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Evidence of Neurological Abnormalities in ME Suppressed in the IOM "ME/CFS" R

Discussion in 'Institute of Medicine (IOM) Government Contract' started by Nielk, Mar 7, 2015.

  1. Nielk

    Nielk

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    https://drive.google.com/a/phoenixrising.me/file/d/0B4uD-VyWmIw2VlR2OVhRbng5Mzg/view

    Evidence of Neurological Abnormalities in Myalgic Encephalomyelitis Suppressed in the IOM "ME/CFS" Report

    By - Jerrold Spinhirne S. E.




    The recent IOM "ME/CFS" report made this claim of page 9:



    The committee deemed the term “myalgic encephalomyelitis,” although commonly endorsed by patients and advocates, to be inappropriate because of the general lack of evidence of brain inflammation in ME/CFS patients, as well as the less prominent role of myalgia in these patients relative to more core symptoms.

    However, the 15-member IOM committee evidently ignored, dismissed, or discounted an overwhelming amount of published, peer-reviewed research evidence to the contrary.

    The 2014 Nakatomi et al. study "Neuroinflammation in Patients with Chronic Fatigue Syndrome/Myalgic Encephalomyelitis: An 11C-(R)-PK11195 PET Study" concluded:

    Neuroinflammation is present in widespread brain areas in CFS/ME patients and was associated with the severity of neuropsychologic symptoms. Evaluation of neuroinflammation in CFS/ME patients may be essential for understanding the core pathophysiology and for developing objective diagnostic criteria and effective medical treatments.
    http://m.jnm.snmjournals.org/content/55/6/945.full.pdf

    It is vitally important to note that this important study used the 2011 ME-ICC to select subjects. (Reference 13 in the paper) Although the Nakatomi et al. paper used the undefined term "CFS/ME" to refer to the disease, this is solely an ME study. That the subjects also met the broader 1994 CDC Fukuda CFS criteria (Reference 12 in the paper) is irrelevant because only a portion of the Fukuda CFS subjects meet the more specific 2011 International Consensus Criteria for ME. The results of this study can be applied reliably only to ME patients – not the overly inclusive group of Fukuda-diagnosed CFS patients.

    The IOM report discussed this study and others finding evidence of brain abnormalities beginning on page 88, but nevertheless the committee concluded that there was a "general lack of evidence of brain inflammation in ME/CFS patients." Nor did the IOM committee conclude there was sufficient evidence of neurological abnormalities associated with their new socially constructed fatigue illness "SEID" to justify making cognitive impairment a required symptom for diagnosing "SEID." By contrast, the 2011 ME-ICC require at least THREE symptoms indicating neurological involvement for an ME diagnosis. This is consistent with the World Health Organization's 46-year classification of ME as a neurological disease.

    Inexplicably, the IOM committee did NOT mention the 2012 International Consensus Primer whatsoever in their 235-page report. The 26 highly qualified and experienced members of the ICC panel from 12 countries concluded on page ii:

    Myalgic encephalomyelitis, a name that originated in the 1950s, is the most accurate and appropriate name because it reflects the underlying multi-system pathophysiology of the disease. Our panel strongly recommends that only the name ‘myalgic encephalomyelitis’ be used to identify patients meeting the ICC because a distinctive disease entity should have one name. Patients diagnosed using broader or other criteria for CFS or its hybrids (Oxford, Reeves, London, Fukuda, CCC, etc.) should be reassessed with the ICC. Those who fulfill the criteria have ME; those who do not would remain in the more encompassing CFS classification.
    http://sacfs.asn.au/download/me_international_consensus_primer_for_medical_practitioners.pdf

    http://www.name-us.org/DefintionsPages/DefinitionsArticles/2012_ICC%20primer.pdf

    These are the neurological abnormalities, with published, peer-reviewed references, that the 2012 IC Primer panel found. Somehow, the inexperienced US IOM committee found that this valuable evidence supporting the continued use of the name of myalgic encephalomyelitis and continued use of the ICC to diagnose ME was not worthy of mention in their report.

