20 patients now found positive for CCI / AAI, there must be many more...

[mattie]

Quote from other thread

I asked him (Dr. Gilete) whether Chronic Fatigue (in his opinion) comes first or CCI/AAI. He responds that based on the subset of patients he has seen which complain about both, they later develop CCI/AAI after getting ME/CFS.

That does not sound encouraging..

 

[jeff_w]

Hi @mattie

I initially thought that I had developed CCI/AAI after developing ME/CFS. Reason being, my overt CCI/AAI symptoms (bobblehead, neck pain) didn't emerge until years into my severe ME.

So when I sought treatment for CCI/AAI, I assumed it was a separate issue on top of ME, and that I would still have ME after treatment. I was shocked when my POTS, PEM, EBV titers, and all other ME symptoms went away.

So if Dr. Gilete said that people develop CCI/AAI after getting ME/CFS, that would be consistent with my own timeline as to the appearance of neck-related symptoms. But Dr. Gilete's observation has no bearing on whether or not CCI/AAI is the cause of ME.

 

[frozenborderline]

I would be interested in how many of those 90% diagnosed that opted for surgery have improved post-surgery. I have read about clear cases like Jeff's story where the recovery is significant, but I have also seen numbers posted from a conference where a significant part of the patients did not improve post-surgery. It raises the question if these CCI findings are similar as EDS, i.e. they are more likely present in a person with ME/CFS, but are not necessarily causative factors in the disease.

These cases are mostly all very recent. Has anyone on this forum besides Jeff and Jen had this surgery yet ?

 

[gm286]

I would like to second @jeff_w, where my neck only got worse years after sudden-onset ME/CFS. It's gotten stiff over time. Around the time when the real stiffness occurred, I'd add: more sensitive gums, slowed or changed ANS processes (slightly erratic swallowing, sweating, dry mouth/dry salivary glands).

What occurred much, much sooner after sudden-onset ME/CFS (in the space of weeks or months): PEM, brain fog, fatigue, sleep issues, chronic GI issues, and perhaps most strikingly, an alarming hip pain as well as lower back stiffness.

And I mean striking to say that it was a stabbing pain, which when walking on a hard surface, would shoot into my hips. I explained this last part quite emphatically to Dr Gilete. "This stabbing pain in my hip bones and lower back, which has been going on for a decade, what could it be?" To mean what is mechanically connecting this pain back to the other stuff.

He said that "maybe my ligaments were weak everywhere" as matter-of-factly as possible. He thought to mention that one of my legs was probably doing more work than another, because he saw some mild scoliosis in my spine. I guess I'm mostly trying to understand the process by which severe and sudden onset illness triggers ligament degradation like this.

Before the sudden-onset ME/CFS: mild fatigue, slightly stiff neck, locking jaw (not sure if this qualifies as TMJ), no brain fog, especially not the way I experienced it after getting ill, when, sitting at a desk, in a chair, and/or in front of a screen for too long instantly triggered it. I always did have a slouched neck (on my recent radiology it was described as "loss of normal cervical lordosis").

I want to reiterate that the doctor did say the essential gist of what I relayed earlier (CFS then CCI/AAI in a co-morbid situation...) but perhaps more along the construct of @jeff_w there is no necessary linear causality between the two.

I am wondering about infections in CFS/ME, if Jeff had other active infections which have abated after surgery (other dissipating viral titers).

 

[frozenborderline]

Hyaluronic acid fillers stretch fibroblasts, boosting collagen production



Platelet rich plasma has also been used in tendon and ligament repair
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3838322/

 

[Belbyr]

Do we know how Jennifer Brea is doing lately? Her social networks have been silent unless I am missing something...

 

[Belbyr]

After doing some digging, I found her updates on twitter. It seems she is still ill and her POTS is back. Looks like there was a second surgery for something that happened after the first surgery. She will be in a 'recovery' phase for a while after having 2 spinal surgeries back to back. It looks like the major thing she gained was her breathing back.

 

[jeff_w]

Hi @Belbyr

Jen Brea is still in the early post-op period, as she had an additional surgery. You will get answers from her, I promise. It will just take some more time. If I had posted how I was doing freshly post-op, you would have had no clear sense of my ultimate outcome.

In the early post-op period after my own surgery, my POTS initially went away for a few days, but then came back strongly from the swelling around the surgical site. You can see for yourself that I reported having the same experience as Jen, happening after my own fusion surgery last year, see my post from early 2018.

Swelling peaks around days 4 to 7. It then takes many weeks for swelling to abate. Also, the post-op swelling compresses the same neuro structures that were a problem prior to surgery. So there's a post-op period where things seem to get worse, before getting better, and this is normal.

You wrote this about Jen Brea, based on her Tweets from several weeks ago:

After doing some digging, I found her updates on twitter. It seems she is still ill and her POTS is back.

I know you're going off of her Tweets from several weeks ago, when she was freshly post-op. A lot has happened in the interim.

