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

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Yes, and actually a SPECT scan is one of the scans Dan Peterson does on all of his patients. Mine showed hypoperfusion.
As you indicate there are some studies that reported hypoperfusion in ME/CFS, but if this was what's causing the enormous disability associated with this illness and hypoperfusion is something that we can actually measure, I would assume that the results stand out more starkly than they did in the studies we have.

This is actually a more general point. ME/CFS causes enormous disability in most patients. It can do that for years without showing much abnormal on standard medical tests. We even have very severe patients, who look as ill as human beings can be, yet their medical tests seem relatively normal.


So I would assume that indicates that whatever is causing the illness is something that we can't see or measure very well with the tools and tests that we currently have. So a theory that proposes that the disability in many ME/CFS patients is caused by a problem that would be visible on these medical tests (like a SPECT for hypoperfusion or an MRI for structural damage) seems rather improbable to me.

This question is really interesting but I don’t fully understand it. Can you explain more?
Don't know if it's a good question really, but I was wondering: if posture makes a big difference and traction can cause spectacular symptom relief wouldn't we see more variability in ME/CFS? Like patients getting worse or better depending on whether they lie down more or sit with a different posture etc. Or isn't that how it works? I remember that you said some symptoms worsened depending on how you hold your head etc.


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
I don't think that website is a reliable source. I contacted them because I thought some info they provided was inaccurate. From their response, it seems that they thought CCI was a condition almost exclusively associated EDS. I wrote about this on the other thread.

The range of CXA in the healthy population is 160 to 145
Range normally means from minimum to maximum, so that doesn't seem right. Jennifer used the studies that reported a CXA in a healthy population, simulated them and came up with an estimate of 3-4% of healthy controls that have a CXA lower than 135. What you report seems more like a range of 1 standard deviation from the mean taken from one of these studies.

The mean CXA reported by this Swedish study seems a bit low but it's almost identical to what Bothelo & Fereira reported in healthy controls (148°± 9.8°) and within one standard deviation of all the other estimates in healthy controls Jennifer summarized on MEpedia. So I think it's correct to say that it looks rather normal.

In the Bolognese and Milhorat study that i posted in this thread and another thread, all of the supine measurements (cxa and others) were within normal range, and then when taken while upright, were quite different and clearly abnormal.
I suspect the reference values refer to supine measurement, no? If upright measurements show more abnormal values, that would also be a bit worrisome because if people are misinterpreting these, it might result in overdiagnosis of CCI.

I just think that it seems like neurosurgeons may see themselves more as artisans than scientists and be less interested in proving their findings than getting results clinically though.
Yes, this is what worries us.
 
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Don't know if it's a good question really, but I was wondering: if posture makes a big difference and traction can cause spectacular symptom relief wouldn't we see more variability in ME/CFS? Like patients getting worse or better depending on whether they lie down more or sit with a different posture etc.

Of the 53 ME/CFS patients positive for CCI in our survey, 36% experience either transient paralysis (eg, breathing muscles fail) in certain head/neck positions, or a worsening of symptoms in certain head/neck positions. So there is head/neck position sensitivity in some ME/CFS CCI patients.

Interestingly enough, more than half the patients with such head/neck position sensitivity had retroflexed odontoid (a type of CCI in which the odontoid its tilted so that it pokes into the brainstem).




Range normally means from minimum to maximum, so that doesn't seem right.

It's just me who put the numbers 160 to 145 in that order. I think you would prefer it written 145 to 160. The full range for CXA is this:

Normal CXA = 160º to 145º, borderline = 144º to 136º, pathological = 135º or less.

Sources: Bolognese 2015 video at 14:28. Also Henderson 2016, Henderson 2018, Henderson 2018 video at 8:17.



The mean CXA reported by this Swedish study seems a bit low but it's almost identical to what Bothelo & Fereira reported in healthy controls (148°± 9.8°) and within one standard deviation of all the other estimates in healthy controls Jennifer summarized on MEpedia. So I think it's correct to say that it looks rather normal.

Interesting. I am not quite sure why that mean clivus-canal angle figure of 148º for healthy controls differs from the mean CXA figure of 158º for healthy controls I mentioned earlier, which I have just found the reference for: this paper says:
Nagashima and Kubota directly measured the normal CXA as 158.2° ± 9.8° in normal adults

Maybe different populations might explain it. Your Bothelo & Fereira study finding 148º was conducted in Brazil, whereas Nagashima and Kubota was conducted in Japan.

