• Decreased brain metabolism found in ME / CFS patients using PET scan. Dr. TM Tavio, Aviano Italy. The greatest impairment was found in the right medial frontal cortex and the brainstem. This may be a bio marker for ME / CFS.

• Natelson BH, Cohen JM, Brassloff I, Lee HJ: A controlled study of brain magnetic resonance imaging in patients with the chronic fatigue syndrome. J Neurol Sci 1993, 120:213-217.

• From Neurology to Mitochondia. Richardson J, Costa DC. J CFS 1998, 4(3)

• J. P. Neary, A. D. W. Roberts, N. Leavins, M. F. Harrison, J. C. Croll and J.R. Sexsmith, "Prefrontal Cortex Oxygenation During Incremental Exercise in Chronic Fatigue Syndrome," Clinical Physiology and Functional Imaging, 2008.

• S. K. Johnson and J. DeLuca, "Chronic Fatigue Syndrome and the Brain," In: J. DeLuca, Ed., Fatigue as a Window to the Brain, MIT Press: Cambridge, Vol. 1, No. 4, MA, 2005, pp. 137-156

• Myalgic Encephalomyelitis: Guidelines for Doctors Journal: J of Chronic Fatigue Syndrome, Vol. 10(1) 2002, John Richardson, MB BS

• Masaaki Tanaka, Akira Ishii, Yasuyoshi Watanabe, Regulatory mechanism of performance in chronic cognitive fatigue. Medical Hypotheses 82 (2014) 567–571.

• Tanaka M, Ishii A, Watanabe Y (2013) Neural Mechanism of Facilitation System during Physical Fatigue. PLoS ONE 8(11): e80731. doi:10.1371/

• Viral Isolation from Brain in Myalgic Encephalomyelitis (A Case Report) J. Richardson J. Richardson is affiliated with Newcastle Research Group, Belle Vue, Grange Road, Ryton, Tyne & Wear, NE40 3LU, England. Journal of Chronic Fatigue Syndrome, Vol. 9(3/4) 2001, pp. 15-19

• Tomoda A, Miike T, Yamada E, Honda H, Moroi T, Ogawa M, Ohtani Y, Morishita S: Chronic fatigue syndrome in childhood. Brain Dev 2001, 22:60-64.

• Lange G, DeLuca J, Maldjian JA, Lee H, Tiersky LA, Natelson BH: Brain MRI abnormalities exist in a subset of patients with chronic fatigue syndrome. J Neurol Sci 2005, 171:3-7.

• Chaudhuri A, Condon B, Gow J, Brennan D, Hadley D: Proton magnetic resonance spectroscopy of basal ganglia in chronic fatigue syndrome. Brain Imaging 2003, 14:225-228.

• Brooks JC, Roberts N, Whitehouse G, Majeed T: Proton magnetic resonance spectroscopy and morphometry of the hippocampus in chronic fatigue syndrome. Br J Radiol 2000, 73:1206-1208.

• T. Okada, M. Tanaka, H. Kuratsune, Y. Watanabe and N. Sadato, "Mechanisms Underlying Fatigue: A Voxel-Based Morphometric Study of Chronic Fatigue Syndrome,"BioMedCentral Neurology, Vol. 4, No. 1, 2004, pp. 14-20.

• Association between serotonin transporter gene polymorphism and chronic fatigue syndrome Masaaki Narita, Naoko Nishigami, Naoko Narita, Kouzi Yamaguti, Nobuo Okado, Yasuyoshi Watanabe, Hirohiko Kuratsune. Biochemical and Biophysical Research Communications Volume 311, Issue 2, 14 November 2003, Pages 264–266

• Brain regions involved in fatigue sensation: reduced acetylcarnitine uptake into the brain. Kuratsune H, Yamaguti K, Lindh G, Evengård B, Hagberg G, Matsumura K, Iwase M, Onoe H, Takahashi M, Machii T, Kanakura Y, Kitani T, Långström B, Watanabe Y.. Neuroimage. 2002 Nov;17(3):1256-65.

• Costa DC, Tannock C, Brostoff J (1995) Brainstem perfusion is impaired in chronic fatigue syndrome. QJM 88:767–773 291. Ichise M, Salit I, Abbey S, Chung DG, Gray B, Kirsh JC, Freedman M (1992) Assessment of regional cerebral perfusion by TcmHMPAO SPECT in chronic fatigue syndrome. Nucl Med Commun 13:767–772

• Basal ganglia hypermetabolism and symptoms of fatigue during interferon-alpha therapy. Capuron L1, Pagnoni G, Demetrashvili MF, Lawson DH, Fornwalt FB, Woolwine B, Berns GS, Nemeroff CB, Miller AH. Neuropsychopharmacology. 2007 Nov;32(11):2384-92. Epub 2007 Feb 28.

• Role of infection and neurologic dysfunction in chronic fatigue syndrome.Komaroff AL, Cho TA.Division of General Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA. Komaroff@hms.harvard.edu. (2011)

• Richard B. Schwartz et al., ' SPECT Imaging of the Brain: Comprison of Findings in Patients with Chronic Fatigue Syndrome, AIDS Dementia Complex, and Major Unipolar Depression ' American Journal of Roentgenology 162 (April 1994): 943-51

• MRI scans and SPET scans show that the brain (in CFS patients) appears to be working harder than in a healthy person doing the same task. Other parts of the brain seem to brought in to help. A. Komaroff, D. Clauw, research paper presented to AACFS 5th International Research, Clinical and Patient Conference, 2001

• Siemionow V, et al. Altered central nervous system signal during motor performance in chronic fatigue syndrome. Clin Neurophysiol 2004 Oct;115(10):2372-81.

• The Emergence of a New Disease: Searching for a Diagnostic Marker and Treatment for Chronic Fatigue Immune Dysfunction Syndrome in a Changing Society, Myra Preston, PhD. CFIDS Journal Winter 1996

• BOLD fMRI scans. Objective evidence of cognitive complaints in Chronic FatigueSyndrome: A BOLD fMRI study of verbal working memory
  Tanaka M et al, “Reduced Responsiveness is an Essential Feature of Chronic Fatigue Syndrome: a fMRI Study,” BMC Neurol Feb 22; 6 (2006): 9.
  Yoshiuchi K, “Patients with Chronic Fatigue Syndrome have Reduced Absolute Cortical Blood Flow.” Clin Physiol Funct Imaging Mar 26(2) (2006): 83-6.
  Lange G et al, "Objective Evidence of Cognitive Complaints in Chronic Fatigue Syndrome: a BOLD fMRI Study of Verbal Working Memory," Neuroimage Jun 26(2) (2005):5 13-24.
  De Lange FP et al, "Gray Matter Volume Reduction in the Chronic Fatigue Syndrome," Neuroimage Jul 1; 26(3)(2005): 777-81.

• A. R. Spitzer and M. Broadman, "Treatment of the Narcoleptiform Sleep Disorder in Chronic Fatigue Syndrome and Fibromyalgia with Sodium Oxybate," Pain Practice, Vol. 10, No. 1, 2010, pp. 54-59.
  Spitzer and Broadman believe that many patients with ME/CFS and FM have a lesion in the ventral-lateral preoptic nucleus of hypothalamus, which is critical to initiating and maintaining sleep. This explains the sleep abnormalities in these illnesses.

• Impaired blood pressure variability in chronic fatigue syndrome—a potential biomarker. J. Frith et al. (2012)

• Detection of Viral-Related Sequences in CFS Patients using Polymerase Chain Reaction W.John Martin (Nightingale Research Foundation: 1989: 1-5)

• Chronic Fatigue Syndrome and the Psychiatrist SE Abbey, PE Garfinkel Canadian Journal of Psychiatry 1990:35:7:625-626

• Detection of Intracranial Abnormalities in Patients with Chronic Fatigue Syndrome: Comparison of MR Imaging and SPECT. RB Schawrtz, BM Garada American Journal of Roentgenology 1994:162:935-941

• Research by Michael Goldberg MD., USA. Shows regional cerebal blood flow (rCBF) was abnormally low in the temporal, parietal and right frontal lobes in CFS patients. SPECT scans were used. Brainstem perfusion is impaired in patients with chronic fatigue syndrome. Costa, DC., Tannock, C and Brostoff; Quarterly Journal of Medicine, 1995, 88, 767-773.

• Kuchinad A, Schweinhardt P, Seminowicz D, Wood P, Chizh B, Bushnell M. Accelerated brain gray matter loss in fibromyalgia patients: premature aging of the brain? J Neurosci. 2007;27:4004–7.

• Abnormal MRI's in many patients with Punctate lesions in the subcortical white mater and periventricular area's.