    From the 2012 IC Primer, pages 4-5:

    Neurological Abnormalities

    Neurocognitive, sleep, autonomic and sensory disturbances, pain, headaches, and paresthesias are prominent neurological signs and symptoms. Cognitive impairments including slow processing of information, poor attention, word finding, and working memory are some of the most functionally disabling symptoms. [1, 73, 74]

    Structural and functional abnormalities within the brain and spinal cord are consistent with pathological dysfunction of the regulatory centers and communication networks of the brain, CNS and ANS, and are essential for effective ongoing self-organization. [1, 75] Reduced brainstem gray matter volume is consistent with insult to the midbrain at fatigue onset.

    Feedback control loops may suppress cerebral motor and cognitive activity, disrupt CNS homeostasis, and reset elements of the ANS. [76] These abnormalities play crucial roles in neurological and neurocognitive symptoms. [1, 5, 11, 57, 65] Greater source activity and more parts of the brain are utilized in cognitive processing, which supports patients’ perception of greater effort. [73, 77, 78] Reduced duration of uninterrupted sleep may explain reported unrefreshed sleep, pain and overwhelming fatigue. [79] These observed pathological changes are consistent with neurological disorders but not psychiatric conditions.

    [Image description] 3D Comparison VS Adult Norms II – Avg. activity sampling By Dr. Ismael Mena 2010 [80]

    Extensive areas of hypoperfusion are characteristic of ME: HMPAO c99m radiopharmaceutical for brain blood flow assessment. Images of the patient are reconstructed and compared against normal age matched data-base by means of Oasis Segami USA Software. In color gray normal perfusion equal to mean + 2 St Dev, colors blue, green and black, 2-5 St dev.below the normal mean denoting hypoperfusion. Left lateral view shows marked hypoperfusion in the lateral aspects of the temporal lobe, extending to the frontal and parietal lobes. Left medial view shows extensive hypoperfusion in the limbic system involving anterior, medial and posterior cingulates. There is left temporal medial hypoperfusion that denotes hypofunction in the projection of the hippocampus. Both posterior cingulate and hippocampal hypofunction denote cognitive impairment. (Ventricular system is in color white.) Finally, there is hypoperfusion in the occipital lobe. Ismael Mena, MD, nuclear medicine [80]

    [Table, pages 4-5]

    Neurological Structural & Functional Abnormalities
    Hypoperfusion [80-84] (Neuro-SPECT, arterial spinning labeling)
    ↓ regional blood flow (rCBF), ↓ absolute cortical blood flow [46, 85]
    ↓ hypoperfusion in brainstem distinguishes ME from depression [83]
    ↓ further reduction in cerebral blood flow after exercise Greater involvement of the brain correlates with greater severity [46]

    Punctate lesions – white matter hyperintensities (MRI)

    Plaque or hyperintensities in the white matter & tracts is consistent with demyelination or inflammation & increase risk of cerebrovascular events [86, 87]
    • brainstem injury and loss of homeostasis [76]

    Reduced brain matter – (MRI)

    ↓ Reduced regional gray and white matter volumes are consistent with impaired memory and visual processing. [88]
    ↓ global reduction of gray matter volume [54, 89]
    ↓ gray matter volume in midbrain & pulse pressure suggest impaired cerebrovascular auto-regulation [76]
    ↓ white midbrain matter volume decreased with fatigue duration [76]

    Hypometabolism – (PET)

    ↓ metabolism of glucose in the brain, [36] ↓ metabolism in brain stem differentiates ME from depression [46, 83]

    Neurocognitive – (fMRI, qEEG & SPECT)

    ↑ Greater effort is required - elevated source current & more regions of the brain are utilized in cognitive activity & fatiguing tasks: poor processing of auditory & spatial information, poor working memory. [73, 77, 78]
    ↓ slower performance in visual imagery & motor tasks - ventral anterior cingulate cortex was active when controls made an error but not in patients. [54]
    ↓ reduced blood flow in temporal lobes may contribute to memory and cognitive impairment & fatigue [80, 81]

    Pain and Fatigue – mRNA assays

    Elevated sensory signaling perceived by the brain as pain and fatigue [11, 57, 90]

    Musculoskeletal – (surface EEG scalp)