I'm in contact with Jen, but I won't speak for Jen, as this information is her own to share. I will just urge you and everyone else to be patient (hard to do, I know!). You can't extrapolate on her outcome based on her Tweets from several weeks ago, when she was freshly post-op with peaking swelling that compresses the very same neurological structures that were a problem prior to surgery.

Again, if I had posted how I was doing freshly post-op, in terms of POTS and exhaustion, you would not have had any clear idea about my ultimate outcome.

Jen's healing will take some time. Knowing the outcome will take some time. Jen will provide updates when she's ready, as she heals.

 

[Belbyr]

Thanks for your response. I see Dr Klimas for the first time in about 18 days about my condition, I will bring this up and see what she thinks. I became ill during high school football and was known for being a 'hitter'. Chronic headache at the back and base of the head with eye symptoms, trigger points in the region, and GI distress.

What was your healing period 'time' you think?

 

[humanrising]

I think I posted this on a different thread so if I did forgive me brain fog continues!

I have had 4 car wrecks resulting in 4 whiplash injuries. I have also had a long history of travel in developing countries where I was in a soup of toxic mess and had over a dozen rounds of antibiotics for bacterial and amoebic dysentery. I had a bad bought of bronchitis about 2 years before I got sick. but it wasn't until I flipped head first into the ground out of a hammock that neck pain, radiating pain and numbness down my arms then insomnia then slowly but surely all the "typical" ME symptoms.
I went to standford to see a surgeon for the neck pain and found out I had 4 damaged cervical discs "not enough" to warrant treatment other then PT but " I will get worse then maybe I will need to have my neck fused". I quit doing massage and catering to not overwork my thoracic cage which helped my arms but not much else.
I have tried and tired to have this conversation with every doc I have seen..... wondering if my neck trauma was contributing to my fatigue brain fog etc. EVERY single one treated me like I was nuts. I have had traditional MRI but nothing else.
If anyone who lives in northern California and knows of anyone I could see that would test for this I would greatly appreciate it!!!!! thanks so much.
this is the most complex illness "complex" I think when it does get more sorted we will find that the cluster of symptoms labeled ME/CFS will have a half dozen or more ways how we got here and will have to be named for those separate triggers or mechanisms.

 

[frozenborderline]

So I still need to get manual traction administered to see I I am surgery candidate before having consult with bolognese. This is proving to be the most difficult thing. I have a referral for pt already but can’t get home pt and am basically too sick to go out. Maybe could go out once I guess. But also the pt people don’t want to necessarily just do traction and would need some kind of order to do this, which I don’t think bolognese has given. If it’s really cci they would be nervous about doing anything without guidance which I think is good sign that they are conscientious ? But uh idk what to do and I’m pretty sick rn

 

[frozenborderline]

https://www.ehlers-danlos.com/2015-annual-conference-files/Henderson_0.pdf
For anyone interested, this is a very long document I think for a presentation Henderson did on this condition/comborbidities. He discusses everything from objective measurements of this condition to nutritional and pharmacological strategies in EDS. But what you all may find interesting is some stuff where he connects the mechanical to the molecular. @Hip , @jeff_w ,
And there’s part specific to intercellular calcium influx after injury which I know people were interested in on this forum.

 

[M Paine]

Just going to weigh in here with a personal anecdote. I have had issues with bladder urgency, shoulder and back pain, and of course ME/CFS. Personally I do find that addressing my back issues has correlated with general improvements in my health. Some of those improvements seem very short term and immediate. I remain pretty skeptical, but at least I can spend some effort on 'something' which feels like it's helping. Yoga has legitimately helped me. Slow, stretching 'Yin' style Yoga which is basically where you hold stretches for several minutes at a time. Perfect when you have zero energy, and a painful back.

 

[Belbyr]

https://uppercervicalawareness.com/proof-fibromyalgia-can-reversed/

Was flipping through articles and thought this was interesting

 

[xrayspex]

Hi @JES



I closely and actively follow research conferences across the world in relation to both ME/CFS and CCI. There has been only one published study on the relationship between ME/CFS and neurosurgery. The paper was a case series in which three ME/CFS patients made a full recovery after neurosurgery for cervical stenosis.

Aside from this one paper from 2018, as far as I am aware, the relationship between ME/CFS and neurosurgical issues had never been noticed or formally studied -- let alone tracked like this.

I am very interested in knowing which conference this was. Can you let us know and post a link? Thanks.

Jeff---I recalled there had been some research back when Rosner and Heffez were noticing CFS and fibro correlated with cervical spine and chiari issues---dug through my old emails and found what I had kept--I apologize that for some reason I didn't keep the links but the whole study so this will be bit long, in case it would be of interest to you:


https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3476600/


https://www.wsj.com/articles/SB942280927444238502

this link might work better:
http://www.anapsid.org/cnd/diagnosis/chiari.html


FORWARD THOUGHTS ON THE HINDBRAIN

Peter G. D’Amour, M.D.

MRI and CSF flow studies are being used to diagnose abnormalities of the posterior fossa, foramen magnum, and cervical spine. In spite of these new techniques, much research is required to make these techniques useful. The medical community and radiologists in particular must analyze additional concepts and challenge the traditional radiologic dogma to further our ability to understand our patients. A review of past, current, and future thoughts will be presented.