• Lake Tahoe Epidemic:
  • A chronic illness characterized by fatigue, neurologic and immunologic disorders, and active Human Herpesvirus Type 6 Infection. Annals of Internal Medicine 1116: 103-13 "Magnetic resonance scans of the brain showed punctate, subcortical areas of high signal intensity consistent with oedema or demyelination in 78% of patients"

• W. J. Shian and C. S. Chi, "Epstein-Barr virus Encephalitis and Encephalomyelitis: MR Findings," Pediatric Radiology, Vol. 26, No. 9, 1996, pp. 690-693

• M. Hausler, V. T. Ramaekers, M. Doenges, K. Schweizer, K. Ritter and L. Schaade, "Neurological Complications of Acute and Persistent Epstein-Barr Virus Infection in Paediatric Patients," Journal of Medical Virology, Vol. 68, No. 2, 2002, pp. 253-263.

• Natelson BH et al. J Neurol Sci/1993; 120: 213

• In the book ' Oslers Web ', Neuropsychologist Sheila Bastien and Dr. Dan Peterson found the following brain abnormalities in CFS patients "What we're finding is that the left temporal lobe, the right parietal lobe, and the left frontal lobe are the three areas with the most damage," she said
  Oslers Web, by Hillary Johnson, Penguin Books 1997, pages 658-659

• Advances in biomedical understanding of ME.  Neil Abbot.  Vance Spence.  InterAction  May 2004

• In 1988 in conjunction with the University of Pittsburgh, the US NIAID held a large research workshop called "Consideration of the Design Studies of Chronic Fatigue Syndrome". There were participants from the Centres for Disease Control and from the National Institutes of Health. One of the presentations was by Dr Sandra Daugherty, who reported that MRI scans on patients demonstrated abnormalities consistent with demyelination and cerebral oedema in 57% of patients studied.

• Morris et al.
  • Central pathways causing fatigue in neuro-inflammatory and autoimmune illnesses. Morris et al. 2015.
  • The Neuro-Immune Pathophysiology of Central and Peripheral Fatigue in Systemic Immune-Inflammatory and Neuro-Immune Diseases Morris et al. 2015.
  • A neuro-immune model of Myalgic Encephalomyelitis/Chronic fatigue syndrome. Morris G, Maes M. Metab Brain Dis. 2013;28:523–40
  • The Putative Role of Viruses, Bacteria, and Chronic Fungal Biotoxin Exposure in the Genesis of Intractable Fatigue Accompanied by Cognitive and Physical Disability, 2015 points to the effects of past infections and continuing chronic infections in the perpetuation of ME over many years or decades. Parvoviruses, HHV6, variants of Epstein-Barr, Cytomegalovirus, Mycoplasma, and Borrelia burgdorferi and Mold infection are mentioned. This would create some differences and subsets between patients.
  • Morris G, Anderson G, Galecki P, Berk M, Maes M. A narrative review on the similarities and dissimilarities between myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and sickness behavior. BMC Med. 2013;11:64.
  • A neuro-immune model of Myalgic Encephalomyelitis/Chronic fatigue syndrome. Morris G, Maes M (2012). Metab Brain Dis. 2013 Dec;28(4):523-40.
  • Morris G, Maes M. Mitochondrial dysfunctions in myalgic encephalomyelitis/chronic fatigue syndrome explained by activated immuno-inflammatory, oxidative and nitrosative stress pathways. Metab Brain Dis 2014;29(1):19–36
  • Myalgic encephalomyelitis/chronic fatigue syndrome and encephalomyelitis disseminata/multiple sclerosis show remarkable levels of similarity in phenomenology and neuroimmune characteristics. Gerwyn Morris and Michael Maes. Morris and Maes BMC Medicine 2013 11:205   doi:10.1186/1741-7015-11-205

• Cook DB et al. Int J Neurosci 2001; 107:1

• http://www.chronicillnet.org/CFS/Ostrom/chp20.html

• Goldstein J. Chronic Fatigue Syndrome - the Limbic hypothesis Haworth Medical Press, Binghampton New York, 1993

• "CFS(ME) patients scanned using Positron Emission Tomography (PET) indicate that areas of their brains are under active in uptake of glucose, the brain’s energy supply f. These early findings could explain the ‘foggy’ brain syndrome, poor concentration, in CFS(ME) and FMS. 
  The rate of blood flow in the brain has been tested in both normal individuals and CFS(ME) patients using SPECT scanning with results indicating that the patients had poorer circulation to those parts of the brain controlling both memory and the movement of body parts including the muscles.
  Brain Electrical Activity Mapping (BEAM) was used to test CFS(ME) and FMS patients with abnormalities in circulation to the brain (temporal lobes) The researchers found that it was impossible to distinguish between CFS(ME) and FMS patients even if the FMS patients did not report difficulties with memory.
  PET (Positron Emission Tomography) research has shown that there is a far lower degree of activity in the frontal lobe of the brain of people with CFS(ME) when compared with normal (control) individuals or when compared with a group of depressed patients who also showed some lowering of activity in these areas.
  Dr Jay Goldstein, using SPECT technology, examined 33 patients with CFS, 15 of whom also met the criteria for FMS. Scans showed marked reduction in blood flow in the right hemisphere of the brain, especially amongst FMS patients.
  James Mountz MD and Laurence Bradley, using SPECT, examined the cerebral blood flow of 10 FMS patients and found a decrease in the region of the caudate nuclei (right and left) which is involved in memory and concentration as well as pain regulation functions."
  
  Leon Chaitow, N.D., D.O., MRO, Senior Lecturer, University of Westminster
  Chronic Fatigue Syndrome & Fibromyalgia: The Brain/Sleep Connection
  ChronicFatigueSyndromeSupport.com
  08-05-2002

• "Dr Jay Goldstein believes that the limbic system, if not functioning normally, could be responsible for many of the symptoms seen in FMS and CFS(ME), including the obvious ‘brain fog’ as well as depression, dizziness, tinitus , intolerance to alcohol, nasal allergies, tendency to gain weight, sensitivity to chemical smells and specific foods, breathing irregularities and many more.
  He believes that the limbic system disturbance may itself be the result of cytokine production by viral agents as well as cytokines produced during exercise activity.
  In support of this theory Dr.Ismael Mena, using SPECT methods, has shown that the blood flow through that part of the brain known as the cerebral cortex, already low in CFS patients, is further reduced rather than increased (as would be normal) after active exercise."
  
  Leon Chaitow, N.D., D.O., MRO, Senior Lecturer, University of Westminster
  Chronic Fatigue Syndrome & Fibromyalgia: The Brain/Sleep Connection
  ChronicFatigueSyndromeSupport.com
  08-05-2002

• Cook DB et al. Relationship of brain MRI abnormalities and physical functional status in chronic fatigue syndrome. International Journal of Neuroscience, 2001, 107, (1-2), 1-6

• The book 'Oslers web' details the lesions found on the brains of most CFS patients. These have been found by eminent medical and scientific people
  Oslers Web, by Hillary Johnson, Penguin Books 1997

• "One of the most disturbing findings made by Dr. Carter and his research team was that CFS patients with abnormally high levels of IL-1 had "anatomic holes" in their brains that were detected by using brain scans. It was not clear to the research team whether the holes were reversible or permanent"
  Dr. William A. Carter is a Professor of Oncology and Hematology at Hahnemann University in Philadelphia
  ' America's Biggest Cover-Up: 50 More Things Everyone Should Know About The Chronic Fatigue Syndrome Epidemic And Its Link To AIDS ',  by Neenyah Ostrom, 1993,  ISBN: 0-9624142-3-9

• Infection(s), chronically activated Immune system and Neuroinflammation & Oxidative and Nitrosative stress and damage in Neurological illnesses
  There are common factors in all of these illnesses, involving activated immune pathways and inflammatory cytokines and inflammatory markers, and neuroinflammation, and high oxidative and nitrosative stress levels and damage, and mitochondria damage, damage to the nervous sytem, with or without infection(s) has been found in neurodegenerative diseases such as Parkinsons, Alzheimers, MS and many others. This causes extreme fatigue and tiredness. This is also found in autoimmune diseases. And they are also found in ME and CFS, a neurological illness according to WHO, with immune system dysfunctions. See research listing below.
  