    CNS signals are altered when controlling voluntary muscle activities, especially when they are fatiguing. [90]

    ↓ poor and slower motor performance 90 & abnormal spatial and temporal symmetry of gait [91]

    Sleep – (EEG)

    ↑ prolonged sleep onset latency [79]
    ↓ disruption of REM sleep & reduced duration of uninterrupted sleep [92, 93]
    ↑ increased alpha intrusion into delta sleep [79]

    Cerebral spinal fluid - (spinal tap) increased opening pressure on lumbar puncture Proteomes distinguish ME from post-treatment Lyme disease and controls. [94]

    ↑ increased lymphocytes 95 and protein [94, 95]
    • IL-10 increased with granulocyte-macrophage (GM), colony-stimulating factor (CSF) suppression [95]
    ↑ elevated lactate is consistent with reduced cortical blood flow, mitochondrial dysfunction & oxidative stress [96]
    Lateral ventricular: 297% vs. anxiety disorder & 348% vs. controls [96]

    Spinal cord and ganglia - (autopsy)
    ↑neuroinflammation in the dorsal root ganglia, (modulators of peripheral sensory information traveling to the brain) [97]

    [References cited above]

    1. Carruthers BM, van de Sande MI, De Meirleir KL, Klimas DG, Broderick G, Mitchell T, Staines D, Powles ACP, Speight N, Vallings R, Bateman L, Baumbarten-Austrheim B, Bell DS, Carlo-Stella N, Chia J, Darragh A, Jo D, Lewis D, Light AR, Marshall-Gradisbik S, Mena I, et al. Myalgic encephalomyelitis: International Consensus Criteria. J Intern Med 2011; 270: 327-338. [PMID: 21777306]
    http://onlinelibrary.wiley.com/doi/10.1111/j.1365-2796.2011.02428.x/pdf

    5. Meeus M, Nijs J, McGregor N, Meeusen R, et al. Unravelling intracellular immune dysfunctions in chronic fatigue syndrome: interactions between protein kinase R activity, RNase L cleavage and elastase activity, and their clinical relevance. In Vivo. 2008; 22: 115-21. [18396793]

    11. Light AR, White AT, Hughen RW, Light KC. Moderate exercise increases expression for sensory, adrenergic and immune genes in chronic fatigue
    syndrome patients but not in normal subjects. J Pain 2009; 10: 1099-112. [PMID: 19647494]

    46. Yoshiuchi K, Farkas I, Natelson BH. Patients with chronic fatigue syndrome have reduced absolute cortical blood flow. Clin Physiol Funct Imaging
    2006; 26: 83-6. [PMID: 16494597]

    54. de Lange FP, Kalkman JS, et al. Gray matter volume reduction in chronic fatigue syndrome. NeuroImage 2005; 26: 777-781. [PMID: 15955487]


    57. Demitract MA, Crofford LJ. Evidence for and pathophysiologic implications of hypothalamic-pituitary-adrenal axis dysregulation in fibromyalgia
    and chronic fatigue syndrome. Ann NY Acad Sci 1998; 840: 684-97. [PMID: 9629295]

    65. Meeus M, Roussel NA, Truijen S, Nijs J. Reduced Pressure pain thresholds in response to exercise in chronic fatigue syndrome but not in chronic low back pain: an experimental study. J Rehabil Med 2010; 42: 884-90. [PMID: 2087801]

    73. Lange G, Steffener J, Cook DB, Bly BM, Christodoulou C, Liu WC, Deluca J, Natelson BH. Objective evidence of cognitive complaints in Chronic Fatigue Syndrome: a BOLD fMRI study of verbal working memory. Neuroimage 2005; 26: 513-24. [PMID: 15907308]

    74. Michiels V, Cluydts R, Fischler B. Attention and verbal learning in patients with chronic fatigue syndrome. J Int Neuropsychol Soc 1998; 4: 456-66.