Another factor might be a possible a difference between the clivus-canal angle of Bothelo & Fereira versus the clivo-axial angle of Nagashima and Kubota.

According to this paper, there are different ways to measure this angle:
The CXA is variably defined as the clivus vertebral angle, the clivus canal angle [15], the clivus-cervical angle, and the clivus-axial angle. Botelho describes the CXA as the angle between the line extending from the top of the dorsum sellae to the basion, and the line between the infero-dorsal to the most superodorsal part of the dens. Others have used a line drawn through the mid potion of the odontoid.

With the goal of standardizing terminology and methodology, the subject of the CXA was recently addressed in multidisciplinary consensus statement that describes the CXA as the angle between the clivus line and the posterior axial line.

Though as far as I can see, the clivus-canal angle looks the same as the clivo-axial angle.
 
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So I would kindly want to ask whether Jeff or Jen could direct me to the scientific articles that do describe CCI as something that closely resembles ME/CFS.

Not sure if this question has been answered, but here is a list of 32 cervical medullary syndrome (CMS) symptoms I found from various sources:

Headache •
Neck pain
Bobble head
Muscle or joint pain •
Weak legs •
Weak arms or hands •
Numb legs and back •
Numb arms/shoulders •
Unsteady walking gait •
Became clumsier •
Chronic fatigue •
Tire very easily •
Memory loss •
Blurred vision •
Double vision •
Urinate every 1-2 hours •
Nausea and vomiting •
Irritable bowel •
Gastrointestinal reflux •
Gastroparesis
Choking on food
Swallowing difficulties
Slurred/hoarse speech
Balance problems •
Vertigo
Dizziness
Raynaud's •
Hearing loss
Ringing in the ears •
Snoring
Sleep apnea
Often wake up in sleep

The ones which are suffixed by the bullet symbol • are those also considered ME/CFS symptoms, going by the comprehensive list of ME/CFS symptoms found on page 104 of the full version of the Canadian consensus criteria.
 
https://jnnp.bmj.com/content/39/4/381

Abstract
Syncope precipitated by sneezing in an adult male associated with an Arnold-Chiari type I malformation and basilar invagination presents a clinical problem in the differential diagnosis and pathological anatomy of Valsalva-related syncope. An abnormally acute clivoaxial angle, small foramen magnum, and type I Arnold-Chiari malformation appear to be a combination of features intolerant of Valsalva-induced changes in cerebral volume, brain-stem position, CSF fluid dynamics, or blood vessel relationships. Proposed mechanisms of pressure transmission to the area of intracranial pathology are discussed.

If someone could dig up the full text of this id be grateful. Its an old case study on a patient with chiari but also an acute cxa--which doesn't prove anything per se but does show that they were thinking about cxa as a proxy for brainstem deformity back then...
 
Thanks. "
The possibility of a strictly mechanical ana-
tomical explanation should also be considered.
It has been reported that flexion of the neck in
patients with Arnold-Chiari malformation at
the time of surgery may result in respiratory
arrest (List, 1941; Mullan and Raimondi, 1962).
Perhaps other cardiovascular events resulting in
syncope could be produced as the result of
percussion of the ventral medulla on the clivus
or temporary vascular occlusion causing brain-
stem ischaemia. An abnormally acute clivo-
axial angle, small foramen magnum, and type I
Arnold-Chiari malformation in concert appear
to be anatomical features intolerant of brief
Valsalva-induced changes in cerebral volume,
brain-stem position, CSF fluid mechanics, or
blood vessel relationships."
 
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
Im not an expert on this type of mathematical modelling but there are certainly branches of science involving systems perhaps even more complex than the human body, where we take modelling quite seriously , like climate science. So I don't think it's fair to say that modelling is only speculation.

I think the discussion of background and metrics is interesting.
"Kubota demonstrated that a clivo-axial angle of less than 130° was associated with delay or failure to recover after foramen magnum decompression.[18] Numerous series of patients report cervicomedullary kyphosis or ventral flattening in the presence of a kyphotic clivo-axial angle or retroflexed odontoid process.[2,5,6,16] Medullary kinking and basilar invagination introduce abnormal deformative stresses in the brainstem and spinal cord,[1923] which result in neurobiological changes that are believed to underlie the pathophysiology of many of the observed neurological changes in this group of patients.[1215,2232]

In a novel approach, the authors applied a finite element analysis (FEA) research tool to compute estimates of preoperative and postoperative mechanical stress within the brainstem and spinal cord in 5 children with medullary kinking due to kyphotic clivo-axial angulation in the context of Chiari malformation or basilar invagination. These stresses were compared with clinical metrics.