  
  • Inflammation and NeuroInflammation and Fatigue
    • Perry VH. Contribution of systemic inflammation to chronic neurodegeneration. Acta Neuropathol. 2010;120:277–86. PubMed Perry VH, Nicoll JA, Holmes C. Microglia in neurodegenerative disease. Nat Rev Neurol. 2010;6:193–201.
    • Mosley RL, Hutter-Saunders JA, Stone DK, Gendelman HE. Inflammation and adaptive immunity in Parkinson's disease. Cold Spring Harb Perspect Med. 2012;2:a009381.
    • Holmes C, Cunningham C, Zotova E, Woolford J, Dean C, Kerr S, et al. Systemic inflammation and disease progression in Alzheimer disease. Neurology. 2009;73:768–74.
    • Heesen C, Schulz KH, Fiehler J, Von der Mark U, Otte C, Jung R, et al. Correlates of cognitive dysfunction in multiple sclerosis. Brain Behav Immun. 2010;24:1148–55.
    • Arai H, Furuya T, Mizuno Y, Mochizuki H. Inflammation and infection in Parkinson's disease. Histol Histopathol. 2006;21:673–8.
    • Perry VH, Cunningham C, Boche D. Atypical inflammation in the central nervous system in prion disease. Curr Opin Neurol. 2002;15:349–54.
    • Perry VH. The influence of systemic inflammation on inflammation in the brain: implications for chronic neurodegenerative disease. Brain Behav Immun. 2004;18:407–13.
    • Beiske AG, Svensson E. Fatigue in Parkinson’s disease: a short update. Acta Neurol Scand Suppl. 2010;190:78–81.
    • Alves G, Wentzel-Larsen T, Larsen JP. Is fatigue an independent and persistent symptom in patients with Parkinson disease? Neurology. 2004;63:1908–11
    • Pal S, Chaudhuri KR, Trenkwalder C, Forbes A, Bridgman K, DiMarco A. The parkinson’s disease sleep scale (pdss): A new instrument for assessment of sleep, nocturnal disability and daytime sleepiness in parkinson’s disease. Mov Disord. 2002;17:S122.
    • Friedman JH, Brown RG, Comella C, Garber CE, Krupp LB, Lou JS, et al. Fatigue in Parkinson’s disease: a review. Mov Disord. 2007;22:297–308.
    • Barone P, Antonini A, Colosimo C, Marconi R, Morgante L, Avarello TP, et al. The PRIAMO study: a multicenter assessment of nonmotor symptoms and their impact on quality of life in Parkinson’s disease. Mov Disord. 2009;24:1641–9.
    • Hagell P, Brundin L. Towards an understanding of fatigue in Parkinson disease. J Neurol Neurosurg Psychiatry. 2009;80:489–92.
    • Londoño D, Cadavid D. Bacterial lipoproteins can disseminate from the periphery to inflame the brain. Am J Pathol. 2010;176:2848–57.
    • Segal B, Thomas W, Rogers T, Leon JM, Hughes P, Patel D, et al. Prevalence, severity, and predictors of fatigue in subjects with primary Sjögren's syndrome. Arthritis Rheum. 2008;59:1780–7.
    • Ahn GE, Ramsey-Goldman R. Fatigue in systemic lupus erythematosus. Int J Clin Rheumtol. 2012;7:217–27.
    • Hewlett S, Ambler N, Almeida C, Cliss A, Hammond A, Kitchen K, et al. Self-management of fatigue in rheumatoid arthritis: a randomised controlled trial of group cognitive-behavioural therapy. Ann Rheum Dis. 2011;70:1060–7.
    • Sattar N, McCarey D, Capell H, McInnes I. Explaining how a "high-grade" systemic inflammation accelerates vascular risk in rheumatoid arthritis. Circulation. 2003;108:2957–63.
    • Ku I, Imboden J, Hsue P, Ganz P. Rheumatoid arthritis: model of systemic inflammation driving atherosclerosis. Circ J. 2009;73:977–85.
    • Repping-Wuts H, van Riel P, van Achterberg T. Fatigue in patients with rheumatoid arthritis: what is known and what is needed. Rheumatology (Oxford). 2009;48:207–9.
    • Repping-Wuts H, Fransen J, van Achterberg T, Bleijenberg G, van Riel P. Persistent severe fatigue in patients with rheumatoid arthritis. J Clin Nurs. 2007;16:377–83.
    • Munoz L, Janko C, Grossmayer G, Frey B, Voll R, Kern P, et al. Remnants of secondarily necrotic cells fuel inflammation in systemic lupus erythematosus. Arthritis Rheum. 2009;60:1733–42.
    • Lee HM, Sugino H, Nishimoto N. Cytokine networks in systemic lupus erythematosus. J Biomed Biotechnol. 2010;2010:676284.
    • Sisto M, Lisi S, Ingravallo G, Lofrumento D, D’Amore M, Ribatti D. Neovascularization is prominent in the chronic inflammatory lesions of Sjögren’s syndrome. Int J Exp Pathol. 2014;95:131–7.
    • Lisi S, Sisto M, D’Amore M, Lofrumento D, Ribatti D. Emerging avenues linking inflammation, angiogenesis and Sjögren’s syndrome. Cytokine. 2013;61:693–703.
    • Muscal E, Brey R. Neurological manifestations of systemic lupus erythematosus in children and adults. Neurol Clin. 2010;28:61–73.
    • Tobón G, Pers J, Devauchelle-Pensec V, Youinou P. Neurological disorders in primary Sjögren’s syndrome. Autoimmune Dis. 2012;2012:645967.
    • Meszaros Z, Perl A, Faraone S. Psychiatric symptoms in systemic lupus erythematosus: a systematic review. J Clin Psychiatry. 2012;73:993–1001.
    • Ramos-Remus C, Duran-Barragan S, Castillo-Ortiz J. Beyond the joints: neurological involvement in rheumatoid arthritis. Clin Rheumatol. 2012;31:1–12.
    • Centonze D, Muzio L, Rossi S, Cavasinni F, De Chiara V, Bergami A, et al. Inflammation triggers synaptic alteration and degeneration in experimental autoimmune encephalomyelitis. J Neurosci. 2009;29:3442–52.
    • Inglese M, Park SJ, Johnson G, Babb JS, Miles L, Jaggi H, Herbert J, Grossman RI (2007) Deep gray matter perfusion in multiple sclerosis: dynamic susceptibility contrast perfusion magnetic resonance imaging at 3 T. Arch Neurol 64(2):196–202 293.
    • Niepel G, Tench CR, Morgan PS, Evangelou N, Auer DP, Constantinescu CS (2006) Deep gray matter and fatigue in MS: a T1 relaxation time study. J Neurol 253(7):896–902
  • Infections and Immunity and Fatigue
    • Alvarez-Lafuente R, De las Heras V, Bartolomé M, Picazo JJ, Arroyo R. Relapsing-remitting multiple sclerosis and human herpesvirus 6 active infection. Arch Neurol. 2004;61:1523–7.
    • Akhyani N, Berti R, Brennan MB, Soldan SS, Eaton JM, McFarland HF, et al. Tissue distribution and variant characterization of human herpesvirus (HHV)-6: increased prevalence of HHV-6A in patients with multiple sclerosis. J Infect Dis. 2000;182:1321–5
    • Miranda-Hernandez S, Baxter AG. Role of toll-like receptors in multiple sclerosis. Am J Clin Exp Immunol. 2013;2:75–93.
    • Horton C, Pan Z, Farris A. Targeting Toll-like receptors for treatment of SLE. Mediators Inflamm. 2010; 2010. doi:10.1155/2010/498980.
    • Nakamura M, Matsuoka T, Chihara N, Miyake S, Sato W, Araki M, et al. Differential effects of fingolimod on B-cell populations in multiple sclerosis. Mult Scler. 2014;20:1371–80.
    • Hauser SL, Waubant E, Arnold DL, Vollmer T, Antel J, Fox RJ, et al. B-cell depletion with rituximab in relapsing-remitting multiple sclerosis. N Engl J Med. 2008;358:676–88.
    • Polman CH, O’Connor PW, Havrdova E, Hutchinson M, Kappos L, Miller DH, et al. A randomized, placebo-controlled trial of natalizumab for relapsing multiple sclerosis. N Engl J Med. 2006;354:899–910.
    • The role of Chronic Lyme disease in Neurological illnesses
    • Research showing Chronic Lyme Disease implicated in the development of Alzheimer's disease
      - Lyme Biofilms Alive in Alzheimer's Disease Plaques
      - Link betwen Lyme disease and Alzheimer's disease
      - Lyme disease relationship to Alzheimer's disease
      - MacDonald, A.B., Miranda, J.M. Concurrent neocortical borreliosis and Alzheimer’s disease. Hum Pathol. 1987; 18(7): 759 - 61
      - Miklossy, J., Khalili, K., Gern, L., Ericson, R.L., Darekar, P., Borrelia burgdorferi persists in chronic Lyme neuroborreliosis and may be associated with Alzheimer disease. J Alzheimers Dis. 2004; 6(6): 639 – 49
      - Miklossy J. Alzheimers disease - a neurospirochetosis. Analysis of the evidence following Kochs' and Hill's criteria. Jounral of Neuroinflammation. 2007;8:90
      - Miklossy J. Alzheimers disease - a neurospirochetosis ? Neuroreport 1993;4(7):841-8
      - Miklossy J. Chronic Inflammation and amyloidogenesis in Alzheimers disese: the role of spirochetes. PhD thesis 2005
      - Miklossy J. Chronic or Late neuroborreliosis: Analysis of evidence compared to chronic or late neurosyphilis. OPen Neurology J. 2012;6(Suppl 1-M9) 146-57
      - Miklossy J. Emerging role of Pathogens in Alzheimers disease. Expert Rev Mol Med. 2011; 13:e30
      - Lyme and co-infections such as Chlamydia severely damage the Golgi structures in Alzheimers disease.
      - Buhner in Healing Lyme and Co-infections (2015) states that Mycoplasmas, Chlamydia and Borrelia are commonly found in the lesions and brains of people who have Alzhiemers, MS and ALS and other neurological illnesses.
      - Alzheimers disease and Herpes infections & Bacteria infections
      