    75. Chen R, Liang FX, Moriay J, et al. Chronic fatigue syndrome and the central nervous system. J Int Med Res 2008; 36: 867-74. [PMID: 18831878]

    76. Barnden LR, Crouch B, Kwiatek R, Burnet R, Mernone A, Chryssidis S, Scroop G, Del Fante P. A brain MRI study of chronic fatigue syndrome: evidence of brainstem dysfunction and altered homeostasis. NMr Biomed 2011; 24: 1302-12. [PMID: 21560176]

    77. Cook DB, O'Connor PJ, Lange G, Steffener J. Functional neuroimaging correlates of mental fatigue induced by cognition among chronic fatigue
    syndrome patients and controls. Neuroimage 2007; 36: 108–22. [PMID: 17408973]

    78. Flor-Henry P, Lind JC, Koles ZJ. EEG source analysis of chronic fatigue syndrome. Psychiatry Res 2010; 181: 155-64. [PMID: 20006474]

    79. Van Hoof E, De Becker P, Lapp C, et al. Defining the occurrence and influence of alph-delta sleep in chronic fatigue syndrome. Am J Med Sci 2007; 333: 78-84. [PMID: 17301585]

    80. Mena I, Villanueva-Meyer J. Study of Cerebral Perfusion by NeuroSPECT in Patients with Chronic Fatigue Syndrome. In: Hyde BM, Goldstein J, Levine P, eds. The Clinical and Scientific Basis of Myalgic Encephalomyelitis, Chronic Fatigue Syndrome. Ottawa, Ontario & Ogdensburg, New York State: The Nightingale Research Foundation; 1992: 432-8.

    81. Goldstein JA, Mena I, Jouanne E, Lesser I. The assessment of vascular abnormalities in late life chronic fatigue syndrome by brain SPECT: Comparison with late life major depressive disorder. J CFS 1995; 1: 55-79.

    82. Goldberg MJ, Mena I, Darcourt J. NeuroSPECT finding in children with chronic fatigue syndrome. J CFS 1996; 3: 61-67.

    83. Costa DC, Tannock C, Brostoff J. Brainstem perfusion is impaired in chronic fatigue syndrome. QJM 1995; 88: 767-773. [PMID: 8542261]

    84. Ichise M, Salit I, Abbey S, Chung DG, Gray B, Kirsh JC, Freedman M. Assessment of regional cerebral perfusion by Tcm-HMPAO SPECT in chronic
    fatigue syndrome. Nucl Med Commun 1992; 13: 767-772. [PMID: 1491843]

    85. Biswal B, Kunwar P, Natelson BH. Cerebral blood flow is reduced in chronic fatigue syndrome as assessed by arterial spin labeling. J Neurol Sci.
    2011; 301: 9-11. [PMID: 21167506]

    86. Lange G, Wang S, Deluca J, Natelson BH. Neuroimaging in chronic fatigue syndrome. Am J Med 1998; 105: 50S-53S. [PMID: 9790482]

    87. Buchwald D, Cheney PR, Peterson DL, Henry B, Wormsley SB, et al. A chronic illness characterized by fatigue, neurologic and immunologic
    disorders, and active human herpes virus type 6 infection. Ann Intern Med 1992; 116: 103-113. [PMID: 1309285]

    88. Puri BK, Jakeman PM, Aqour M, Gunatilake KD, Fernando KA, et al. Regional grey and white matter volumetric changes in myalgic encephalomyelitis (chronic fatigue syndrome): a voxel-based morphometry 3 T MRI study. Br J Radiol 2012; 85: e270-3. [PMID: 22128128]

    89. Okada T, Tanaka M, Kuratsune H, Watanabe Y, Sadato N. Mechanisms underlying fatigue: a voxel-based morphometric study of chronic fatigue
    syndrome. BMC Neurol 2004; 4: 14. [PMID: 15461817]

    90. Siemionow V, Fang Y, Calabrese L, Sahgal V, Yue GH. Altered central nervous system signal during motor performance in chronic fatigue
    syndrome. Clin Neurophysiol. 2004; 115: 2372-81. [PMID: 15351380]

    91. Saggini R, Pizzigallo E, Vecchiet J, Macellari V, Giacomozzi C. Alterations of spatial-temporal parameters of gait in Chronic Fatigue Syndrome
    patients. J Neurol Sci 1998; 154: 18-25. [PMID: 9543318]