CAN SPINAL CORD COMPRESSION CAUSE THE
FIBROMYALGIA SYNDROME?


Dan S. Heffez¹ M.D., Daniel G. Malone² M.D., Sam R. Banner¹ M.D., Alan Shepard¹ M.D., Ruth E. Ross¹ Ph.D. and James W. Robertson¹ B.S. (Sponsored by Daniel Malone)¹ Chicago Institute of Neurosurgery and Neuroresearch, Chicago, IL 60614 and ²University of Wisconsin at Madison, Madison, WI 53706



The symptoms of cervical myelopathy mimic those of fibromyalgia. We established a prospective database to catalogue neurological findings in patients with fibromyalgia to examine the possible etiological role of spinal cord compression. The principal criterion for referral is cervical spinal canal or foramen magnum stenosis on a screening MRI scan. Patients complete a detailed questionnaire regarding current symptoms and past medical care and are examined by a neurologist and a neurosurgeon. Measures of balance, strength, coordination, and cognitive function are obtained using a battery of standardized tests. To date, forty-five consecutive fibromyalgia patients (87% female, median age 44 years, median duration of illness 6 years) have been evaluated for myelopathy. Neurological symptoms included fatigue (93%), fatigue upon exertion (98%), cognitive impairment (96%), diffuse pain (93%), headache (89%), weakness (89%), impaired balance (80%), paresthesiae (82%), clumsiness (71%), numbness (73%), dizziness (62%), and diplopia (71%). Neurological signs included hyperreflexia (80%), spinothalamic sensory level (79%), recruit of reflexes (44%), impaired tandem walk (32%), positive Romberg sign (31%), clonus (28%), Hoffman sign (26%), dysdiadokokinesia (28%), impaired position sense (19%) and dysmetria (19%). Only 3 patients had a normal neurological examination. Detailed MRI imaging of the cervical spine and foramen magnum revealed cervical stenosis (n=21), brainstem compression due to tonsillar ectopia (n=12) or, both cervical stenosis and tonsillar ectopia (n=11). We conclude that some patients with fibromyalgia have cervical myelopathy on the basis of spinal cord or cervicomedullary compression. We recommend a thorough neurological examination and a screening MRI scan of the cervical spine and brain in all patients with fibromyalgia who do not respond to conventional medical therapy.


PATIENTS WITH FIBROMYALGIA HAVE QUANTIFIABLE
NEUROLOGICAL DEFICITS


Pamela S. Johnson¹ M.S./P.T., Helen Bourke-Taylor¹ O.T.R./L., Dan s. Heffez¹ M.D., Daniel G. Malone² M.D., Ruth E. Ross¹ Ph.D. and James W. Robertson¹ B.S. (Sponsored by Daniel Malone) ¹Chicago Institute of Neurosurgery and Neuroresearch, Chicago, IL 60614 and ²University of Wisconsin at Madison, Madison, WI 53706



An association has been proposed between fibromyalgia and cervical myelopathy. As part of an investigation of a possible neurological etiology of fibromyalgia, 42 consecutive patients with fibromyalgia were evaluated using a series of standardized tests of neurological function. We assessed upper extremity function including coordination and dexterity (Jebsen-Taylor Hand Test and nine-hole peg test) and strength (Jamar dynamometer and pinch gauge). Mobility and static and dynamic balances were assessed using the Berg Balance Scale and timed measures of ambulation. The median age of patients was 44 years. Patients carried the diagnosis of fibromyalgia for a median of 6 years. Eighty-seven percent of patients were female.

Data analysis indicated that 68% of patients had balance deficits as shown by the Berg Balance Scale, including impaired functional reach (31%), tandem stance (24%) and single limb stance (26%). The sample size allowed for the analysis of the Jebsen-Taylor hand test of dexterity only for the 30 right-handed females; a statistically significant slowing as compared to accepted standard of normal was identified in 6 of 7 subtests (p<.01). Forty-six percent and 33% of patients fell below the 25th percentile on nine-hole peg testing of the dominant and non-dominant hands, respectively. Tests of grip strength and dexterity showed a lack of the normal dominance pattern in 60% of patients.

We conclude that some patients with fibromyalgia have neurological dysfunction that can be objectively quantified. This database will allow for prospective objective analysis of the response of fibromyalgia to the treatment of cervical myelopathy.