Finite element analysis is a mathematical method that reduces a continuous structure into discrete finite brick elements. This method allows the approximation of partial differential equations with a linear system of ordinary differential equations, which can then be solved by numerical methods with the appropriate boundary conditions. In this particular case, the equations concern mechanical strain, out-of-plane loading and material properties such as Young’s modulus of elasticity or Poisson’s ratio.

A model of the brainstem and spinal cord that incorporates patient-specific anatomical data such as deformity over the odontoid process, lengthening of brainstem and spinal cord with flexion, and numerous other features such as compression of the spinal cord by a herniated disc or spur has been developed to parametrically generate specific finite element models for each patient. The computations derived from these models undergoing flexion and extension generate estimates of the stresses existing within the brainstem and spinal cord in the neutral, flexion and extension conditions. The estimated stresses reflect the dynamic change in stress exerted on the neural tissue. The importance of biomechanical stress has recently been demonstrated in the neurobiological, clinical, experimental and biomechanical literature.

The FEA estimations of deformative strain, generated postoperatively, were used to test the hypothesis that reduction of abnormal stresses improved neurological deficits. The 5 patients studied herein underwent open reduction (normalization of the clivo-axial angle) and posterior translation to normalize the craniospinal relationship. This reduction was followed by occipitocervical fusion and stabilization.[1,7,16] Correlation of computed mechanical stresses with clinical outcome indices suggested a direct relationship between reduction of deformative stress and clinical improvement....
An FEA program (PRIMEGen) was adapted for the purpose of modeling the brainstem and cervical and upper thoracic spinal cord under dynamic loading and strain. The resulting Spinal Cord Stress Injury Analysis (SCOSIA©) technology computes probable magnitude and location of stress within the brainstem and upper spinal cord. The Von Mises stress is the aggregate of both in-line strain, or stretching; and the stress due to “out-of-plane loading,” such as from odontoid compression.

Computer-driven stress analysis–based finite element formulations provide a unique perspective on the biomechanical behavior of the human cervical spine under normal, degenerative and iatrogenically surgically altered conditions. Due to the reproducibility and repeatability of finite element models, detailed parametric analysis with regards to the geometrical conditions and material property changes can be performed, and biomechanical responses can be evaluated using FEA. FEA is routinely used to study spine mechanics.[3747] More recently, FEA has been applied to spinal disorders[48] and spinal cord pathologies.[20,21,49]

Due to the displacement-based formulation of structural finite elements, nodal displacements are primary output variables and nodal stresses are computed variables using nodal displacements. In other words, stresses are predicted based upon the deformation or stretching of specific nodes, with specific Cartesian coordinates within the system."

As for no study with a control group, I did fins a Milhorat/Bolognese study on measurements supine vs upright which had a healthy control group as well as a group with only chiari and no ctd, posted in other thread , i couldn't upload the PDF from scihub but it's there, if anyone cares to read full text.


https://thejns.org/spine/view/journals/j-neurosurg-spine/7/6/article-p601.xml
Just take the doi from this study and put it into scihub

I do think it's possible that the mathematical modelling is very relevant to this discussion, but I don't know much about it. I know there must be someone on this board who's an engineer or understands the physics that might understand it.
 
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PS—neurologists in general are very bad at diagnosing these conditions. I do not know why. I think they tend to treat conditions that can be managed with medications, and so are much more focused on MS and Parkinson’s. From what I’ve seen, you need to work hard with your neurologist or skip them entirely and go to a spine neurosurgeon or interventional radiologist, depending on the diagnosis. That may sound “fishy” but this can be true even of some fairly standard (if “rare”) diagnoses. For one, most neurologists only order brain MRIs and if they can’t find anything wrong, they are done with you. That has been my universal experience. They are not skilled in diagnosing many of these conditions, either by ordering the right imaging or even doing the right physical exam.
That was my exact experience times four neurologists. It took one neurosurgeon less than 10 minutes to solve my case. I am post op ACDF to relieve compression of my spinal cord. Too soon to say anything for sure, but I am confident that I have ended the progression of my symptoms if nothing else. I'm having a pretty decent recovery period and looking forward to what may come after the inflammation goes away.
 