      
    • Research showing role of Lyme disease in MS
      - Fritzsche, M. Geographic and seasonal correlation of multiple sclerosis to sporadic schizophrenia. Int J Health Geogr.2002; 1(1): 5
      - Fritzsche, M. Seasonal correlation of sporadic schizophrenia to Ixodes ticks and Lyme borreliosis. Int J Health Geogr. 2002; 1(1): 2
      - Chmielewska-Badora, J., Cisak, E., Dutkiewicz, J. Lyme borreliosis and multiple sclerosis: any connection? Ann Agric Environ Med. 2000; 7: 141 - 3
      - Brorson, O., Brorson, S.H., Henriksen, T.H., Skogen, P.R.,Schoyen, R. Association between multiple sclerosis and cystic structures in cerebrospinal fluid. Infection 2001; 29(6): 315 - 9
      - http://www.dailymail.co.uk/health/article-2343062/Mother-diagnosed-MS-facing-life-wheelchair-cured--discovered-symptoms-TICK-BITE.html
      - Lyme and co-infections such as Chlamydia severely damage the Golgi structures in MS.
      - Buhner in Healing Lyme and Co-infections (2015) states that Mycoplasmas, Chlamydia and Borrelia are commonly found in the lesions and brains of people who have Alzhiemers, MS and ALS and other neurological illnesses.
    • Romme Christensen J, Börnsen L, Hesse D, Krakauer M, Sørensen PS, Søndergaard HB, et al. Cellular sources of dysregulated cytokines in relapsing-remitting multiple sclerosis. J Neuroinflammation. 2012;9:215.
    • Beck J, Rondot P, Catinot L, Falcoff E, Kirchner H, Wietzerbin J. Increased production of interferon gamma and tumor necrosis factor precedes clinical manifestation in multiple sclerosis: do cytokines trigger off exacerbations. Acta Neurol Scand. 1988;78:318–23.
    • Maimone D, Gregory S, Arnason BG, Reder AT. Cytokine levels in the cerebrospinal fluid and serum of patients with multiple sclerosis. J Neuroimmunol. 1991;32:67–74.
    • Navikas V, Link H. Review: cytokines and the pathogenesis of multiple sclerosis. J Neurosci Res. 1996;45:322–33.
    • Gold SM, Krüger S, Ziegler KJ, Krieger T, Schulz KH, Otte C, et al. Endocrine and immune substrates of depressive symptoms and fatigue in multiple sclerosis patients with comorbid major depression. J Neurol Neurosurg Psychiatry. 2011;82:814–8.
    • Heesen C, Nawrath L, Reich C, Bauer N, Schulz KH, Gold SM. Fatigue in multiple sclerosis: an example of cytokine mediated sickness behaviour? J Neurol Neurosurg Psychiatry. 2006;77:34–9.
    • Flachenecker P, Bihler I, Weber F, Gottschalk M, Toyka KV, Rieckmann P. Cytokine mRNA expression in patients with multiple sclerosis and fatigue. Mult Scler. 2004;10:165–9.
    • Nagyoszi P, Wilhelm I, Farkas AE, Fazakas C, Dung NT, Haskó J, et al. Expression and regulation of toll-like receptors in cerebral endothelial cells. Neurochem Int. 2010;57:556–64.
    • Andersson A, Covacu R, Sunnemark D, Danilov AI, Dal Bianco A, Khademi M, et al. Pivotal advance: HMGB1 expression in active lesions of human and experimental multiple sclerosis. J Leukoc Biol. 2008;84:1248–55.
    • Bsibsi M, Ravid R, Gveric D, van Noort JM. Broad expression of Toll-like receptors in the human central nervous system. J Neuropathol Exp Neurol. 2002;61:1013–21.
    • Brydon L, Harrison NA, Walker C, Steptoe A, Critchley HD (2008) Peripheral inflammation is associated with altered substantia nigra activity and psychomotor slowing in humans. Biol Psychiatry 63(11):1022–9. doi:10.1016/j.biopsych.2007.12.007
    • Eisenberger NI, Berkman ET, Inagaki TK, Rameson LT, Mashal NM, Irwin MR (2010) Inflammation-induced anhedonia: endotoxin reduces ventral striatum responses to reward. Bi
  • Oxidative and Nitrosative Stress and Mitochondria damage, and Fatigue
    • Blake C, Spitz E, Leehey M, Hoffer B, Boyson S. Platelet mitochondrial respiratory chain function in Parkinson’s disease. Mov Disord. 1997;12:3–8.
    • Shinde S, Pasupathy K. Respiratory-chain enzyme activities in isolated mitochondria of lymphocytes from patients with Parkinson’s disease: preliminary study. Neurol India. 2006;54:390–3
    • Perl A, Hanczko R, Doherty E. Assessment of mitochondrial dysfunction in lymphocytes of patients with systemic lupus erythematosus. Methods Mol Biol. 2012;900:61–89.
    • Perl A, Nagy G, Gergely P, Puskas F, Qian Y, Banki K. Apoptosis and mitochondrial dysfunction in lymphocytes of patients with systemic lupus erythematosus. Methods Mol Med. 2004;102:87–114.
    • Pagano G, Castello G, Pallardó FV. Sjøgren’s syndrome-associated oxidative stress and mitochondrial dysfunction: prospects for chemoprevention trials. Free Radic Res. 2013;47:71–3.
    • Segal BM, Thomas W, Zhu X, Diebes A, McElvain G, Baechler E, Gross M (2012) Oxidative stress and fatigue in systemic lupus erythematosus. Lupus 21(9):984–92. doi:10.1177/0961203312444772 101.
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    • Gironi M, Borgiani B, Mariani E, Cursano C, Mendozzi L, Cavarretta R, et al. Oxidative stress is differentially present in multiple sclerosis courses, early evident, and unrelated to treatment. J Immunol Res. 2014;2014:961863.
    • Miller E, Walczak A, Saluk J, Ponczek MB, Majsterek I. Oxidative modification of patient’s plasma proteins and its role in pathogenesis of multiple sclerosis. Clin Biochem. 2012;45:26–30.
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    • Stavropoulou C, Zachaki S, Alexoudi A, Chatzi I, Georgakakos VN, Terzoudi GI, et al. The C609T inborn polymorphism in NAD(P)H:quinone oxidoreductase 1 is associated with susceptibility to multiple sclerosis and affects the risk of development of the primary progressive form of the disease. Free Radic Biol Med. 2011;51:713–8.
    • Fiorini A, Koudriavtseva T, Bucaj E, Coccia R, Foppoli C, Giorgi A, et al. Involvement of oxidative stress in occurrence of relapses in multiple sclerosis: the spectrum of oxidatively modified serum proteins detected by proteomics and redox proteomics analysis. PLoS One. 2013;8:e65184.
    • Oliveira SR, Kallaur AP, Simão AN, Morimoto HK, Lopes J, Panis C, et al. Oxidative stress in multiple sclerosis patients in clinical remission: association with the expanded disability status scale. J Neurol Sci. 2012;321:49–53.
    • Ljubisavljevic S, Stojanovic I, Cvetkovic T, Vojinovic S, Stojanov D, Stojanovic D, et al. Erythrocytes’ antioxidative capacity as a potential marker of oxidative stress intensity in neuroinflammation. J Neurol Sci. 2014;337:8–13.
    • Lu F, Selak M, O’Connor J, Croul S, Lorenzana C, Butunoi C, et al. Oxidative damage to mitochondrial DNA and activity of mitochondrial enzymes in chronic active lesions of multiple sclerosis. J Neurol Sci. 2000;177:95–103.
    • Mahad D, Lassmann H, Turnbull D. Review: mitochondria and disease progression in multiple sclerosis. Neuropathol Appl Neurobiol. 2008;34:577–89.
    • Reinke S, Broadhurst D, Sykes B, Baker G, Catz I, Warren K, et al. Metabolomic profiling in multiple sclerosis: insights into biomarkers and pathogenesis. Mult Scler. 2014;20:1396–400
    • Lutz NW, Viola A, Malikova I, Confort-Gouny S, Audoin B, Ranjeva JP, et al. Inflammatory multiple-sclerosis plaques generate characteristic metabolic profiles in cerebrospinal fluid. PLoS One. 2007;2:e595.
    • Lutz NW, Cozzone PJ. Metabolic profiling in multiple sclerosis and other disorders by quantitative analysis of cerebrospinal fluid using nuclear magnetic resonance spectroscopy. Curr Pharm Biotechnol. 2011;12:1016–25.
    • Tajima S, Yamamoto S, Tanaka M, Kataoka Y, Iwase M, Yoshikawa E, Okada H, Onoe H, Tsukada H, Kuratsune H, Ouchi Y, Watanabe Y (2010) Medial orbitofrontal cortex is associated with fatigue sensation. Neurol Res Int 2010:671421. doi:10.1155/2010/671421 271.
    • Chaudhuri A, Behan PO (2004) Fatigue in neurological disorders. Lancet 363(9413):978–88
    • Bruno RL, Cohen JM, Galski T, Frick NM (1994) The neuroanatomy of post-polio fatigue. Arch Phys Med Rehabil 75(5):498–504
    • Blomstrand E, Perrett D, Parry-Billings M, Newsholme EA (1989) Effect of sustained exercise on plasma amino acid concentrations and on 5-hydroxytryptamine metabolism in six different brain regions in the rat. Acta Physiol Scand 136(3):473–81
• TLR2/4 activation and upregulation
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  • Andersson A, Covacu R, Sunnemark D, Danilov AI, Dal Bianco A, Khademi M, Wallström E, Lobell A, Brundin L, Lassmann H, Harris RA (2008) Pivotal advance: HMGB1 expression in active lesions of human and experimental multiple sclerosis. J Leukoc Biol 84(5):1248–55 169.
  • Bsibsi M, Ravid R, Gveric D, van Noort JM (2002) Broad expression of Toll-like receptors in the human central nervous system. J Neuropathol Exp Neurol 61(11):1013–21
  • Kim C, Ho DH, Suk JE, You S, Michael S, Kang J, Joong Lee S, Masliah E, Hwang D, Lee HJ, Lee SJ (2013) Neuron-released oligomeric α-synuclein is an endogenous agonist of TLR2 for paracrine activation of microglia. Nat Commun 4:1562
  • Tiffin N, Adeyemo A, Okpechi I (2013) A diverse array of genetic factors contribute to the pathogenesis of systemic lupus erythematosus. Orphanet J Rare Dis 8:2. doi:10.1186/1750-1172-8-2 173.
  • Low HZ, Witte T (2011) Aspects of innate immunity in Sjögren’s syndrome. Arthritis Res Ther 13(3):218. doi:10.1186/ar3318 174.
  • Goh FG, Midwood KS (2012) Intrinsic danger: activation of Tolllike receptors in rheumatoid arthritis. Rheumatology (Oxford) 51(1):7–23. doi:10.1093/rheumatology/ker257
  • Wang PF, Fang H, Chen J, Lin S, Liu Y, Xiong XY, Wang YC, Xiong RP, Lv FL, Wang J, Yang QW (2014) Polyinosinicpolycytidylic acid has therapeutic effects against cerebral ischemia/reperfusion injury through the downregulation of TLR4 signaling via TLR3. J Immunol 192(10):4783–94. doi:10.4049/ jimmunol.1303108
  • 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.
  • White AT, Light AR, Hughen RW, Vanhaitsma TA, Light KC. Differences in metabolite-detecting, adrenergic, and immune gene expression after moderate exercise in patients with chronic fatigue syndrome, patients with multiple sclerosis, and healthy controls. Psychosom Med. 2012;74:46–54.
  • Gow JW, Hagan S, Herzyk P, Cannon C, Behan PO, Chaudhuri A. A gene signature for post-infectious chronic fatigue syndrome. BMC Med Genomics. 2009;2:38.
• Glutamate and Quinolic acid
  • Esposito Z, Belli L, Toniolo S, Sancesario G, Bianconi C, Martorana A (2013) Amyloid β, glutamate, excitotoxicity in Alzheimer’s disease: are we on the right track? CNS Neurosci Ther 19(8):549–55. doi:10.1111/cns.12095 209.
  • Zinger A, Barcia C, Herrero MT, Guillemin GJ (2011) The involvement of neuroinflammation and kynurenine pathway in Parkinson’s disease. Parkinsons Dis 2011:716859. doi:10.4061/2011/716859 210.
  • Vaarmann A, Kovac S, Holmström KM, Gandhi S, Abramov AY (2013) Dopamine protects neurons against glutamate-induced excitotoxicity. Cell Death Dis 4:e455. doi:10.1038/cddis.2012.194 211.
  • abnormal high levels of Quinolic acid in Chronic Lyme infection
  • Anitha A, Nakamura K, Thanseem I, Yamada K, Iwayama Y, Toyota T, Matsuzaki H, Miyachi T, Yamada S, Tsujii M, Tsuchiya KJ, Matsumoto K, Iwata Y, Suzuki K, Ichikawa H, Sugiyama T, Yoshikawa T, Mori N (2012) Brain region-specific altered expression and association of mitochondria-related genes in autism. Mol Autism 3(1):12. doi:10.1186/2040-2392-3-12 212.
  • Kostic MS, Rajkovic RJ, Potic Floranovic MS, Dimov ID, Pavlovic D (2013) Multiple sclerosis and oxidative stress—a clinical perspective. Neurochem J 7(1):77–86 213. Lim CK, Brew BJ, Sundaram G, Guillemin GJ (2010) Understanding the roles of the kynurenine pathway in multiple sclerosis progression. Int J Tryptophan Res 3:157–67 214.
  • . Kincses ZT, Toldi J, Vécsei L (2010) Kynurenines, neurodegeneration and Alzheimer’s disease. J Cell Mol Med 14(8):2045–54. doi: 10.1111/j.1582-4934.2010.01123.x 219.
  • Brouns R, Verkerk R, Aerts T, De Surgeloose D, Wauters A, Scharpé S, De Deyn PP (2010) The role of tryptophan catabolism along the kynurenine pathway in acute ischemic stroke. Neurochem Res 35(9):1315–22. doi:10.1007/s11064-010-0187-2
    