    92. Togo F, Natelson BH, Cherniack NS, FitzGibbons J, Garcon C, Rapoport DM. Sleep structure and sleepiness in chronic fatigue syndrome with or
    without coexisting fibromyalgia. Arthritis Res Ther 2008; 10: R56. [PMID: 18474105]

    93. Kishi A, Struzik ZR, Natelson BH, Togo F, Yamamoto Y. Dynamics of sleep stage transitions in healthy humans and patients with chronic fatigue
    syndrome. Am J Physiol Regul Integr Comp Physiol 2008; 294: R1980-7. [PMID: 18417644]

    94. Schutzer SE, Angel TE, Liu T, Schepmoes AA, Clauss TR, Adkins JN, Camp DG, Holland BK, et al. Distinct cerebrospinal fluid proteomes differentiate post-treatment lyme disease from chronic fatigue syndrome. PLoS ONE 2011; 6: e17287. [PMID: 21383843]

    95. Natelson BH, Weaver SA, Tseng CL, Ottenweller JE. Spinal fluid abnormalities in patients with chronic fatigue syndrome. Clin Diagn Lab Immunol
    2005; 12: 52-5. [PMID: 15642984]

    96. Mathew SJ, Mao X, Keegan KA, Levine SM, Smith EL, et al. Ventricular cerebrospinal fluid lactate is increased in chronic fatigue syndrome compared with generalized anxiety disorder: an in vivo 3.0 T (1)H MRS imaging study. NMR Biomed 2009; 22: 251-8. [PMID: 18942064]

    97. Chaudhuri A. Abstract presentation at the Royal Society of Medicine Meeting 2009.
     
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  2. alex3619

    alex3619 Senior Member

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    I just wrote this to FB but its applicable to this very issue:

    Most of the ignored things have insufficient evidence under EBM rules. Its not about the evidence, its about the rules of evidence. So they are excluded by the methodology. However, and I have not yet read deeply enough to be sure of this, its possible they also failed to apply EBM correctly.

    There are conditions where study quality can be upgraded or downgraded due to things like effect size. I hope to be looking later to see if this is done. I suspect it wasn't , most EBM reviews use cookie cutter approaches as its cheaper and easier and quicker.

    EBM is inappropriate in biased research bases, and that includes biases induced by lack of funding and research, emphasis on small studies, non-replication etc. All of which abound in ME research. So much of this is neither a surprise nor due to the authors of the report.

    Nearly everything considered a hot topic today in the research is actually old. Its just been sitting there for the most part because nobody had the funds or other resources.

    I have made a point, and others have too (Ellie Stein, Leonard Jason) that the IOM report should have started with a study to validate the definition.

    Let me expand on that. This is an evidence based review. So they come up with a theoretical diagnostic criteria. Which they then fail to validate empirically. Evidence based without testing? I consider that a contradiction, and a failure of the process.
     
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  3. Marco

    Marco Grrrrrrr!

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    Abnormal neurological findings, no matter how robust, do not necessarily equate to 'encephalomyelitis'.
     
  4. Jon_Tradicionali

    Jon_Tradicionali Alone & Wandering

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    Goldstein has been convinced for a long time that limbic encephalopathy of the brain is the root cause.

    After the Dubbo findings and Japanese study, Peterson (if I'm not mistaken) said there was no other possibility other than to accept that there is low-grade encephalomyelitis in the brain.
     
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  5. Marco

    Marco Grrrrrrr!

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    He's entitled to his opinion of course but neuroinflammation or encephalo'pathy' is not the same as a demyelinating inflammation of the brain and spinal cord.
     
  6. Nielk

    Nielk

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    It is interesting to note that 26 experts including Klimas and Bateman who authored the ME-IC Primer in 2012 found enough evidence for the use of the name ME.
     
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  7. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    Good work @Nielk.

    Never made sense to me for them to say no inflammation when there is research showing elevated inflammatory cytokines.

    I also think muscle pain is alot more common then they think its just that its not the main issue for some or its cyclic type of pain.
     
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  8. Jon_Tradicionali

    Jon_Tradicionali Alone & Wandering

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    What do you believe to be the case then?

    I don't think its demyelinating Neuroinflammation either.