Not sure if this question has been answered, but here is a list of 32 cervical medullary syndrome (CMS) symptoms I found from various sources:

Headache •
Neck pain
Bobble head
Muscle or joint pain •
Weak legs •
Weak arms or hands •
Numb legs and back •
Numb arms/shoulders •
Unsteady walking gait •
Became clumsier •
Chronic fatigue •
Tire very easily •
Memory loss •
Blurred vision •
Double vision •
Urinate every 1-2 hours •
Nausea and vomiting •
Irritable bowel •
Gastrointestinal reflux •
Gastroparesis
Choking on food
Swallowing difficulties
Slurred/hoarse speech
Balance problems •
Vertigo
Dizziness
Raynaud's •
Hearing loss
Ringing in the ears •
Snoring
Sleep apnea
Often wake up in sleep

The ones which are suffixed by the bullet symbol • are those also considered ME/CFS symptoms, going by the comprehensive list of ME/CFS symptoms found on page 104 of the full version of the Canadian consensus criteria.

There are a few additional symptoms @Hip that are considered to be a part of the ICC. I believe dizziness and gastroparesis (described as GI dysmotility) are in the ICC. There are also several additional CCI symptoms mentioned in case reports. Some are symptoms I associate more with intracranial hypertension like cognitive dysfunction, pressure in the head, pain behind the eyes, and visual disturbances (all mentioned in ICC). Dyspnea (shortness of breath) is also mentioned in the ICC and is a CCI symptom.
 
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Not sure if this question has been answered, but here is a list of 32 cervical medullary syndrome (CMS) symptoms I found from various sources:

I had understood criteria like the ICC and CCC to be offering extensive lists of symptoms in different body systems to indicate that in order to be diagnosed with ME, a patient needs to experience symptoms across a range of functions including neurological, muscular, cognitive, and immunological, and that which from the pick and mix list any individual experiences can vary widely.

The vast lists of symptoms in these ME criteria does not mean all these symptoms are specific to ME, and the more symptoms listed, the bigger the overlap with any other condition that lists a wide ranges of symptoms. Surely the longer the lists, the more conditions any of us will overlap with.

For example, chronic neurological conditions like Parkinsons' disease and MS will be likely to overlap with a lot of the listed symptoms for both ME and cervical medullary syndrome.

For differential diagnosis, the important symptoms are not the ones that occur in both conditions being considered, they are the ones that differ and are more specific to that condition.

So if I were confronted with someone's symptom list and asked if I thought they had ME or CMS, I would not look for general things that occur on both symptom lists, I would look for the things that distinguish them.
 
So if I were confronted with someone's symptom list and asked if I thought they had ME or CMS, I would not look for general things that occur on both symptom lists, I would look for the things that distinguish them.

That's right. In differential diagnosis the only symptoms that are if interest are the ones that are NOT common to the possible diagnoses. It is not helpful for diagnostic criteria to include long lists of symptoms that occur in lots of conditions.

Also note that 'cervical medullary syndrome' is a speculative syndrome that most neurosurgeons do not recognise. Symptoms of CMS are not generally recognised symptoms of CCI.
 
I had understood criteria like the ICC and CCC to be offering extensive lists of symptoms in different body systems to indicate that in order to be diagnosed with ME, a patient needs to experience symptoms across a range of functions including neurological, muscular, cognitive, and immunological, and that which from the pick and mix list any individual experiences can vary widely.

I believe this is part of why the ICC is actually thought to be more likely to pick up a wider range of diagnoses than the CCC: it has many more symptoms.

So if I were confronted with someone's symptom list and asked if I thought they had ME or CMS, I would not look for general things that occur on both symptom lists, I would look for the things that distinguish them.

I think this is exactly right. The challenge for my case is that many of the symptoms that were “classic” CCI or tethered cord syndrome were not my most pressing symptoms or were intermittent, so I never reported them to the doctor (PEM and POTS were the most disabling). Also, these symptoms are still present in many descriptions of ME (e.g., ICC and Ramsay) even though they are not required for diagnosis.

I’m sorry to repost this Venn Diagram but I think it is pertinent to this conversation. My lower body/leg symptoms, for examp,e would have been very important for diagnosing tethered cord syndrome. However, enough of them were a part of the ICC (or CCC, or Ramsay ME) to be considered “a part of ME” by ME/CFS doctors. Conversely, if I had ONLY presented with the symptoms in green to a neurologist, they may have recognized my tethered cord syndrome. It was the fact that I ALSO had the symptoms in pink, purple, yellow that made me such a confusing case.