• Muscle fatigue
  • .Stockton K, Iah K, Paratz DJ, Bennell K (2012) Fatigue, muscle strength and vitamin D status in women with systemic lupus erythematosus compared with healthy controls. Lupus 21(3):271–278
  • Tench C, Bentley D, Vleck V, Mccurdie I, White P, D’cruz D (2002) Aerobic fitness, fatigue, and physical disability in systemic lupus erythematosus. J rheumatology 29(3):474–481
  • Kanellopoulos P, Baltoyiannis C, Tzioufas A (2002) Primary Sjögren’s syndrome associated with inclusion body myositis. Rheumatology 41(4):440–444 302. Vrethem M, Lindvall B, Holmgren H, Henriksson K, Lindström F, Ernerudh J (1990) Neuropathy and myopathy in primary Sjögren’s syndrome: neurophysiological, immunological and muscle biopsy results. Acta Neurol Scand 82(2):126–131
  • Willer, B., Stucki, G., Hoppeler, H., Brühlmann, P. and Krähenbühl, S. 2000. Effects of creatine supplementation on muscle weakness in patients with rheumatoid arthritis. Rheumatology, 39 (3), pp. 293– 298
  • Yates D (1963) Muscular changes in rheumatoid arthritis. Ann Rheum Dis 22(5):342–347
  • Friedman JH, Abrantes AM (2012) Self perceived weakness in Parkinson’s disease. Parkinsonism Relat Disord 18(7):887–889
  • Stevens-Lapsley J, Kluger BM, Schenkman M (2012) Quadriceps muscle weakness, activation deficits, and fatigue with Parkinson disease. Neurorehabil Neural Repair 26(5):533–541
• impaired PGC- 1 expression
  • Eschbach J, Schwalenstöcker B, Soyal SM, Bayer H, Wiesner D, Akimoto C, Nilsson AC, Birve A, Meyer T, Dupuis L, Danzer KM, Andersen PM, Witting A, Ludolph AC, Patsch W, Weydt P (2013) PGC-1α is a male-specific disease modifier of human and experimental amyotrophic lateral sclerosis. Hum Mol Genet 22(17):3477– 84. doi:10.1093/hmg/ddt202 255.
  • Tsunemi T, La Spada AR (2012) PGC-1α at the intersection of bioenergetics regulation and neuron function: from Huntington’s disease to Parkinson’s disease and beyond. Prog Neurobiol 97(2): 142–51. doi:10.1016/j.pneurobio.2011.10.004 256.
  • Witte ME, Nijland PG, Drexhage JA, Gerritsen W, Geerts D, van Het Hof B, Reijerkerk A, de Vries HE, van der Valk P, van Horssen J (2013) Reduced expression of PGC-1α partly underlies mitochondrial changes and correlates with neuronal loss in multiple sclerosis cortex. Acta Neuropathol 125(2):231–43. doi:10.1007/s00401-012- 1052-y
  • Austin S, St-Pierre J (2012) PGC1α and mitochondrial metabolism—emerging concepts and relevance in ageing and neurodegenerative disorders. J Cell Sci 125(Pt 21):4963–71. doi:10.1242/jcs. 113662 268.
  • Tufekci KU, Civi Bayin E, Genc S, Genc K (2011) The Nrf2/ARE pathway: a promising target to counteract mitochondrial dysfunction in Parkinson’s disease. Parkinsons Dis 2011:314082. doi:10. 4061/2011/314082
• Central pathways causing fatigue in neuro-inflammatory and autoimmune illnesses. Morris et al. 2015.
• The Neuro-Immune Pathophysiology of Central and Peripheral Fatigue in Systemic Immune-Inflammatory and Neuro-Immune Diseases Morris et al. 2015.
• A neuro-immune model of Myalgic Encephalomyelitis/Chronic fatigue syndrome. Morris G, Maes M. Metab Brain Dis. 2013;28:523–40
• The Putative Role of Viruses, Bacteria, and Chronic Fungal Biotoxin Exposure in the Genesis of Intractable Fatigue Accompanied by Cognitive and Physical Disability, 2015 points to the effects of past infections and continuing chronic infections in the perpetuation of ME over many years or decades. Parvoviruses, HHV6, variants of Epstein-Barr, Cytomegalovirus, Mycoplasma, and Borrelia burgdorferi and Mold infection are mentioned. This would create some differences and subsets between patients.
• Morris G, Anderson G, Galecki P, Berk M, Maes M. A narrative review on the similarities and dissimilarities between myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) and sickness behavior. BMC Med. 2013;11:64.
• A neuro-immune model of Myalgic Encephalomyelitis/Chronic fatigue syndrome. Morris G, Maes M (2012). Metab Brain Dis. 2013 Dec;28(4):523-40.
• Morris G, Maes M. Mitochondrial dysfunctions in myalgic encephalomyelitis/chronic fatigue syndrome explained by activated immuno-inflammatory, oxidative and nitrosative stress pathways. Metab Brain Dis 2014;29(1):19–36
• Myalgic encephalomyelitis/chronic fatigue syndrome and encephalomyelitis disseminata/multiple sclerosis show remarkable levels of similarity in phenomenology and neuroimmune characteristics. Gerwyn Morris and Michael Maes. Morris and Maes BMC Medicine 2013 11:205   doi:10.1186/1741-7015-11-205