SURGICAL TREATMENT OF MYELOPATHY RELIEVES SOME
SYMPTOMS OF FIBROMYALGIA


Dan S. Heffez¹ M.D., Sam R. Banner¹ M.D., Daniel G. Malone² M.D., Alan Shepard¹ M.D. and Ruth E. Ross¹ Ph.D. (Sponsored by Daniel Malone) ¹Chicago Institute of Neurosurgery and Neuroresearch, Chicago, IL 60614 and ²University of Wisconsin at Madison, Madison, WI 53706

An association has been suggested between fibromyalgia and cervical myelopathy. If so, treatment of myelopathy could relieve some symptoms of fibromyalgia. Twenty-two fibromyalgia patients with cervical myelopathy (82% female, mean duration of illness 6.1 years +/-4.49) were evaluated. Symptoms included fatigue (100%), cognitive impairment (100%), exertion intolerance (95%), diffuse pain (86%), headache (86%), clumsiness and instability (91%), nonrestorative sleep (82%), nausea (64%), dizziness (59%) and numbness (59%). Neurological signs included hyperreflexia (86%), recruitment of reflexes (46%), impaired tandem walk (41%), positive Romberg sign (37%), spinothalamic sensory level (32%), nystagmus (27%) and appendicular ataxia (23%). MRI imaging revealed foramen magnum stenosis due to cerebellar tonsillar herniation (n=8), cervical spinal stenosis (n=7) or both (n=7). Surgical decompression of the foramen magnum (n=13), the cervical spinal canal (n=7) or both (n=2) was performed. After a minimum 6-month follow-up, (range: 0.5-2.5 years), 81% of patients reported sustained improvement in the distribution and intensity of pain. Cognitive dysfunction (75%), dizziness (77%), numbness (77%), fatigue (70%), headache (68%), nausea (65%), capacity for exertion (65%) and quality of sleep (50%) also improved. Improved performance on neurological examinations was noted. We conclude that fibromyalgia patients with myelopathy can experience an improvement in symptoms of fibromyalgia following surgical decompression of the cervical spine or foramen magnum. We have developed a database to identify any etiological link between cervical myelopathy and fibromyalgia.


FIBROMYALGIA: A Neurological Perspective

Roger W. Kula, M.D.

Gowers, a neurologist, first described FMS in 1904 as a possibly inflammatory condition. When no evidence of inflammation could be found an association was noted with depression and stress, the concept of “psychogenic rheumatism” was advanced (Boland 1947). A number of studies have since established that FMS is neither a psychosomatic nor somatiform disorder and that when present, anxiety and depression are more likely to be the result than the cause of FMS (Goldenberg 1989, Yunus 1994). Although FMS is now a better defined clinical syndrome, comprehensive patient evaluation continues to include a wide differential diagnosis including many diverse and sometimes obscure neurological and neuromuscular conditions.

Pathological findings in muscle in painful neuromuscular syndromes and neurophysiological abnormalities of sleep in FMS will be reviewed. Although there have been many abnormalities of laboratory and others tests reported in FMS, none is sufficiently sensitive or specific to be useful diagnostically. Patients with FMS should have a comprehensive medical evaluation as part of their work-up. A preliminary lab screening should include CBC, ESR, Rheumatoid factor, ANA, SPEP, IFE, Thyroid function testing (T?, TSH), Hgb A1C, and CK (x3). Both prescribed and surreptitious drug use should be explored. Sleep and exercise behaviors should be examined. Clinical consideration of a wide range of diagnostic possibilities may include: Acute or chronic inflammatory demyelinating or axonal polyneuropathy, autonomic neuropathy, secondary hyperparathyroidism, obstructive sleep apnea, periodic limb movements, restless legs syndrome, Chiari I malformation, cervical spinal stenosis, polymyalgia rheumatica, polymyositis, inclusion body myositis, nodular fasciitis, steroid withdrawal syndrome, chronic antacid use (milk-alkali syndrome), myoadenylate deaminase deficiency or other metabolic myopathies, periodic paralysis, and myasthenia gravis.

New data including a comparative symptom analyses of FMS and Chiari I malformation patients will be highlighted (Milhorat, 1999). Poorly understood symptoms such as dysequilibrium, orthostatic hypotension, tachycardia, musculoskeletal pain, impaired concentration, and sleep disturbances common to patients with FMS, CFS and Chiari I malformation will be approached from the standpoint of possibly disordered brainstem function.






PAIN: An Overview


John D. Loeser, M.D. and Ronald Melzack

Until the 1960s, pain was considered an inevitable sensory response to tissue damage. There was little room for the affective dimension of this ubiquitous experience, and none whatsoever for the effects of genetic differences, past experience, anxiety, or expectation. In recent years, great advances have been made in our understanding of the mechanisms that underlie pain and in the treatment of people who complain of pain. The roles of factors outside the patient’s body have also been clarified. Pain is probably the most common symptomatic reason to seek medical consultation. All of us have headaches, burns, cuts, and other pains at some time during childhood and adult life. Individuals who undergo surgery are almost certain to have postoperative pain. Aging is also associated with an increased likelihood of chronic pain. Health-care expenditures for chronic pain are enormous, rivalled only by the costs of wage replacement and welfare programs for those who do not work because of pain. Despite improve knowledge of underlying mechanisms and better treatments, many people who have chronic pain receive inadequate care.
PAIN SYNDROMES AND C-SPINE/FORAMEN MAGNUM CORD COMPRESSION. TWO YEAR EXPERIENCE OF A UNIVERSITY-BASED RHEUMATOLOGIST


