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.  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.  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  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  [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  ↓ further reduction in cerebral blood flow after exercise Greater involvement of the brain correlates with greater severity  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  Reduced brain matter – (MRI) ↓ Reduced regional gray and white matter volumes are consistent with impaired memory and visual processing.  ↓ global reduction of gray matter volume [54, 89] ↓ gray matter volume in midbrain & pulse pressure suggest impaired cerebrovascular auto-regulation  ↓ white midbrain matter volume decreased with fatigue duration  Hypometabolism – (PET) ↓ metabolism of glucose in the brain,  ↓ 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.  ↓ 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.  ↓ poor and slower motor performance 90 & abnormal spatial and temporal symmetry of gait  Sleep – (EEG) ↑ prolonged sleep onset latency  ↓ disruption of REM sleep & reduced duration of uninterrupted sleep [92, 93] ↑ increased alpha intrusion into delta sleep  Cerebral spinal fluid - (spinal tap) increased opening pressure on lumbar puncture Proteomes distinguish ME from post-treatment Lyme disease and controls.  ↑ increased lymphocytes 95 and protein [94, 95] • IL-10 increased with granulocyte-macrophage (GM), colony-stimulating factor (CSF) suppression  ↑ elevated lactate is consistent with reduced cortical blood flow, mitochondrial dysfunction & oxidative stress  Lateral ventricular: 297% vs. anxiety disorder & 348% vs. controls  Spinal cord and ganglia - (autopsy) ↑neuroinflammation in the dorsal root ganglia, (modulators of peripheral sensory information traveling to the brain)  [References cited above] 1. 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