• Using neuro-imaging techniques, MRI has revealed punctate areas of abnormality in 78% cases, particularly in the subcortical areas. SPECTscans have shown defects in perfusion and metabolism
  Research findings presented by Professor Anthony Komaroff (Boston, Mass) to The Sydney ME / CFS Clinical and Scientific Conference, December 2001

• Rey Casse (Adelaide SA) used SPECTscans to study regional cerebral blood flow in CFS. He recommended that a triple headed camera be used for accuracy and reliability. 13 CFS patients' scans were compared with 11 people suffering from other conditions with normal scans. Visually, deficit in regional cerebral blood flow was found in the temporal areas in 7 patients, and equivocal in 3. Statistical Parametric Mapping was applied to show location and amplitude of significant focal deficits. Most deficits were found in the brainstem, temporal lobes, frontal lobe and anterior cingulate gyrus.
  Research findings presented by Rey Casse (Adelaide, SA) to The Sydney ME / CFS Clinical and Scientific Conference, December 2001

• SPECT Imaging of the Brain: Comparison of Findings in Patients with Chronic Fatigue Syndrome, AIDS Dementia Complex, and Major Unipolar Depression
  Richard B. Schwartz' Anthony L. Komaroff Basem M. Garada Marcy Gleit Teresa H. Doolittle' David W. Bates' Russell G. Vasily B. Leonard Holman

• "There is no doubt SPET scans are a breakthrough in the diagnosis and recognition of CFS as a real illness. They consistently show reduced perfusion to all parts of the brain, especially frontal, temporal and parietal lobes and the deep basal ganglia. However, what is unique to CFS sufferers is very poor perfusion of blood in the brain stem. Whilst other diseases such as dementia and depression show reduced blood flow to the thinking areas of the brain, brain stem perfusion is normal."
  Dr. Sarah Myhill, Wales, UK
  http://www.drmyhill.co.uk 
  
  

• "The most alarming is the neurologic and neurocognitive elements of this disease. Half have abnormal MRI scans, 80% have abnormal SPECT scans, 95% have abnormal cognitive evoked EEG brain maps. Most have abnormal neurologic examinations."
  Paul R. Cheney M.D., Ph.D Charlotte, NC
  Testimony before the FDA Scientific Advisory Committee, February 1993

• Role of infection and neurologic dysfunction in chronic fatigue syndrome.Komaroff AL, Cho TA.Division of General Medicine, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts 02115, USA. Komaroff@hms.harvard.edu. (2011)

• EEG spectral coherence data distinguish chronic fatigue syndrome patients from healthy controls and depressed patients-A case control study, Frank H Duffy, Gloria B McAnulty, Michelle C McCreary, George J Cuchural, and Anthony L Komaroff. BMC Neurology 2011, 11:82

• Event-related potentials in Japanese childhood chronic fatigue syndrome. Akemi Tomoda, Kei Miyuno, Nobuki Murayama, Takaka Joudoi, Tomohiko Igasaki. Journal of Pediatric Neurology, January 2007.

• Regland B, Andersson M, Abrahamsson L, et al. Increased concentrations of homocysteine in the cerebrospinal fluid in patients with fibromyalgia and chronic fatigue syndrome. Scand J Rheumatol 1997;26:301-307

• Betrayal by the Brain: The Neurologic Basis of Chronic Fatigue Syndrome, Fibromyalgia Syndrome, and Related Neural Network Disorders (The Haworth ... networks in health & illness) by Jay Goldstein

• Acheson ED (1956), "A New Clinical Entity?", Leading Article, Lancet, 26 mei, pp. 789-90

• Acheson ED (1959), "The clinical syndrome variously called benign myalgic encephalomyelitis, Iceland disease, and epidemic neuromyasthenia", Am J Med Apr;26(4):569-95, PMID: 13637100

• Chaudhuri A, Behan OB (2000), "Neurological Dysfunction in Chronic Fatigue Syndrome", JFCS 6(3/4):51-68,

• Chronic fatigue syndrome--a neuroimmunological model. Arnett SV, Alleva LM, Korossy-Horwood R, Clark IA. Med Hypotheses. 2011 Jul;77(1):77-83

• The following video shows a British woman who had ME / CFS and was given a bogus psychiatric diagnosis and psychiatric treatments by British doctors. She died. A post-mortem revealed that she had a virus infection of the spinal cord and nervous system and a lot of inflammation of the spinal cord. Psychiatric treatments could not treat ME / CFS , but some British doctors insisted on psychiatric treatment which ultimately led to her death. Click on videos below to watch them.

  The Hippocratic oath taken by medical doctors states that a doctor should do no harm. Improper diagnosis and treatments and neglect of this woman through the wrong use of psychiatric medicine meant that serious harm was done to this woman. And, unfortunately many other ME / CFS patients are suffering similarly. There was another case of an ME / CFS patient in England who had serious enteroviral infection of the brain and nervous system and he was told by doctors that he was suffering from depression. He was given psychiatric drugs which made him worse. This neglect by doctors made him very ill and he deteriorated rapidly. He committed suicide. An autopsy revealed that he had serious enterovirus infection of the brain and nervous system. Read article here - https://listserv.nodak.edu/cgi-bin/wa.exe?A2=ind0112a&L=co-cure&F=&S=&P=62

• Neuromuscular Abnormalities in Patients with Chronic Fatigue Syndrome. Carolyn L. Warner, Reid R. Heffner, D Cookfair. In.. The Clinical & Scientific Basis of ME / CFS. ed.. B.M. Hyde J Goldstein, P Levine. pub. The Nightingale Research Foundation, Ottawa 1992

• Davey NJ, Puri BK, Nowicky AV, Main J, Zaman R: Voluntary motor function in patients with chronic fatigue syndrome. J Psychosom Res 2001, 50:17-20.

• Davey NJ, Puri BK, Catley M, Main J, Nowicky AV, Zaman R: Deficit in motor performance correlates with changed corticospinal excitability in patients with chronic fatigue syndrome. Int J Clin Pract 2003, 57:262-264

• I. J. Elenkov, R.L. Wilder, G. P. Chrousos and E. S. Vizi, "The Sympathetic Nerve—An Integrative Interface Between Two Supersystems: The Brain and the Immune System," Pharmacological Reviews, Vol. 52, No. 2, 2000, pp. 595-638.

• Oxidative and Nitrosative Stress and Immune-Inflammatory Pathways in Patients with Myalgic Encephalomyelitis (ME)/Chronic Fatigue Syndrome (CFS). Maes et al. Curr Neuropharmacol. 2014 Mar;12(2):168-85.

• Starr A, Scalise A, Gordon R, Michalewski H, Caramia M: Motor excitability in chronic fatigue syndrome. Clin Neurophysiol 2000, 111:2025-2031.