Daniel G. Malone, M.D., University of Wisconsin, Madison, WI


At the September 1997 seminar sponsored by the National Fibromyalgia Research Association I learned of the connection between fibromyalgia/CFIDS/chronic pain, and cervical spine/foramen magnum compression abnormalities. Since that time I have done thorough neurological examinations on nearly all patients referred to me with chronic pain. Total patients seen with pain syndromes = 335, and those evaluated neurologically = 271. Of the 271, neurological abnormalities resulted in 144 recommendations for C-spine MRI, done according to a special protocol to assess true canal diameter at each cervical level. Axial cuts were made through the foramen magnum in a plane parallel to the foramen magnum to assess true cerebellar tonsillar ectopia. Eighty-eight such MRIs were done. Almost all were interpreted by the UW radiology staff as normal, as showing only minimal disc bulging, as showing DDD/DJD, or mild thecal sac effacement. Only one was read as showing a Chiari malformation, and 7 as showing frank stenosis of a moderate or severe degree. In contract, 79 of these MRIs were interpreted by the author and by Dr. Dan S. Heffez: 12 – normal, 16 – minimal abnormality, 18 – significant cerebellar tonsillar ectopia, 21 – significant stenosis, and 24 – stenosis and ectopia. Thirty-nine patients were seen and evaluated by Dr. Heffez. Twenty-three had at least one operative procedure done, and three were not considered surgical candidates. Of the remaining 3, surgery was recommended for 11, and follow-up with possible surgery for 2.


CHIARI I MALFORMATION REDEFINED: Clinical and Radiographic Findings for 364 Symptomatic Patients


Thomas H. Milhorat, M.D., Mike W. Chou, M.D., Elizabeth M. Trinidad, M.D., Roger W. Kula, M.D., Menachem Mandell, M.D., Chantelle Wolpert, M.B.A., P.A.-C., Marcy C. Speer, Ph.D.

Departments of Neurosurgery (THM, MWC, EMT), Neurology (RWK), and Radiology (MM), State University of New York Health Science Center at Brooklyn, Brooklyn, New York; The Long Island College Hospital (THM, MWC, EMT, RWK), Brooklyn, New York; and the Department of Medicine (CW, MCS), Section of Medical Genetics, Duke University Medical Center, Durham, North Carolina



OBJECTIVE: Chiari malformations are regarded as a pathological continuum of hindbrain maldevelopments characterized by downward herniation of the cerebellar tonsils. The Chiari I malformation (CMI) is defined as tonsillar herniation of at least 3 to 5 mm below the foramen magnum. Increased detection of CMI has emphasized the need for more information regarding the clinical features of the disorder.

METHODS: We examined a prospective cohort of 364 symptomatic patients. All patients underwent magnetic resonance imaging of the head and spine, and some were evaluated using CINE-magnetic resonance imaging and other neurodiagnostic tests. For 50 patients and 50 age- and gender-matcher control subjects, the volume of the posterior cranial fossa was calculated by the Cavalieri method. The families of 21 patients participated in a study of familial aggregation.

RESULTS: There were 275 female and 89 male patients. The age of onset was 24.9 ± 15.8 years (mean ± standard deviation), and 89 patients (24%) cited trauma as the precipitating event. Common associated problems included syringomyelia (65), scoliosis (42%), and basilar invagination (12%). Forty-three patients (12%) reported positive family histories of CMI or syringomyelia. Pedigrees for 21 families showed patterns consistent with autosomal dominant or recessive inheritance. The clinical syndrome of CMI was found to consist of the following: 1) headaches, 2) pseudotumor-like episodes, 3) a Meniere’s disease-like syndrome, 4) lower cranial nerve signs, and 5) spinal cord disturbances in the absence of syringomyelia. The most consistent magnetic resonance imaging findings were obliteration of the retrocerebellar cerebrospinal fluid spaces (364 patients), tonsillar herniation of at least 5 mm (332 patients), and varying degrees of cranial base dysplasia. Volumetric calculations for the posterior cranial fossa revealed a significant reduction of total volume (mean, 13.4 ml) and a 40% reduction of cerebrospinal fluid volume (mean, 10.8 ml), with normal brain volume.

CONCLUSION: These data support accumulating evidence that CMI is a disorder of the para-axial mesoderm that is characterized by underdevelopment of the posterior cranial fossa and overcrowding of the normally developed hindbrain. Tonsillar herniation of less than 5 mm does not exclude the diagnosis. Clinical manifestations of CMI seem to be related to cerebrospinal fluid disturbances (which are responsible for headaches, pseudotumor-like episodes, endolymphatic hydrops, syringomyelia, and hydrocephalus) and direct compression of nervous tissue. The demonstration of familial aggregation suggests a genetic component of transmission. (Neurosurgery 44:1005-1017, 1999)




DISTRIBUTION OF SUBSTANCE P IN THE SPINAL CORD OF PATIENTS WITH SYRINGOMYELIA


Thomas H. Milhorat, M.D., Harrison T. M. Mu, M.D., Carole C. LaMotte, Ph.D., and Ade T. Milhorat, M.D.