I had all the right symptoms for an ME/CFS diagnoses, too many symptoms to be accurately diagnosed with any of my underlying pathologies.

Another problem is that the way many intake processes work, the symptoms you report become a sort of foregone conclusion. Pre-surgery, I would have passed the intake process in any current US ME/CFS research study because they would have asked me about a range of “pink” and “purple” symptoms and I would have checked off all the boxes that needed checking off. Same goes for clinical intake. The questions asked may not have surfaced the “green” and “yellow” only symptoms at all. Ask me enough about my pink and purple symptoms, I started forgetting about the green and yellow ones, especially if they are not the most constant or disabling (again, PEM and POTS were).

My symptoms in bold.

Note: the symptoms I list as CCI symptoms are not CMS symptoms but rather symptoms that appeared in various case reports and review studies, ideally in more than one source.

FF7072B8-113F-47E2-8D97-75D171CEF9EC.jpeg
 
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I believe this is part of why the ICC is actually thought to be more likely to pick up a wider range of diagnoses than the CCC: it has many more symptoms.



I think this is exactly right. The challenge for my case is that many of the symptoms that might have distinguished me or were “classic” CCI or tethered cord syndrome were not my most pressing symptoms, and so I never even reported them to the doctor (PEM and POTS were the most disabling). Also, these symptoms are still present in many descriptions of ME (e.g., ICC and Ramsay) even though they are not required for diagnosis.

I’m sorry to repost this Venn Diagram but I think it is pertinent to this conversation. My lower leg symtpoms were really important for diagnosing tethered cord syndrome. However, enough of them were a part of the ICC (or CCC, or Ramsay ME) to I think be considered “a part of ME” by ME/CFS doctors. Conversely, if I had ONLY presented with the symptoms in green to a neurologist, they may have recognized my tethered cord syndrome. It was the fact that I ALSO had the symptoms in pink, purple, yellow that made me such a confusing case.

I had all the right symptoms for an ME/CFS diagnoses, too many symptoms to be accurately diagnosed with any of my underlying conditions.

Another problem is that the way many intake processes work, the symptoms you report become a sort of foregone conclusion. Pre-surgery, I would have passed the intake process in any current US ME/CFS research study because they would have asked me about range of “pink” and “purple” symptoms and I would have checked off all the boxes that needed checking off. Same goes for clinical intake. The questions asked may not have surfaced the “green” and “yellow” only symptoms at all. Ask me enough about my pink and purple symptoms, I started forgetting about the green and yellow ones, especially if they are not the most constant or disabling (again, PEM and POTS were).

My symptoms in bold.

Note: the symptoms I list as CCI symptoms are not CMS symptoms but rather symptoms that appeared in various case reports and review studies, ideally in more than one source.

View attachment 9334

It is also worth mentioning that some symptoms not captured above by the ICC or Ramsay are mentioned in other case reports of ME outbreaks.
For example, stiffness of the neck and spine is mentioned in:
  1. Sigurdsson, B(May 1956). "The Lancet". Clinical findings six years after outbreak of Akureyri disease. 270: 766–7.
  2. Jump up to: 4.04.14.24.34.4 Dr R.A. Pellew, "A Clinical Description of a Disease resembling Poliomyelitis, seen in Adelaide, 1949-1951" Medical Journal of Australia, Medical Journal of Australia 1951, June 30 Vol. 1 No. 26 pp. 944-6
  3. Jackson, B (May 1957). "A disease resembling poliomyelitis; report of an outbreak in Johannesburg". South African Medical Journal. 31: 514 – 517.
  4. Jump up to: 9.009.019.029.039.049.059.069.079.089.099.109.119.129.139.149.159.169.179.18 Hill, RC (Apr 4, 1959). "Epidemic myalgic encephalomyelopathy: the Durban outbreak". The Lancet. 1: 689–693.
See: https://www.me-pedia.org/wiki/Epidemic_myalgic_encephalomyelitis#Symptoms
 
I would forget Venn diagrams. I would also forget ICC and Ramsay criteria and go with something more realistic like CCC or IOM.

From the perspective of a physician trained in neurology and spinal disease I would say:

None of the clinical features that specifically lead to a diagnosis of ME are localising neurological symptoms or signs.

All of the clinical features that specifically lead to a diagnosis of CCI are localising neurological symptoms or signs.

No overlap. No need for a diagram.