    In reference to Neuroinflammation and in particular low-grade encephalitis, HSV-1 would be the number one candidate I'd say.
     
  9. alex3619

    alex3619 Senior Member

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    The rules of evidence were different.

    Its long been the case that a government body, agency or whatever can limit the rules of evidence, limit the scope and so limit the possible outcomes. Sometimes this is a good thing, but it can be used to distort and manipulate outcomes too.
     
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  10. duncan

    duncan Senior Member

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    It may be irrelevant, but I find it interesting that mainstream Lyme doctors and researchers - at least in the United States - try to downplay both the prevalence and severity of neuroborreliosis.

    Within the patient community, it is widely known NB is everywhere, probably more common than swollen knees. Anecdotal evidence of brain involvement, often profound involvement, is abundant. ILADS practitioners acknowledge the problem and try to address it.

    But the official position from the CDC and IDSA seems to be that TBDs, and in particular Lyme, with CNS or brain involvement, are the exception rather than the rule. They seem intent on denying what is right in front of their eyes, and ignoring literally thousands that can demonstrate associated defects.
     
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  11. melamine

    melamine Senior Member

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    If I were to name my most disabling symptom this would be it. It's why I feel frozen out of IOMs disease, whatever they want to call it. ICC is where my illness resides.

    My muscle pain is of a type that when it's not prominent, such as it was for several years following a flu-like infection, I tend to forget to tell doctors about it because it's become part of the new "normal" background noise. My muscles fatigue rapidly resulting in abnormal pain or/and weakness, and sometimes tremor or stiffness. How much and how soon depends on the location of them and is relative to my general condition. When my lower back muscles stopped supporting me effectively while sitting upright it was not a matter of deconditioning, since I sat nearly every day during the time it first began.
     
    Last edited: Mar 8, 2015
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  12. Sidereal

    Sidereal Senior Member

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    Same here. Breathing muscles became weak next. I'd love to hear how the deconditioning hypothesis can account for that.
     
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  13. melamine

    melamine Senior Member

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  14. Marco

    Marco Grrrrrrr!

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    I think there's sufficient evidence from cognitive and autonomic impairments to refer to encephalopathy whether structural or functional and some evidence to support neuroinflammation (i.e. primed/activated glia).
     
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  15. jimells

    jimells Senior Member

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    I have been wondering how they can spend a million dollars to come up with a new hypothesis without actually testing it, and still call it "science". I don't even recall the ever-present research conclusion of, "Our conclusion is this hypothesis needs more research money, and a new grant application is in the mail."
     
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  16. Iquitos

    Iquitos Senior Member

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    Yes, I noticed that, too. Made me wonder how those two, Klimas and Bateman, could have let these ideas be ignored by the IoM.
     
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  17. alex3619

    alex3619 Senior Member

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    That is the trick. It is NOT science. Its a managerial review.
     
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  18. Izola

    Izola Senior Member

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    What does?
     
  19. Esther12

    Esther12 Senior Member

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    Were any of the various criteria for ME/CFS tested before they were published?

    To me it seems pretty normal for them to just publish whatever they think some committee thinks is worthwhile.
     
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  20. WillowJ

    WillowJ คภภเє ɠรค๓թєl

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    I haven't read the entire report, but some of those items are indeed in the report.

    Some of this is definitely there.

    I know there is a section on sleep, but I don't know what's in it exactly.

    I didn't see the same kind of "this study doesn't meet criteria for being a 'worthy' study to be included" way of sorting out papers like was done in P2P and in other EBM reviews. Instead they just said it was a difficult field due to low funding & etc., lots of studies were small, and said what the specific limitations of the studies were as they reviewed them.

    But I also didn't read the whole paper and didn't check to see whether certain things were excluded.

    Because they didn't wait a year or so, all the interesting new papers like the qEEG study, Stanford's fancy MRI study, the PET study, the CII cytokine paper, and so on--none of those made it in. Hopefully someone will follow through with a review in a couple years or so with all these new findings, including the open-label rituximab paper due out soon and the rituximab stage III clinical trial when it comes out.
     
    Last edited: Mar 24, 2015
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