinking down, leading to Less space for the odontoid process , therefore causing it to slip backwards compressing the brainstem ?

I admit the BDI thing has me a little stumped because in the consensus statement, which @Hip provided in the post i quoted, they only speak of a pathologically high BDI, not pathologically low or lower limit.
And in most of the literature i could find, BDI is only spoken of being pathologically high (as in thr case of total atlantooccipital dissociation which has a far higher mortality rate than CCI). Usually as in above 12 mm.

However , if that paper established that a) these changes in measurements are associated with improvements in symptoms (as they did with x ray fluoroscopy while doing traction) then I would like to see those measurements considered as indicators of pathology although it would also be good to do a blinded study.

However you also stated that you think its obvious how an acute cxa could be causing pathology and one doesn't need any modelling (such as the modelling in the Henderson paper) to account for that. What I think is not obvious is how acute the cxa needs to be to create problems , and that's what the modelling was trying to establish.

So again, if upright imaging shows both a pathological cxa (as opposed to the supine position ) and a reduced BDI, perhaps they are making an indirect inference that reduced BDI is associated with kyphosis?

I am still curious about the history of these measurements. I don't know if really strong normal ranges have ever been fully established. It seems like before the consensus statement hundreds of measurements were used and the consensus statwment was an attempt to simplify measurements. So while it may be a fair criticism that these measurements need double blinded studies to show clinical value , I'm not sure if the measurements used for diagnosis of cci before the consensus statement were validated in the way you suggest is important.

Michiel Tack said:
Can the persons who think this consensus is important point out where it can be found and who the exact authors were?
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Hip did in the post i quoted below.
Hip said:
A copy of the consensus statement provided in this post.
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I was trying to find double blinded studies assessing the utility of the cxa and I found none, but I did find this interesting study suggesting the use of a different measurement (clivo palate angle)versus cxa that does have controls, but the paper is short and doesn't provide much indication of how they originally differentiated BI and controls to start with.

As for the idea that traction would not help because most of the damage in CCI is caused by neuronal death that is irreversible, a)what is the evidence for that, b) arent there examples of neural strain or compression where the strain is not enough to cause large amounts of neuron death but is enough to cause other issues (maybe raised glutamate , hypoperfusion, abnormal immune signalling) and c) couldn't even intermittent compression cause many significant symptoms?
 
debored13 said:
Are you saying that the smaller the bdi is, the safer, because the smaller position allows for less horizontal movement, and therefore less retroflexion of the odontoid?

Because the paper we are discussing found that the cxa was more acute (kyphotic) when upright and the BDI was also smaller , in the same group of patients, on average.

So it seems like a smaller BDI is correlated with a more acute cxa. And a more acute cxa leads to kyphosis. So is this indication that a sufficiently small BDI would mean the skull is sinking down, leading to Less space for the odontoid process , therefore causing it to slip backwards compressing the brainstem ?

I admit the BDI thing has me a little stumped because in the consensus statement, which @Hip provided in the post i quoted, they only speak of a pathologically high BDI, not pathologically low or lower limit.
And in most of the literature i could find, BDI is only spoken of being pathologically high (as in thr case of total atlantooccipital dissociation which has a far higher mortality rate than CCI). Usually as in above 12 mm.

However , if that paper established that a) these changes in measurements are associated with improvements in symptoms (as they did with x ray fluoroscopy while doing traction) then I would like to see those measurements considered as indicators of pathology although it would also be good to do a blinded study.

However you also stated that you think its obvious how an acute cxa could be causing pathology and one doesn't need any modelling (such as the modelling in the Henderson paper) to account for that. What I think is not obvious is how acute the cxa needs to be to create problems , and that's what the modelling was trying to establish.

So again, if upright imaging shows both a pathological cxa (as opposed to the supine position ) and a reduced BDI, perhaps they are making an indirect inference that reduced BDI is associated with kyphosis?

I am still curious about the history of these measurements. I don't know if really strong normal ranges have ever been fully established. It seems like before the consensus statement hundreds of measurements were used and the consensus statwment was an attempt to simplify measurements. So while it may be a fair criticism that these measurements need double blinded studies to show clinical value , I'm not sure if the measurements used for diagnosis of cci before the consensus statement were validated in the way you suggest is important.


Hip did in the post i quoted below.
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As someone whose BDI used to be lower and who is vastly better at a “moderate” BDI, I do think the BDI should have a lower bound. It just has not been conceptualized this way and there’s no research to tell us what the lower bound should be.
 
debored13 said:
I admit the BDI thing has me a little stumped because in the consensus statement
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I also noticed that sometimes BDI seems 'too big' and sometimes 'too small'. I think what I said in a previous post holds. The change in CXA just reflects change in posture and the BDI is measured in a way that gives spurious indications of 'functional settling' with posture because it becomes oblique.

