New study on “craniocervical obstruction” and ME

Large study of ME patients finds high rates of hypermobility, fibromyalgia, signs of intracranial hypertension and Chiari

I just wanted to share with you a very important new study for anyone with myalgic encephalomyelitis (ME), hypermobile EDS (hEDS), or fibromyalgia. In my view, this publication has brought us closer to finding the cause of ME symptoms for a significant subset of patients than anything I have ever read. I know that is a bold statement. I hope the research to follow will help us better understand if that is indeed true and if so, what we can do about it.

A group of clinicians in Sweden collected preliminary data from 234 #MECFS patients meeting the Canadian Consensus Criteria. This same team is currently undertaking a more extensive MRI study comparing patients and controls. Imaging will include supine brain/spine MRIs and upright flexion/extension MRIs at Medserena in London.

Summary

• 49% had hypermobility, 20% met criteria for hEDS

• 96% had fibro pain, 67% met fibro criteria

• 55% had increased diameter of their optic nerve sheath. This is another way of saying they had cerebrospinal fluid in their optic nerve sheath, a sign of intracranial hypertension. (I had this on my MRI.)

• There were other signs of intracranial hypertension that I know less about found in 83% and 32% of patients

• Herniation of the cerebellar tonsils was found in 56% of patients. This was severe enough in 13.2% of patients to be considered a Chiari Malformation. Note that this is the same rate of Chiari Malformation Hip is finding in his Phoenix Rising survey.

Read the study: https://osf.io/qwn5h/

My takeaways

• This study provides evidence that strongly supports the hypothesis/observation that “structural” neurological issues are at play in a significant subset of ME patients

• A very large proportion of patients had signs of intracranial hypertension (elevated pressure in the skull). This study did not investigate all causes of intracranial hypertension, of which low-lying cerebellar tonsils are just one.

• As I have written previously, what ties together the diagnoses that I am anecdotally seeing in a large proportion of ME patients (Chiari malformation, cervical stenosis, craniocervical instability, atlantoaxial instability, vascular stenosis, Eagle’s syndrome) is that they can all cause or be associated with intracranial hypertension

• We need more research, specifically high-quality imaging data that can assess for a wider range of structural problems, where the radiologists interpreting the imaging are blind to whether those images belong to patients or controls. I believe this is exactly the study this Swedish group is working on

• There were other signs of intracranial hypertension that I know less about found in 83% and 32% of patients

• The high rates of co-morbidity are a clear indication (in my opinion) of what I have been saying for some time: many people with ME have hypermobility or hEDS and that is significant.

However, not all people with hEDS have the symptoms of ME. Many are perfectly able to do PT and be physically active without “crashing.” Others have no symptoms of chronic illness whatsoever. Moreover, many people with ME do not have hypermobility. This means the causes of these symptoms, including the causes of the connective tissue damage, are likely to be either more complex or more varied than a simple story of hypermobility or autosomal dominant inheritance. It is likely to involve an interplay of genetic risks and environmental factors like mold or infection, mediated, perhaps, by MCAS. And as we know, hypermobility is not correlated with illness severity.

• We need more research on the overlap of syndromes (symptoms) of ME, hEDS, fibro and MCAS, so we can get away from categorizing people by their symptoms and move toward classifying patients by their pathologies (the nature of the tissue damage).

• Pathology is not the same as cause, but it is one step closer to the cause. Correcting the pathology in my experience (and I hope clinical trials will eventually show) may improve or even remit many symptoms.

• This is not on the radar of most of our clinicians or researchers. If you believe this line of inquiry is important, talk to the doctors who treat you or the researchers you support. Send them this paper. Ask that their work address these questions.

• We do need more neurologists, neurosurgeons, and neuroscientists in the field, but the damage has a *molecular* cause. Truly understanding those causes, providing nonsurgical options for treatment, providing early diagnosis and prevention, is going to require understanding the genetics, molecular biology, immunology of all of this.

• We also need ME, hEDS, fibro, MCAS and POTS/dysautonomia clinicians and researchers to start to work together and to stop being ignorant of each other’s fields. I think patients have a role to play in encouraging and supporting this collaboration.

Read the study: https://osf.io/qwn5h/

Some related research (a Twitter thread): https://twitter.com/jenbrea/status/1200085632900448257

Some related Medium articles:

• CCI + tethered cord series: https://medium.com/@jenbrea/cci-tethered-cord-series-e1e098b5edf

• Path to diagnosis: Part I (An empty sella) — how I started on my path to getting diagnosed with CCI: https://medium.com/@jenbrea/path-to-diagnosis-part-i-an-empty-sella-9b984a5ac6ca