Department of Neurosurgery, State University of New York Health Science Center at Brooklyn and the Kings County Hospital Center, Brooklyn, New York; Departments of Surgery and Anesthesiology, Yale University School of Medicine, New York, New York



The distribution of substance P, a putative neurotransmitter and pain-related peptide, was studied using the peroxidase-antiperoxidase immunohistochemical method in the spinal cords obtained from autopsy of 0 patients with syringomyelia and 10 age- and sec-matched, neurologically normal individuals. Substance P immunoreactivity was present in axons and in terminal-like processes in close apposition to neurons in the first, second, and third laminae of the dorsal horn. Smaller amounts of peroxidase-positive staining were found in the fifth lamina of the dorsal horn, the intermediolateral nucleus, the intermediomedial nucleus, and the ventral horn. In nine of 10 patients with syringomyelia, there was a substantial increase in substance P immunoreactivity in the first, second, third, and fifth laminae below the level of the lesion. A marked reduction or absence of staining was present in segments of the spinal cord occupied by the syrinx. Central cavities produced bilateral abnormalities, whereas eccentric cavities produced changes that were ipsilateral to the lesion. No alterations in staining were found in the spinal cord of an asymptomatic patient with a small central syrinx. The authors conclude that syringomyelia can be associated with abnormalities in spinal cord levels of substance P, which may affect the modulation and perception of pain.


Craniocervical Decompression, Cerebral Blood Flow and Neuropsychological Dysfunction in FMS and CFS

Michael J. Rosner, M.D., F.A.C.S., F.C.C.M., Sharon E. Guin, C.R.N.P.,
Alice Johnson, R.N and Sheila D. Rosner, B.S.N., M.S.N.

Acknowledgements
The authors gratefully acknowledge Drs. J. M. Mountz and E. San Pedro of the Division of Nuclear Medicine at the University of Alabama at Birmingham for SPECT scan data.

Introduction: Because others have reported that rCBF measured by SPECT scan was abnormal in patients with fibromyalgia syndrome, the hypothesis was tested that rCBF as measured by SPECT scan would improve after craniovertebral surgery in similar patients.

Methods: Sixteen patients underwent pre-operative rCBF SPECT scan who had been offered decompressive craniovertebral surgery for Chiari syndrome, congenital cervical stenosis, or both. Detailed neurologic history and physical examination were recorded in a prospective standardized interview and examination. Pre-operative grip strength was measured and the spinal cord was measured in its AP and transverse diameters. After surgery, the interviews, standardized exams, grip strength, the spinal cord measurements, and the rCBF SPECT scan were repeated. A parallel group of patients later were given a more detailed questionnaire pre- and post-operatively which included a number of questions related to neuropsychological complaints. These were graded by the patients for severity using a 0-3 scale where 0 = no problem and 3 was severe, or a visual analog scale of 0-100 where 100 represented the worst imaginable degree of severity. A group of well controls completed the same instrument.

Results: Generalized bi-hemispheric increases in rCBF SPECT measures of blood flow occurred in a statistically reliable fashion. Generalized blood flow increases averaged 3 to 4 percent for global cortical measures. The left frontal lobe increased by approximately 10 percent and the right occipital and parietal regions by 4 and 12 percent respectively (p<.05--.001).
The neurologic complaints and exams of this group generally improved with reduction in hyperreflexia, Babinski responses, improvement in strength, etc. Grip strength improved from 23.2 ± 5.9 Kg. to 30.3 ± 11.4 Kg. (p = .03). In those patients undergoing cervical decompression (n = 8), spinal cord area increased by as much as 40 percent (p < .001).

Complaint Pre-Op (n=36) Post-Op (n=20) Control (n=6)
Neuropsychological
Mean SD Median Mean SD Median Mean SD Median
Memory 1.5 (1.1) [2] 0.5 (0.8) [0] 0.0 (0.0) [0]
Concentration 1.8 (1.4) [2] 0.7 (0.8) [0] 0.0 (0.0) [0]
Abnl logic 0.9 (1.0) [1] 0.3 (0.6) [0] 0.2 (0.4) [0]
Anxiety 1.2 (1.1) [1] 0.5 (0.8) [0] 0.2 (0.4) [0]
Depression 1.4 (1.1) [1.5] 1.1 (1.0) [1] 0.5 (0.8) [0]
Irritability 1.6 (1.0) [2] 1.0 (1.0) [1] 0.7 (0.8) [0.5]
Abnl Fatigue 1.9 (1.1) [2] 1.4 (1.1) [1] 0.2 (0.4) [0]

Sleep
Insomnia 1.9 (1.2) [2] 1.2 (1.2) [1] 0.3 (0.5) [0]
Poor sleep 2.2 (1.0) [3] 1.4 (1.2) [1] 0.3 (0.5) [0]
Awaken tired 2.2 (0.9) [3] 1.4 (1.1) [1] 1.0 (0.6) [1]
Pain awakens 1.9 (1.1) [2] 1.3 (1.2) [1] 0.0 (0.0) [0]

Visual Analog Scales

Feel Rested 71 (35) [90] 42 (34) [32] 32 (16) [36]
Awaken Tired 74 (34) [90] 49 (38) [43] 10 (17) [17]
Nervous 44 (31) [49] 19 (23) [49] 5 (9 ) [9]
Depressed 44 (35) [37] 22 (28) [7] 4 (10) [6]

There is substantial improvement in Neuropsychological/neurocognitive complaints after surgery, which parallels the improvements seen in a separate but otherwise similar population of FMS/CFS patients.

