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

Messages
5
Hello everyone,

I have just received Upright MRI findings of atlantoaxial subluxation. I am waiting on a full report from Dr Gilete.

I was diagnosed with ME/CFS in 2007 and developed neurological symptoms in 2009, at which point I was told it was ‘functional’.

I am apprehensive about the road ahead and am looking for some support to understand this condition.
 

suevu

Senior Member
Messages
170
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.

In my own case pain in the neck area appeared also much later after all the other symptoms.

however prior to fatigue I had some symptoms that seem to be related to CCI, much before fatigue, I had a lot of issues with sound and light sensitivity especially very thin sounds like forks, plates, rings, etc... also white lights were a nightmare for me, and I didnt have any fatigue at all, I actually used to run like 10-20 km a day as prescribed by "doctors" to overcome my neurologial issues, what I did was only getting worse. I hope these guys end up in jail some day for all what they did to me.
 

Yuno

Senior Member
Messages
118
Hi @mattie I wonder, if you could help me with a quick question.
Dr. Gilete wants me to do a venogram and Amy has been wanting to send me the request form with the details for a week now, but they seem to be so utterly drowned in work, that she doesnt seem to get to do it.

There is a different terminology in German, so if I understood correctly they need not only veins, but veins and arteries from head and neck down to T1?
They need it with contrast and they need it to rule out any kind of blood vessel stenosis and check for signs of IHH. Is that right and is that what you had done ?

Sorry for the bother and thank you so much !
 

mattie

Senior Member
Messages
384
Hi Yuno,
They need it with contrast and they need it to rule out any kind of blood vessel stenosis and check for signs of IHH. Is that right and is that what you had done ?
Correct, contrast is needed and it is to look for stenosis in veins and especially the internal jugular veins and transverse sinuses.

I couldn't tell you how to order this scan in German,
but here is exactly how Amy wrote it up for me:

Kindly request the fufillment of the following scan:
-MRI angio/venogram, gadolinium enhanced, reviewing intracraneal venous system and cervical (neck) venography especially internal jugular vein trajectory from lateral sinus to subclavian vein. Evaluate for possible compression of the jugular vein.


Please note that: Stenosis or a compressed vein on a MRI is not hard evidence for IIH.
IIH can be confirmed by checking for papilledema by an opthomologist,
and / or by measuring opening pressure with lumbar puncture.

And a few doctors (Higgins / Kenneth Liu) diagnose IIH by measuring pressure gradients around found stenosis.
 
Last edited:

bread.

Senior Member
Messages
499
@mattie

hi mattie,

how are you doing these days? what do you think was your overall improvement and are you positive it was the surgery?

thank you so much.
 

Yuno

Senior Member
Messages
118
Hi Yuno,

Correct, contrast is needed and it is to look for stenosis in veins and especially the internal jugular veins and transverse sinuses.

I couldn't tell you how to order this scan in German,
but here is exactly how Amy wrote it up for me:

Kindly request the fufillment of the following scan:
-MRI angio/venogram, gadolinium enhanced, reviewing intracraneal venous system and cervical (neck) venography especially internal jugular vein trajectory from lateral sinus to subclavian vein. Evaluate for possible compression of the jugular vein.


Please note that: Stenosis or a compressed vein on a MRI is not hard evidence for IIH.
IIH can be confirmed by checking for papilledema by an opthomologist,
and / or by measuring opening pressure with lumbar puncture.

And a few doctors (Higgins / Kenneth Liu) diagnose IIH by measuring pressure gradients around found stenosis.

Mattie, did you do you Angio/Venogram with a Tesla 3.0 or with a 1.5?
I guess a 3.0 is preferable, but the insurance doesn’t wanna pay, so I’m considering paying the difference myself. Just wondering if it’s worth it.
Thank you again!
 

mattie

Senior Member
Messages
384
Mattie, did you do you Angio/Venogram with a Tesla 3.0 or with a 1.5?
I guess a 3.0 is preferable, but the insurance doesn’t wanna pay, so I’m considering paying the difference myself. Just wondering if it’s worth it.
Thank you again!
I had a 1.5 T MRV with contrast.
 
Messages
7
I find myself ever more the skeptic after 35 years of this now, but this is beginning to feel like TMJ in the late 80s/early 90s. It seemed like everyone who couldn't be diagnosed with anything else was diagnosed with a TMJ problem back then...including me. The doctor who diagnosed me was "very confident" based on all the xrays that TMJ was my problem, and extensive orthodontics was the solution. I declined "treatment" because my nonsense alarm kept going off, and I'm glad I did. A lot of people found out the hard way that orthodontics can cause some serious problems.