I find this statement useful:
Scott, of Boston's Children's Hospital, said he was alarmed some five years ago, when parents began showing up in his office with kids who'd undergone what he called "huge operations with negative [normal] MRI studies" at the Chiari Institute — with long incisions and giant medical bills.

Scott said he took his concerns to the American Association of Neurological Surgeons ethics committee. Nothing happened

None of the pictures I have seen in these discussions of CCI show anything I would think needs an operation. I was prepared to believe I was missing something but if a neurosurgeon at Boston Children's agrees I think I have reason to think I was not.

Prior to this 'consensus' we decided to operate if we could see the cord distorted or if the peg of axis was sticking out above the atlas. You do not really need measurement if you can see the problem in front of you.
 
So the Henderson paper i cited earlier in the thread, which discusses surgical corrections of cxa but doesn't have a control group, did cite this paper that involves a form of mathematical modelling of deformative stress on the brainstem at different angles, that i think may be important: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2940090/

Anyone here know what finite element analysis is? @JenB , @Hip ?
 
Cheshire said:
You can keep up with all your speculations, as long as you cite studies with no control group or mathematical model, that's all it is: speculation.
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Which goes back to the earlier interesting discussion in this thread regarding how to evaluate evidence.

Mod note: please continue the discussion about how to evaluate evidence in general on the linked thread.
 
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Michiel Tack said:
I don't know where these figures are from but the consensus documents says that 135 or less is only potentially pathological.
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Yes, that's right, as I understand it, pathological range craniocervical measurements alone are not sufficient for a CCI diagnosis.

Rather the diagnosis of CCI is made via a combination of factors, which includes the patient's craniocervical measurements like CXA, Grabb-Oakes and BAI, but also involves factors like whether or not the patient has the symptoms of CCI (the so-called cervical medullary syndrome symptoms, especially severe headaches and neck pain), and whether there is a reasonable explanation for the lax ligaments at the patient's craniocervical junction.

Dr Henderson in this 2012 video at 13:12 says that the above 3 (bolded) components are required for a diagnosis of CCI.

Dr Henderson in this 2019 paper on diagnosing CCI in the patient population with hereditary hypermobility connective tissue disorders says that CCI diagnosis also depends on whether the patient displays certain neurological deficits that are linked to CCI.


A list of reasonable explanations for the lax ligaments is the following:

Acute causes:
• Physical trauma (like a car accident or sporting injury)
Chronic causes:
• Developmental Chiari
• Occipitalization of atlas (congenital fusion of the atlas to the occipital bone of the skull)
• Klippel-Feil syndrome (congenital musculoskeletal condition involving fusion of at least two vertebrae)
Degenerative or inflammatory causes:
• Rheumatoid arthritis
• Lupus
• Neoplasm (an abnormal growth of tissue, such as cancer)
• Infections
• Surgery
Genetic hypermobility connective tissues disorder causes:
• Hypermobile EDS
• Marfan syndrome
• Stickler syndrome
• Down's syndrome


A list of neurological deficits associated with CCI found here (midway through document):
  • Tender C1-C2
  • Decreased gag reflex
  • Hypoesthesia to pinprick
  • Decreased vibratory sensation
  • Hyperreflexia
  • Dysdiadochokinesia
  • Romberg
  • Difficulty with heel to toe walking
  • Abnormal gait
  • Weakness
  • Loss of abdominal reflex
  • Babinski, Hoffman’s signs

That is how Dr Henderson diagnoses CCI, and Dr Gilete I believe follows similar criteria. Dr Bolognese's criteria also include examining the cervical medullary syndrome symptoms, but he additionally adds the further criterion that a patient must improve under invasive neck traction before he considers the possibility of fusion surgery. (Note that invasive neck traction is the gold standard; home over-the-door traction devices and physiotherapist applied traction are not as definitive as invasive neck traction).

Bolognese in this 2018 video at 1:12:44 says that some patients have pathological measurements indicating CCI, but show no symptoms. No surgery is advised for these patients.




Michiel Tack said:
I suspect it's possible for people like gymnastics or ballet dancers to have a CXA lower than 135 but be perfectly healthy.
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I am not entirely sure about the differences between regular patients and EDS patients when it comes to the craniocervical measurements. Obviously EDS patients have a greater range of joint motion than normal people.

I read that about 1 in 15 people with EDS will go on to develop CCI due to a lack of connective tissue support at the craniocervical junction. Ref: 1
 
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JES said:
Everything else we discuss is mere speculation, if we set a hard limit that we need to have blinded and controlled (plus replicated) evidence, in case of treatment preferably phase 3 studies. Everything Ron Davis does is on the same rationale mere speculation.
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Yes, it is. Is someone claiming that it isn't?
 
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