Conclusion: Abnormalities of rCBF are present in a group of FMS/CFS patients and provide an objective, physiological basis for complaints of decreased cognition, and related “neuropsychological” complaints. rCBF abnormalities may resolve with craniovertebral decompression in parallel with neuropsychological improvement; these data strengthen the concept of a physiological basis in the majority of patients for such complaints. Since rCBF studies provide objective evidence for such complaints, they may help guide the need for adjunctive therapy when rCBF abnormalities resolve but complaints persist. However, persistence of such abnormalities may suggest persist structural disease, or inadequate therapy and warrant reinvestigation of the patient.
Neurally Mediated Hypotension: Its surgical evaluation, management and early outcome as part of the Fibromyalgia—Chronic Fatigue Syndrome

Michael J. Rosner, MD, Peter D’Amour, MD and Peter C. Rowe, MD

Introduction: Correlation of MR findings in those patients with FMS and CF-IDS is difficult, in part due to wide variations in the population carrying these diagnoses. Because the subset of patients with NMH is rigorously defined by tilt table and other objective abnormalities and also may carry the diagnosis of FMS and/or CF-IDS, we analyzed their clinical symptoms, signs and MR findings. The latter was especially of concern since the radiological confirmation of structural disease in the FMS CF-IDS population is often vague, elusive and has significant overlap with asymptomatic patients.

Methods: Patients referred for potential surgical treatment with tilt table proven Neurally Mediated Hypotension (NMH) underwent a standardized interview, neurological evaluation, magnetic resonance (MR) evaluation including CINE MR of the posterior fossa. They also completed a 75 item questionnaire which rated the degree of a spectrum of complaints on a 0-3 scale (0=none, 3=severe) or a visual analog scale with 100 being the most severe possible degree.

Results: Fifteen patients have been evaluated; eleven have undergone craniovertebral decompression; two await surgery:
1. All patients have had resolution of syncope and hypotension. One remains on a low dose of fludrocortisone and a second on a low dose of dexadrine.
2. POTS has also improved or resolved in all cases, but the rate of resolution of the POTS has been slower than that of the NMH. There seems to be a phase of increased sensitivity to endogenous catecholamine release, which also resolves with time. Deconditioning, which is prominent in these patients, may also cause tachycardia, etc., and be confused with symptoms of POTS.
3. Concomitant symptoms of FMS and/or CF-IDS resolve in parallel with normalization cardiovascular responses. These symptoms include cognitive dysfunction, pain syndromes and a broad array of dysautonomic problems.

Complaint Pre-Op (n=13) Post-Op (n=5) Control (n=6)
Mean SD Median Mean SD Median Mean SD Median
Profuse sweat 1.6 (1.1) [1.5] 1.0 (0.8) [1] 0.0 (0.0) [0]
Dizziness 2.2 (0.9) [2.5] 1.4 (1.1) [1] 0.0 (0.0) [0]
SOB 1.6 (1.1) [2.0] 1.0 (1.4) [0] 0.0 (0.0) [0]
Chest Pain 1.4 (1.2) [1.0] 0.4 (0.9) [0] 0.0 (0.0) [0]
Palpitations 1.1 (1.1) [1.0] 0.2 (0.4) [0] 0.0 (0.0) [0]
Color changes 1.4 (1.3) [2.0] 0.8 (0.8) [1] 0.0 (0.0) [0]
Overall (0-3) 1.6 (1.0) [1.8] 1.1 (1.0) [0.7] 0.0 (0.0) [0]

Days felt good 0.6 (0.9) [0] 4.0 (4.2) [3] 6.8 (0.4) [7]
Missed work 5.8 (2.0) [7] 3.2 (2.2) [3] 0.0 (0.0) [0]

Visual Analog (%)
Pain Interferes 88 (13) [90] 57 (29) [48] 3 (16) [8.1]
Severity of pain 78 (25) [91] 48 (21) [47] 1 (17) [2.2]
Tiredness 91 (9) [92] 69 (29) [64] 10 (17) [17]
Awaken rested 93 (9) [96] 67 (31) [57] 32 (16) [36]

4. The MR differences between the patients with NMH vs. a group of normal control patients related to the
craniovertebral junction region. The foramen magnum was smaller, 35.5 ± 2.7 vs. 39 ± 4.8, p<0.03)
and the vertebral vessels impacted the brainstem to a greater degree and more often than controls
((p<0.03). The cerebellar tonsils were lower, 2.0 ± 1.1 vs. 1.25 ± 1.1 (p=0.14), and the C2 canal was
smaller, 11.3 ± 4.3 v s. 13.6 ± 1.7 (p=0.07); the latter two differences could have been due to chance.
5. No patient with NMH/POTS had a normal neurological exam. Neurological signs also improved following craniovertebral surgery.