• The Differential Diagnosis between Multiple Sclerosis and Chronic Fatigue Postviral Syndrome. Charles M. Poser. ibid

• A chronic fatigue syndrome - related proteome in human cerebrospinal fluid.  Baraniuk, JN., Casado, B., Maibach, H., Clauw, DJ., Pannell, LK and Hess, S.  BMC Neurology, 2005, 5:22.

• Neuroscience of Fatigue and CFS/ME by Using PET Molecular Imaging and Functional Neuroimaging
  Yasuyoshi Watanabe, Masaski Tanaka, Kei Mizuno, Akira Ishii, Emi Yamano, Sanae Fukuda, Yasuhito Nakatomi, Kouzi Yamaguti, and Hirohiko Kuratsune. IACFS/ME Conference. Translating Science into Clinical Care. March 20-23, 2014 • San Francisco, California, USA

• Detection of intracranial abnormalities in patients with chronic fatigue syndrome. RE Schwartz et al. Am J Roentgenology 1994:162:935 941

• A 56 year old woman with CFS. AL Komaroff. JAMA 1997.. 278..14:1179 1184

• Pathophysiology of a Central Cause of Post-Polio Fatigue Richard Bruno et al Annals of the New York Academy of Sciences 1995:753:257-275

• Encephalomyelitis resembling benign myalgic encephalomyelitis. SGB Innes Lancet 1970: 969 971

• A. M. Bakheit, P.O Behan, T. G. Dinan and V. O'Keane, "Possible Upregulation of Hypothalantic 5-Hydroxytry- Ptamine Receptors in Patients with Postviral Fatigue Syndrome, British Medical Journal, Vol. 304, 1992, pp. 1010-1012. (Subgroup of CFS).

• Prevalence in the cerebro spinal fluid of the following infectious agents in a cohort of 12 CFS subjects: Human Herpes Virus 6 & 8; Chlamyclia Species; Mycoplasma Species, EBV; CMV and Coxsackie B Virus. Susan Levine JCFS 2001: 9: 91-2:41-51

•  Enterovirus in the chronic fatigue syndrome. McGarry F, Gow J and Behan PO Ann Intern Med 1994:120:972 973

• Chronic Fatigue Syndrome Findings now point to Central Nervous System Involvement. DS Bell Postgrad Med 1994:96:6:73 81

• M Fremont, K De Meirleir et al. JCFS 2006:13(4):17-28

• Brainstem perfusion is impaired in patients with chronic fatigue syndrome. Costa DC, Tannock C and Brostoff J. Quarterly Journal of Medicine 1995:88:767 773

• Brain positron emission tomography (PET) in chronic fatigue syndrome: preliminary data. Tirelli U et al. Am J Med 1998:105: (3A): 54S-58S

• S. Yamamoto, Y. Ouchi, H. Onoe, E. Yoshikawa, H. Tsukada, H. Takahashi, et al., "Reduction of Serotonin Transporters of Patients with Chronic Fatigue Syndrome," Brain Imaging, Vol. 15, No. 17, 2004, pp. 2571-2574. (Subgroup of CFS).

• Neurological dysfunction in chronic fatigue syndrome. Chaudhuri, A and Behan PO. JCFS 2000:6: (3-4):51-68

• Behan WM, McDonald M, Darlington LG, Stone TW. Oxidative stress as a mechanism for quinolinic acid-induced hippocampal damage: protection by melatonin and deprenyl. Br J Pharmacol. 1999;128:1754–60.

• Relationship of brain MRI abnormalities and physical functional status in chronic fatigue syndrome. Cook DIB, Natelson BH et al Int J Neurosci 2001:107: (1-2):1-6
• Perception of cognitive performance in patients with chronic fatigue syndrome
  ImmuneSupport.com
  07-16-2002
  Source: Ann Behav Med 2002 Spring;24(2):106-12 Metzger FA, Denney DR.
  Department of Psychology, University of Kansas, Lawrence 66045-7556.

• Patients have poor concentration, short term memory loss and disturbances of sensation. Action for ME, Britain.

• Brain Link to Chronic Fatigue Syndrome
  ImmuneSupport.com
  07-15-2002
  An area of the brain that controls the stomach receives substantially less blood in some people with chronic fatigue syndrome, a study shows. The finding adds more weight to the argument that the controversial illness is biological, not psychological.
  Brain scans of 40 chronic fatigue patients were carried out by Adelaide scientists and compared against the scans of healthy people. The director of nuclear medicine at Queen Elizabeth Hospital, Dr Steven Unger, who headed the study along with neurologist Dr Rey Casse, said: "There was a very strong change in cerebral blood flow in patients."

• Relation between neuropsychological impairment and functional disability in patients with chronic fatigue syndrome. Journal of Neurology, Neurosurgery, and Psychology; April 1998, Volume 64 Number 4, C Christodoulou, J DeLuca, G Lange, S K Johnson, S A Sisto, L Korn, B H Natelson

• Dr. Susser reports - after exercise, brain circulation in CFS patients gets worse, unlike what happens with healthy persons. Dr. Sussser tests patients after exercise for decreased brain circulation. In addition, he tests the cortisone levels in the blood, which decrease in CFS patients after exercise. Low levels of this hormone (which is vital in dealing with stress) can indicate the likelihood of CFS

• Short-term memory, general memory, retrieval from semantic memory and memory requiring cognitive effort have been found to be impaired.

• Riccio M et al. Br J Clin Psychol 1992; 31: 111

• Sandman CA et al. Biol Psychiatry 1993; 33: 618

• Smith AP et al. Br. J Psychol 1993; 84: 411

• McDonald E et al. J Neurol Neurosurg Psychiatry 1993; 56: 812
  

• Brain Link to Chronic Fatigue Syndrome
  ChronicFatigueSyndromeSupport.com
  07-15-2002

• Dr Jay Goldstein, using SPECT technology, examined 33 patients with CFS, 15 of whom also met the criteria for FMS. Scans showed marked reduction in blood flow in the right hemisphere of the brain, especially amongst FMS patients.
  ChronicFatigueSyndromeSupport.com
  08-05-2002
  By Leon Chaitow, N.D., D.O., MRO, Senior Lecturer, University of Westminster

• In their presentation to the US Assembly Committee, Drs Dharam Ablashi and Kristin Loomis said:

  “Reasons to suspect viruses as a cause of CFS and MS: In CFS, symptoms wax and wane; antiviral pathways are activated; symptoms are similar to many viral conditions; geographic outbreaks have been reported; gene expression profiling found genetic variants that reduce antiviral defences.  In MS, antiviral pathways are activated; geographic outbreaks have been reported; all demyelinating disorders with known aetiology have been caused by viruses; symptoms wax and wane and worsen with viral infections.

  “Evidence of central nervous system abnormalities in (ME)CFS are similar to those in MS: reduced grey matter  volume in bilateral prefrontal cortex; abnormal uptake of acetyl-L carnitine in the prefrontal cortex; enlarged ventricle volumes; increased small punctate lesions on MRI in MS and in a subset of (ME)CFS; fatigue is present in more than 85% of people with MS and in 100% of people with (ME)CFS; reduced information processing speed; memory and cognitive problems”.

  Ablashi and Loomis pointed out that an analysis of studies of HHV-6 in (ME)CFS differentiated between active and latent virus, with 83% being positive (Assessment and Implications of Viruses in Debilitating Fatigue in CFS and MS Patients. Dharam V Ablashi et al.   HHV-6 Foundation, Santa Barbara, USA. Submission to Assembly Committee/Ways & Means, Exhibit B1-20, submitted by Annette Whittemore 1st June 2005).

• Goldenberg Fibromyalgia, chronic fatigue syndrome and myofascial pain syndrome Current Opinion in Rheumatology 1993;5:199-20810

• Deluca J et a1. Arch Neurol 1993; 50: 301

• DeLuca J et al. J Neurol Neurosurg Psychiatry 1995; 58: 38

• B Evengard (Stockholm) concluded that there are different neurobiological profiles in CFS patients when compared with those with burnout and healthy controls. This suggests different underlying pathological processes.
  B Evengard (Stockholm) research paper submitted to the AACFS 5th International Research, Clinical and Patient Conference, 2001

• "Professor Komaroff concluded that in view of the above evidence, CFS has an organic basis, and in many of the patients there are abnormalities of the limbic system in the brain and abnormal regulation of the immune system, which is possibly a result of limbic system abnormalities. A single cause seems unlikely, but multiple triggering agents (infections, toxins, stress) could be involved." 
  Research findings presented by Professor Anthony Komaroff (Boston, Mass) to The Sydney ME / CFS Clinical and Scientific Conference, December 2001

• Jones DE, Hollingsworth KG, Taylor R, Blamire AM, Newton J (2010), "Abnormalities in pH handling by peripheral muscle and potential regulation by the autonomic nervous system in chronic fatigue syndrome", J Intern Med Apr;267(4):394-401,

• Demitrack MA et al. Biol Psychiatry 1992; 32: 1065

• ME outbreaks suggesting brain and neurological abnormalities and role of viruses and other pathogens
  Viruses have been isolated from the muscles of ME patients during epidemics. Using PCR methods, 50% or more of patients had evidence of such infection.