I've also lost confidence that without a biomarker, patient reports of improvement are unreliable. Case in point being the Rituxan trial, where when double blinding was applied as many people "improved" from nothing (placebo) as improved from Rituxan...which calls into question whether anyone improved due to Rituxan, or whether it was just the random waxing and waning characteristic of CFS that was being reported as improvement. I think the jury is still out.

I'm sure there are clear cut cases of CCI and Chiari, but I also have a sense that when someone has only a hammer everything looks like a nail.

I also am highly skeptical of this turning into a “fad treatment” and urge caution as the surgeries are not without risk. I especially like your hammer and nail quote as that has been the mantra of so many doctors I have seen.
 
Messages
52
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.


-----------------------------

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


Okay I realize I'm totally late to the party on this thread, but want to say that I am seeing Dr. Rosner for my first consult at the end of the month because of suspected mechanical issues causing my ME. It should be noted that he does do upright flexion and extension MRI's for those looking to get this kind of imaging done. I understand he's been treating ME/CFS and Fibro with neurosurgery (for those exhibiting Chiari and/or stenosis) for decades, mostly under the radar. I'm sure he wouldn't be surprised at all at the recent results Jeff, Jen, and others have experiences from fusion and TC release surgeries (although I don't know if he performs these surgeries).

I've reached out to at least a dozen of Rosner's patients, and almost all of them have said something along the lines of "he saved my life." I've never heard such raving reviews of a doctor (these were all patients who went under the knife).

I have ME/CFS, Fibro, POTS, hypermobility (likely EDS), scoliosis, and I suspect stenosis, CCI/AAI, and/or tethered cord, but am waiting for dx from Rosner and others on the last three, will try to keep people posted on my experience with him. He could be someone to add to the list of neurosurgeons able to help with mechanical etiologies of ME, but need to clarify with him when I see him about which surgeries he does. Just thought I'd weigh in!
-----------------------------------------------------------------------------------
EDIT - I was wrong, Dr. Rosner does NOT do upright MRI's. He does supine flexion and extension.
 
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Yuno

Senior Member
Messages
118
@mbunke thank you for posting all that Info. That’s super interesting!! Could you please ask Dr. Rosner, if he was open to Skype consultations for patients abroad ? It would be immensely helpful to have the possibility of a second opinion in addition to Dr. Gilete. Thanks!
 
Messages
52
@mbunke can I ask how you contacted him ? I can’t seem to find his email address. Thanks
I will do my best to remember to ask him that! I'm creating a list of questions so I'll add that to it.

I don't have an email address, but his website with phone and address listed is here: http://www.mjrosner.com/

They are a small and busy office so you'll likely get voicemail if you call, just leave a message and they usually call you back pretty quickly.
 

Yuno

Senior Member
Messages
118
I will do my best to remember to ask him that! I'm creating a list of questions so I'll add that to it.

I don't have an email address, but his website with phone and address listed is here: http://www.mjrosner.com/

They are a small and busy office so you'll likely get voicemail if you call, just leave a message and they usually call you back pretty quickly.


THANKS!!
 
Messages
52
Okay I realize I'm totally late to the party on this thread, but want to say that I am seeing Dr. Rosner for my first consult at the end of the month because of suspected mechanical issues causing my ME. It should be noted that he does do upright flexion and extension MRI's for those looking to get this kind of imaging done. I understand he's been treating ME/CFS and Fibro with neurosurgery (for those exhibiting Chiari and/or stenosis) for decades, mostly under the radar. I'm sure he wouldn't be surprised at all at the recent results Jeff, Jen, and others have experiences from fusion and TC release surgeries (although I don't know if he performs these surgeries).

I've reached out to at least a dozen of Rosner's patients, and almost all of them have said something along the lines of "he saved my life." I've never heard such raving reviews of a doctor (these were all patients who went under the knife).

I have ME/CFS, Fibro, POTS, hypermobility (likely EDS), scoliosis, and I suspect stenosis, CCI/AAI, and/or tethered cord, but am waiting for dx from Rosner and others on the last three, will try to keep people posted on my experience with him. He could be someone to add to the list of neurosurgeons able to help with mechanical etiologies of ME, but need to clarify with him when I see him about which surgeries he does. Just thought I'd weigh in!

Okay it looks like Dr. Rosner actually does not perform Upright MRI's, he does supine flexion and extension. Sorry for the misinformation!
 

bread.

Senior Member
Messages
499
Okay it looks like Dr. Rosner actually does not perform Upright MRI's, he does supine flexion and extension. Sorry for the misinformation!


how does he do that? lying on the back or side? I am very severe and cant do a sitting anymore.
 
Messages
52
how does he do that? lying on the back or side? I am very severe and cant do a sitting anymore.
I'm not sure...doesn't seem to make much sense. I'll chat with them next week and try to get more details. I know he can give Ativan for those who need it for the imaging.
 
Messages
52
Story of EDS teen making impressive recovery after TC release and CCI from Henderson's website
 

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