Discussion in 'BioMedical ME/CFS Research' started by Andy, Feb 2, 2018.
Open access at https://rd.springer.com/article/10.1186/s12967-018-1397-7
Very interesting....but a little scary as well.
Most ME/CFS manifestations are refractory to treatment - if only because no one know nothing about treatments which consistently work for any subsets, let alone across subsets. "The prompt restoration of normal function" is at best a myth for most pwME.
Fascinating article, and it was heartening to read the level of improvement reported in the three patients in question. It was surprising (it probably shouldn't have been) to me to realise that beyond typical numbness/pain/other neuropathy, pressure on the spinal cord in the neck could cause such systemic issues. Made me wonder (highly speculative) whether this could be considered more evidence that neuroinflammation is a key driver for a lot of ME/CFS sufferers - i.e. whether a different pathology causing such inflammation could be similar to a spinal stenosis in its effect on the CNS and sickness responses.
Well, yes, but if doctors can find even a small subset who are responsive to this treatment - and from the three case studies, highly responsive - then that's still pretty good news. And in the unlikely event it provides clues to possible aetiologies for other ME/CFS subsets, even better.
I have occasional come across comments relating to a UK doctor who asserts specific spinal problems are a diagnostic feature of ME. I remember being confused by this at the time, but can not recall any further information. However usually here there will be someone with the details more readily at hand.
I think improvement may have been overstated. The Karnofsky scores from the physician went from around 50% to around 90%, which is defined as "Able to carry on normal activity; minor signs or symptoms of disease." But the self-rated SF36-PF scores went from about 15 to about 30 for all three cases, which is still extremely low. I don't think a score of 30 on the SF36-PF can be reconciled with a Karnofsky score of 90%.
From the PR thread
Denise - I thought so also so I queried Rowe who said they did not norm the SF-36 (to be x/100) so the results were 30 out of 30 and 26 out of 30.
They need to make this clearer.
To clarify- the PR thread was about the 2016 IACFSME poster http://iacfsme.org/ME-CFS-Primer-Education/News/IACFSME-2016-Program.aspx page 121
(broken up to make it easier to read - I hope)
Cervical spine stenosis as a cause of severe ME/CFS and orthostatic intolerance symptoms
Peter C. Rowe, M.D*, Colleen L. Marden, Scott Heinlein, PT, Charles Edwards II, M.D.
Comparatively little has been published on the clinical features and management of severe forms of ME/CFS.
To describe the presenting symptoms and neurological examination findings in three young adult women whose disabling ME/CFS symptoms and orthostatic intolerance improved after the recognition and surgical management of cervical spine stenosis (CSS).
This retrospective case series includes three consecutive individuals who (1) met the Fukuda and criteria for CFS, (2) had evidence of refractory orthostatic intolerance, (3) were unable to work or attend school, and (4) were minimally responsive to medical and psychiatric management.
To investigate pathological reflex findings, all underwent MRI evaluations. CSS was considered present if the AP cervical spinal canal diameter (SCD) was less than 10 mm at any level.
Overall function was assessed before and after cervical disc replacement surgery using (1)a clinician-assigned Karnofsky score (range 0 to 100) and (2) the SF-36 physical function (PF) subscale score (range 10-30). Higher scores indicate better function on both measures.
Age at onset of symptoms was 12, 29, and 29 years. The onset of ME/CFS was acute in all three.
Neurological exam findings included>3+ (brisk) deep tendon reflexes (DTR) in 2/3, positive Hoffman sign in 2/3,tremor in 2/3, and absent gag reflex in 1/3. Diagnosis was delayed for 6-9 years after the onset of symptoms. Brain MRIs were normal.
The youngest patient had congenital CSS with a single level disc protrusion at C5-6 that caused further ventral cord compression and a SCD of 7 mm. Her mother also has cervical stenosis.
A second patient had two disc protrusions at C5-6 and C6-7 with SCD of 7 and 9 mm, and myelomalacia (this patient has a sibling with Chiari I malformation).
The third had acquired CSS due to a single level disc bulge at C5-6 (SCD = 8.5 mm).
Improvements were evident within 2 months of single-level cervical disc replacement surgery (one patient also had fusion at an adjacent level). After 16-40 months of follow-up, all reported improved fatigue, cognitive dysfunction,PEM, lightheadedness, and anxiety.
The pre-to post-op SF-36 PF scores improved from 13 to 30, 18 to 30, and 16to 26, respectively, and the Karnofsky scores improved from 40 to 90, 40 to 90, and 50 to 100, respectively.
Standing tests conducted at variable intervals from pre- to post-op showed a reduction in the maximal heart rate(HR) change during 5 minutes of standing from 64 to 22 bpm, 42 to 29 bpm, and 34 to 27 bpm, respectively.
This case series draws attention to the potential for CSS to contribute to ME/CFS and orthostaticsymptoms, extending work by Heffez in fibromyalgia (Eur Spine J 2004;13:516).
Further work is needed to define indications for surgery. However, the improvements in HR and function following surgery emphasize the importance of detecting and treating CSS, especially in the subset of those with ME/CFS whose severe symptomsare refractory to other interventions.
My son's osteopath, using the Perrin technique, said that one of the diagnostic features of people with ME/CFS is three or four vertebrae which are straightened or flatened.
I'll believe that if and only if I see a properly conducted study with bone scanning evidence that shows this.
If Only they would listen to patients, the Ramsey days (the why of the name ME). I think you are spot on, and it is the inflammation creating the pressure and symptoms, because I feel my spine and brain on fire, and can feel the inflammation (my neuro said is impossible). But maybe if they do upright scans when we are symptomatic we would find the issue.
Just wanted to remind everyone that this paper exists.
Reminder: there's a big difference between a subgroup with some specific features that may in some cases be amenable to surgery (some cases do not have a surgical remedy), and a diagnostic test or feature of ME in general. This is saying a few people may have this in addition to ME, and may feel better by correcting the structural problem.
I guess if ME gets worse from any little thing, why not this, too.
female patient 1, who went severe mecfs/pots by 12 (i understand), sounds close to things reported "here"
This is quite amazing and describes me perfectly. I also had the same trigger (viral gastrointestinal illness) and it happened at the same age (12). My symptoms were quite similar, except my illness had been mild until it started getting much worse a few years ago.
The more I read about this CCI / neck issues connection, the more it seems to make sense. I wouldn't at all be surprised if in a quite large subset of CFS / ME patients the disease is caused by CCI / neck issues.
What I find also perplexing is how many of these people had a sudden onset. This sounds very untuitive: how could a structural issue start causing symptoms overnight? There could be several logical explanations for this, I could thik of two:
- Maybe the structural issue was always there, but a viral infection somehow transformed it from an asymptomatic to a symptomatic problem.
- Maybe a viral infection initiated some kind of reaction (immune) which would lead to the structural problem. Initially the fatigue would be from the virus, but once the virus was cleared, the fatigue remained, but now not due to the virus, but the structual issues that were initiated by the virus. This would make it seem like the disease started overnight.
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