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  • Byrne E, Trounce I, Dennett X. Chronic relapsing myalgia (Post viral): clinical, histological, and biochemical studies. Aust N Z J Med. 1985 Jun;15(3):305-8. PMID: 3864422
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  • Calder BD, Warnock PJ. Coxsackie B infection in a Scottish general practice. J R Coll Gen Pract. 1984 Jan;34(258):15-9. PMID: 6319691 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1959663/pdf/jroyalcgprac00169-0017.pdf
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  • Know your organizations: the Myalgic Encephalomyelitis Association. Health Visit. 1982 Jul;55(7):350. PMID: 6921182
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  • Parish JG. Myalgic encephalomyelitis. Lancet. 1981 Apr 25;1(8226):950-1. PMID: 6112360 
  • Layzer RB. Myoglobinaemia in benign myalgic encephalomyelitis. Lancet. 1981 Mar 21;1(8221):670. PMID: 6110899
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  • Church AJ. Myalgic encephalomyelitis. Med J Aust. 1980 Aug 23;2(4):224. PMID: 7432298
  • Behan PO. Epidemic myalgic encephalomyelitis. Practitioner. 1980 Aug;224(1346): 805-7. PMID: 7433399
  • Bishop J. Epidemic myalgic encephalomyelitis. Med J Aust. 1980 Jun 14;1(12):585-6, 609. PMID: 7402153
  • Ramsay AM, Rundle A. Clinical and biochemical findings in ten patients with benign myalgic encephalomyelitis. Postgrad Med J. 1979 Dec;55(654):856-7. PMID: 548947 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2425703/?tool=pubmed
  • Pampiglione G, Harris R, Kennedy J. Electro-encephalographic investigations in myalgic encephalomyelitis. Postgrad Med J. 1978 Nov;54(637):752-4. PMID: 746023 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1606252/pdf/brmedj00135-0058a.pdf
  • Behan PO. Post-infectious encephalomyelitis: some aetiological mechanisms. Postgrad Med J. 1978 Nov;54(637):755-9. PMID: 34143 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1606252/pdf/brmedj00135-0058a.pdf
  • Wookey C. Epidemic myalgic encephalomyelitis. Br Med J. 1978 Jul 15;2(6131):202. PMID: 678851
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  • Acheson ED. Benign myalgic encephalomyelitis. Lancet. 1957 Apr 20;272(6973):834-5. PMID: 13417614
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  • Blattner RJ. Benign myalgic encephalomyelitis (Akureyri disease, Iceland disease). J Pediatr. 1956 Oct;49(4):504-6. PMID: 13358047 
  • A new Clinical Entity ? Lancet 1956
  • Outbreak at the Royal Free. E.D Acheson. The Lancet, Volume 266, Issue 6886, Pages 394 - 395, 20 August 1955.
  
  
  

  Years of Epidemics
  1917 Van Economo reports an illness involving brain and neurological inflammation and great fatigue and some deaths. See paper 'New Clinical Entity' published in the Lancet in 1956.
  1918 - 1924, several outbreaks of an illness involving brain and neurological inflammation and fatigue reported throughout Europe. See paper 'New Clinical Entity' published in the Lancet in 1956.
  1924 England and Wales 5,039 cases of encephalitis lethargica. See paper 'New Clinical Entity' published in the Lancet in 1956.
  1934 Los Angeles County Hospital. Called 'Atypical Poliomyelitis'
  1936 Fond Du Lac, Wisconsin - St. Agnes Convent - Encephalitis
  1937 Erstfeld, Switzerland - Abortive Poliomyelitis
  1937 St. Gallen, Switzerland - Frohburg Hospital – Abortive Poliomyelitis
  1939 Middlesex, England - Harefield Sanatorium
  1939 Degersheim, Switzerland - Abortive Poliomyelitis
  1945 Pennsylvania. Hospital of the University of Pennsylvania - epidemic Pleurodynia
  1946 Iceland disease resembling Poliomyelitis with the character of Akureyri disease
  1948 Iceland, North Coast towns - epidemic simulating Poliomyelitis
  1949 Adelaide, South Australia - a disease resembling Poliomyelitis
  1949 Cambridgeshire, England - aberrant poliomyelitis. Involvement of other Enteroviruses suspected.
  1950 Louisville, Kentucky -- St. Joseph 's Infirmary - epidemic Neuromyasthenia
  1950 Upper State New York -- outbreak resembling the Iceland disease, simulating " acute Anterior Poliomyelitis
  1952 London, England - Middlesex Hospital Nurses ' Home - Encephalomyelitis associated with Poliomyelitis virus
  1952 Copenhagen, Denmark - epidemic Myositis
  1952 Lakeland, Florida - epidemic Neuromyasthenia
  1953 Coventry and District, England - an illness resembling Poliomyelitis observed in nurses
  1953 Rockville, Maryland - Chestnut Lodge Hospital - Poliomyelitis-like epidemic Neuromyasthenia
  1953 Jutland, Denmark - epidemic Encephalitis with vertigo
  1954 Seward, Alaska - benign Myalgic Encephalomyelitis (Iceland Disease)
  1954 Berlin, Germany - British army - further outbreak of a disease resembling Poliomyelitis
  1954 Liverpool, England - outbreak among medical and nursing staff in a local hospital
  1955 Dalston, Cumbria, England – epidemic and sporadic outbreak of an unusual disease
  1955 London, England - Royal Free Hospital - outbreak in staff and patients of Benign Myalgic Encephalomyelitis
  1955 Hampstead, London
  1955 Perth, Australia - virus epidemic in waves
  1955 Gilfac Goch, Wales - outbreak of benign Myalgic Encephalomyelitis
  1955 Durban City, South Africa - Addington Hospital - outbreak among nurses of Durban Mystery Disease
  1955 Segbwema, Sierra Leone - outbreak of Encephalomyelitis
  1955 Patreksfjorour and Porshofn, Iceland - unusual response to polio vaccine
  1955 Northwest London, England - nurses ' residential home - acute Infective Encephalomyelitis simulating poliomyelitis
  1956 Ridgefield, Connecticut - epidemic Neuromyasthenia
  1956 Punta Gorda Florida - outbreak of epidemic Neuromyasthenia
  1956 Newton-le-Willows, Lancashire, England - Lymphocytic Meningoencephalitis with myalgia and rash
  1956 Pittsfield and Williamstown, Massachusetts - benign Myalgic Encephalomyelitis
  1956 Coventry, England - epidemic malaise, benign Myalgic Encephalomyelitis
  1957 Brighton, South Australia - Cocksakie Echo virus Meningitis, epidemic Myalgic Encephalomyelitis
  1958 Athens, Greece - nurses ' school - outbreak of benign Myalgic Encephalomyelitis with periostitis and arthopathy noted.
  1958 Southwest London, England - reports of sporadic cases of Myalgic Encephalomyelitis
  1959 Newcastle Upon Tyne, England - outbreak of benign Myalgic Encephalomyelitis
  1961 Basel, Switzerland - sporadic cases of benign Myalgic Encephalomyelitis
  1961 New York State - outbreak of epidemic Neuromyasthenia in a convent
  1964 Northwest London, England - epidemic malaise, epidemic Neuromyasthenia
  1964 Franklin, Kentucky - outbreak of Neuromyasthenia in a factory
  1967 Edinburgh, Scotland - sporadic cases resembling benign Myalgic Encephalomyelitis
  1968 " Fraidek, Lebanon - benign Myalgic Encephalomyelitis
  1969 Brooklyn, New York - State University of New York Downstate Medical Center - epidemic Neuromyasthenia, unidentified symptom complex
  1970 Lackland Air Force Base, Texas - epidemic Neuromyasthenia
  1970 London, England - Great Ormond Street Hospital for Children - outbreak of Neuromyasthenia among nurses
  1975 Sacramento, California - Mercy San Juan Hospital - Infectious Venulitis, epidemic " Phelobodynia
  1976 Southwest Ireland - epidemic Neuromyasthenia, benign Myalgic Encephalomyelitis
  1977 Dallas – Fort Worth, Texas - epidemic Neuromyasthenia
  1979 Southampton, England - Myalgic Encephalomyelitis
  1980 West Kilbridge, Ayrshire, Scotland - epidemic Myalgic Encephalomyelitis
  1980 San Francisco, California – epidemic persistent flu-like illness
  1981 Stirlingshire, Scotland - sporadic Myalgic Encephalomyelitis
  1982 West Otago, Dunedin and Hamilton, New Zealand - Myalgic Encephalomyelitis
  1983 Los Angeles, California - initial cases of an unknown, chronic symptom complex involving profound "fatigue"
  1984 Lake Tahoe Area of California/Nevada - start of a yearlong epidemic involving " over 160 cases of chronic illness eventually characterized as Chronic Fatigue Syndrome
  Source: Paradigm Change web site

  
  

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