Conclusions:
1. A population of patients with NMH/POTS responds to suboccipital craniectomy and/or cervical laminectomy.
2. If patients carry the diagnosis of FMS or CF-IDS, then these symptoms also resolve in parallel with the cardiovascular symptoms of NMH/POTS following craniovertebral decompression.
3. The MR/radiographic appearance of these patients is characterized by minimal abnormality and can easily be read as “normal.” However, the essential findings are consistent with the hypoplastic posterior fossa and/or congenital-cervical stenosis. There is, as yet, no pathognomonic radiographic change, which allows diagnosis independently of a careful and thorough history and physical examination.
4. While the radiological diagnosis of the hypoplastic posterior fossa can be difficult, the clinical outcome after decompressive surgery warrants a thorough evaluation and aggressive surgical approach.


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you can also search Andrew Holman's study of fibro and cervical stenosis; positional cord compression

 

[xrayspex]

I think that these 2 news stories in regard to neuro-surgeon Dr. Rosner sort of give an idea why the area of spinal issues and CFS has seemed so slow moving.....although I have heard it can take many years for research to become practice in any area of medicine (ie Marshall and antibiotics S. Pylori took forever to be accepted practice)

Sounds like Rosner was considered brilliant in research academics and practice and innovation.... but ran into some opposition because of course not 100% of people are going to like their surgical outcomes with challenging medical issues especially new territory and a group of other surgeons/docs targeted him it sounds like but now he is getting back on his feet:

today:

https://www.hendersonvillelightning...JKY28KfEkPEBxjUdsczsmF4DgOTv2ruUlgdKfg0EUb7vk


yesterday:


https://www.wsj.com/articles/SB942280927444238502

this link might work better:
http://www.anapsid.org/cnd/diagnosis/chiari.html

 

[jeff_w]

Hi @xrayspex,

Thank you for the links! This is interesting information about cord compression and Chiari Malformation as they relate to Fibromyalgia and ME/CFS. There is a neurosurgical connection on multiple fronts.

The articles you posted discuss "craniovertebral decompression," which opens up the skull, and is a different surgery than the one I had. There is also research about alleviating spinal cord compression causing remission of ME/CFS, whereas I had a skull to C2 fusion for CCI/AAI, which alleviated brainstem compression.

Thus far, no articles have been published about CCI/AAI fusion surgeries, which I had, as they relate to ME/CFS. So there have not yet been conference presentations about situations like mine, where an ME/CFS patient had CCI/AAI surgically corrected.

 

[xrayspex]

Hi @xrayspex,

Thank you for the links! This is interesting information about cord compression and Chiari Malformation as they relate to Fibromyalgia and ME/CFS. There is a neurosurgical connection on multiple fronts.

The articles you posted discuss "craniovertebral decompression," which opens up the skull, and is a different surgery than the one I had. There is also research about alleviating spinal cord compression causing remission of ME/CFS, whereas I had a skull to C2 fusion for CCI/AAI, which alleviated brainstem compression.

Thus far, no articles have been published about CCI/AAI fusion surgeries, which I had, as they relate to ME/CFS. So there have not yet been conference presentations about situations like mine, where an ME/CFS patient had CCI/AAI surgically corrected.

yep thanks Jeff......I just thought though that it is interesting the cranial cervical junction sure seems to play into this and efforts made in past with research to identify some of it
I still haven't arranged scans to rule out CCI or AAI.........I would bet money I have cervical instability but I dont know if its above or below atlas area yet or both.....just dreading putting neck in extension because trying to work for a while with accoms and that would surely foil me.....I will know when am ready (had enough)

 

[frozenborderline]

Hi everyone. So like I said in other thread , I’ve been told that if bolognese doesn’t see anything, he says “we can’t help you” and if he does see something, he has you do traction for diagnostic purposes before he sees you. This is proving to be a big hurdle. I live in a very rural area and it’s hard to go out at all. There are no home pts here and the one pt recommended to deal with cci specifically is booked until March. Bolognese wants me to do traction six times before getting back to him. Going out once would already be tricky. Going out six times way moreso. Also no guarantee the pt will even want to do traction. Not sure that my doctor wrote the order specifically for that (he doesn’t understand this cci thing) and the pt isn’t just going to do traction because I ask, yet bolognese won’t write the order directly. I wonder if I can just show bolognese email to the Pt or to my doctor. Or if he can talk to my doctor directly. I feel that wearing the collar all the time has weakened my neck, but it’s extra hard to recondition with PEM. I certainly think the collar has been helpful but I originally thought this process could be faster than it has been and that the collar would be a temporary measure to hold me together for a month tops. Now it’s been two months. And I’m not close to diagnosis or treatment.

It worries me that bolognese May think of me as a borderline case b/c I think normally he would just ask for traction once? Not sure.

 

[frozenborderline]

If anyone could help me figure this whole deal out so I can get help quicker that would be much appreciated. Also still can’t get into the freaking beyond the measurement group ! What the hell