If localising neurological symptoms PWME are attributed to ME because of ICC criteria, that is a good reason for ditching the criteria. There is no justification for attributing local neurological symptoms to ME.
 
I think amateurs like me at our peril try to create meaning in the form of Venn diagrams from lists of symptoms. I personally find them so oversimplified as to be useless. They may simply indicate that the symptom lists on some ME definitions are so broad ranging to be meaningless.

A symptom, stated in a couple of words like, for example, 'leg pain', may be part of so many different disorders that it indicates practically nothing. Just becuase those two words appear on a symptom list doesn't mean that the leg pain I have is anything like the leg pain someone with another condition has.

If medicine were that simple, all we would need would be computer algorithms to diagnose us, not experienced doctors who have learned to distinguish one leg pain from another and to understand what that leg pain means in the context of the patient's other symptoms, signs, history, test results etc.
 
I think amateurs like me at our peril try to create meaning in the form of Venn diagrams from lists of symptoms. I personally find them so oversimplified as to be useless. They may simply indicate that the symptom lists on some ME definitions are so broad ranging to be meaningless.

A symptom, stated in a couple of words like, for example, 'leg pain', may be part of so many different disorders that it indicates practically nothing. Just becuase those two words appear on a symptom list doesn't mean that the leg pain I have is anything like the leg pain someone with another condition has.

If medicine were that simple, all we would need would be computer algorithms to diagnose us, not experienced doctors who have learned to distinguish one leg pain from another and to understand what that leg pain means in the context of the patient's other symptoms, signs, history, test results etc.

The point of the diagram is to illustrate why a patient with craniocervical instability and tethered cord syndrome might be diagnosed with ME/CFS on the basis of the symptoms they describe to their doctors, especially if those symptoms began after a viral infection.

These are our definitions and this is what is in the literature. What do you recommend as an alternative?

In my view, it’s the doctors who have the hardest time parsing the nuances of our symptoms, not us “amateurs.” This is why doctors need to rely on objective signs. They have no idea what we are really feeling any more than any of us can truly know what someone else is feeling. At least we can spend thousands of hours talking to each other and comparing our experiences. In that, we are experts.

Moreover, until encountering neurosurgeons, I never had a doctor much bother trying to distinguish between my 10 flavors of headache or leg pain. You’re talking about a level of care/precision that, while admirable and something to strive for, I have rarely experienced in either a clinic or at a research study. For 7+ years, whether I had pressure in my head, stabbing occipital pain, burning in my brain, aching in my forehead, or stiffness in my neck etc., it was all just “headache.” Whether my leg pain was muscle aching or neuropathic and migratory, it was all just “leg pain.” That’s not my amateurish lack of specificity. That’s doctors translating my faithful and specific accounts of my symptoms into something simple and standard, while often erasing vital information. It was so frustrating, a part of the problem.

I do not think most ME/CFS experts were better in this regard. They were looking for what they were looking for and did not know to look for anything else. Again, I saw seven.

I also saw at least a half dozen doctors at Harvard and almost as many at Stanford. Where are the experienced doctors that are supposed to know so much more than the amateurs? They don’t know more (yet), and that is part of why we are in this mess.
 
If medicine were that simple, all we would need would be computer algorithms to diagnose us, not experienced doctors who have learned to distinguish one leg pain from another

Indeed, every medical student is taught that for any symptom of pain six further questions are required. Some have up to a dozen possible answers but if each had two any good maths teacher will know that there are 64 distinguishable scenarios you may discover. If there were only three possible answers to each it would be 729 scenarios. And that is just the first symptom.
 
The point of the diagram is to illustrate why a patient with craniocervical instability and tethered cord syndrome might be diagnosed with ME/CFS on the basis of the symptoms they describe to their doctors, especially if those symptoms began after a viral infection.

These are our definitions and this is what is in the literature. What do you recommend as an alternative?

So how do you respond to my comment above @JenB - that in fact there is no overlap in the discriminatory features?

These are not the definitions in 'the literature'. They are definitions in fringe publications as far as the medical community is concerned, and everyone knows that.

What I recommend as an alternative is

what is in the generally accepted literature. CCC and IOM are not bad for ME. The features CCI have little to do with the speculative 'cervical medullary syndrome'.

I don't want to lecture but I think it is important not to give the impression you are quoting accepted medical evidence when it is in fact highly controversial material from a few people with a very strong financial conflict of interest.

They were looking for what they were looking for and did not know to look for anything else.

And the neurosurgeons?
 
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