I know it's been talked about before, chiari, please help.

Discussion in 'Fibromyalgia Main Forum' started by misskoji, Oct 15, 2008.

  1. misskoji

    misskoji Member

    Hi all.

    I'm hoping you don't mind if I bring this subject up again. I read through every Chiari post I could find on the board and it's been helpful.

    I'm hoping, however, to hear from those that have been dx with it, or suspect it, and have had the surgery or have decided against it. And what if any improvments/worsening you experienced. Or alternatives, if any other than surgery? I read a little about the axis thing, have to read more on that.

    Just an aside, I have not officially been dx, just really researching all I can before I spend money on journying to the specialist and/or making any kinds of decisions.

    I know what works for some doesn't always work for others too and we're all different, but I'm thirsting for information here.

    Thanks so much for any help.

  2. misskoji

    misskoji Member

    I hope someone out there will see this. Thanks so much.
  3. SkeptikSharon

    SkeptikSharon New Member

    Hi Misskoji,

    I wish I could help you with this, but actually, I just thought I'd bump this up, because I am also curious about this.

    Does anyone know if this is something that is automatically ruled out with an MRI? Or do you have to specifically ask for it to be considered?
  4. simonedb

    simonedb Member

    mmmm I am too tired to type a lot
    did you google and research? should be a lot of info out there. maybe at neurotalk etc

    anyway I did all the testing for that about 8 years ago or so and they decided the cervical stenosis was more the problem but its similar.
    you do have to go to someone, not just any neurologist, that really knows the issue, and the mri does have to be taken a very specific way or they can miss it. there is controversy in the field about when its bad enough for surgery.
    you could go to dan rosner on east coast or dan heffez in midwest or i am sure there are a bunch of docs known to specialise in it everywhere, but do not mention fms or cfs to a regular neurosurgeon or they may not give you a fair evalution.
  5. spacee

    spacee Member

    Have seen a good neurologist and he said that I didn't have it.

  6. misskoji

    misskoji Member

    Sharon, I'm a research nut at times. :) Sometimes I'll fill my whole day up with reasearch. But from what I've read, (and was able to retain) Chiari is tough to diagnose. And it varies from neurologist to neurologist what their criteria for the malformation will be.

    I've found a couple of specialists, the one I decided to go with is Dr. Heffez, as someone else mentioned. He's based in Milwaukee, WI now. I figured it can't hurt to know right? He is a neurosurgeon, but will also help in testing and diagnosing for Chiari. Anway, I haven't made the appointment yet, as I'm spending some money seeking out Dr. Lerner first. But, I fully intend to see him.

    There is a lot of controversy surrounding Chiari Malformation, it's diagnosis and it's treatment. Some of the neuro's have caught a lot of flack from their peers about this, and some hold strong to their beliefs and conclusions and protocol for it.

    From what I gather, some years back they were linking the malformation to FMS/CFS. But like all treatments, nothing is foolproof and not everyone recovered. Also, some of the patients did not fare well after the surgery to correct it. I mean it is neurosurgery, so it's not to be taken lightly and the risks are obviously there.

    But I did read a couple of posts and stories where people talked about having the surgery and going into full remission of symptoms.

    There are also alternatives to surgery, and I did find those protocols too. So I guess all in all it's no cure all end all, but I think it's worth at least testing for.

    I was just hoping to hear from a few more that had personal experiences to share. I hope you'll update on if you decide to test for it Sharon. I'll be sure to post my findings.

    Good Luck,

  7. simonedb

    simonedb Member

    hey definitely post what happens. i saw him in 99/00 when all the good and bad press exploded and after the link to fms the neurosurgeon i Had seen in town treated me alike a pariah cus i had a fms dx, its really unfortunate how that went down for everyone. also i do recall some people reacting very badly to the surgery and that getting alot of attention but yea i remember some did better after surgery.
    I am so sensitive to meds with p45o problem I am way afraid to put self thru the trauma of another surgery. i get messed up just from doing the catscan that was part of the eval. hopefully he doesnt do that anymore cus putting one's head back in extension like that is rough on ya if you have stenosis. i didnt do the surgery and then saw rosner in like 02 for another opinon and he would have done laminectomy and fusion if i wanted and keep a watch on what he thought was mild chiari, but it all scared me and I am not sure if thats the main issue or just another issue.
    i do ok if i dont jump around with my neck but its always an accident waiting to happen, i have paid for a lot of myofascial work over the years.

    what made you think of getting the eval? do u think you have another issue too like mitochondrial? is there any good website right now for chiari etc? there used to be a bunch back in the day but i havent really looked for years other than at neurotalk which used to be brainchat i think, very occasionally peek there.
  8. misskoji

    misskoji Member

    Thanks for sharing your experience. What led me to wanting the evaluation was research. I can spend hours upon hours researching and (trying to retain the information) to learn new things. I'm not sure what symptom exactly led me to Chiari, but I'm thinking it was the specific type of headaches I get as well as an easily aggrivated neck. Then upon further research, the thickening of finger joints and vertigo, and on and on. Many of my symptoms match those listed with Chiari. A few don't, but that is to be expected. Then again, a lot of those same symptoms are the same with CFS and FMS.

    What is the p45o problem you have? That's not one I've heard of before. I can certainly understand being scared of surgery though. Especially one this intensive and risky. Have you been reconsidering Chiari and treatment for it lately? The only one site I have stored in my list is http://chiarione.org/index.html It seems to be a bit dated. There were quite a few other ones I stumbled on, but for some reason only stored this one.


  9. simonedb

    simonedb Member

    I havent been thinking about the surgery lately, but this is reminding me that one of my docs suggested getting an updated eval on it.
    I should probably have an mri from time to time......just havent sensed its a crisis right now so want to come at things from another angle for now to support self other ways ie nutritional etc.
    surgery is too much of a crap shoot for me unless my arm goes numb and I cant use it or something.
    I did try to find my old forum on it i went to back in 2000 and cant remmeber or find it but i did find an old email from one of the members who sent me all the pertinent research at the time. I dont know if its progressed much since then.

    p450 refers to the cytochrome system if you go to wikipedia to start it can explain but its part of my chemical sensitivity, can't detox cus of genetic limitiations or mitochondrial damage and thats why surgery scares me with the anesthesia, maybe thats why this chiari stuff didnt take off cus they havent found away to protect us from the trauma of surgery, i looked into dr jho in pittsburgh back in 02 cus at least he does minimally invasive surgery but still anesthesia.....
    good luck keep posting

    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.


    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.


    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.


    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.


    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)


    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.

    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)
    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]

    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.

    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.
  10. Dinee

    Dinee New Member

    Maybe I can help, I've had very successful surgery in '06 by Michael Rosner MD in Hendersville NC

    let me know,
  11. misskoji

    misskoji Member

    I'm very glad to hear of your outcome, and thank you for coming to share your experience here.

    I have decided to take a break from the medical community, in terms of serious protocols anyway. So, I have not yet met Dr. Hefez as planned. For now, I'm just trying to get my pain relieved and hoping for a little recovery before seeking out anything else.

    Can I ask you, on a percentage level, how much better do you feel after the surgery?

    Is there anything further you need to do after surgery with the surgeoun or neuros? (Check ups, MRI's, ect?)

    Thanks so much

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