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Chronic Fatigue Syndrome: HELP
Articles from Miscellaneous institutions in Melbourne
Based on 11 articles published since 2010
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These are the 11 published articles about Fatigue Syndrome, Chronic that originated from Miscellaneous institutions in Melbourne during 2010-2020.
 
+ Citations + Abstracts
1 Review Myalgic encephalomyelitis or chronic fatigue syndrome: how could the illness develop? 2019

Morris, Gerwyn / Maes, Michael / Berk, Michael / Puri, Basant K. ·IMPACT Strategic Research Centre, School of Medicine, Barwon Health, Deakin University, Geelong, Victoria, Australia. · Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. · Department of Psychiatry, Royal Melbourne Hospital, University of Melbourne, Parkville, Victoria, Australia. · Florey Institute for Neuroscience and Mental Health, University of Melbourne, Parkville, Victoria, Australia. · Orygen, The National Centre of Excellence in Youth Mental Health, Parkville, Victoria, Australia. · Department of Medicine, Imperial College London, Hammersmith Hospital, London, England, W12 0HS, UK. basant.puri@imperial.ac.uk. ·Metab Brain Dis · Pubmed #30758706.

ABSTRACT: A model of the development and progression of chronic fatigue syndrome (myalgic encephalomyelitis), the aetiology of which is currently unknown, is put forward, starting with a consideration of the post-infection role of damage-associated molecular patterns and the development of chronic inflammatory, oxidative and nitrosative stress in genetically predisposed individuals. The consequences are detailed, including the role of increased intestinal permeability and the translocation of commensal antigens into the circulation, and the development of dysautonomia, neuroinflammation, and neurocognitive and neuroimaging abnormalities. Increasing levels of such stress and the switch to immune and metabolic downregulation are detailed next in relation to the advent of hypernitrosylation, impaired mitochondrial performance, immune suppression, cellular hibernation, endotoxin tolerance and sirtuin 1 activation. The role of chronic stress and the development of endotoxin tolerance via indoleamine 2,3-dioxygenase upregulation and the characteristics of neutrophils, monocytes, macrophages and T cells, including regulatory T cells, in endotoxin tolerance are detailed next. Finally, it is shown how the immune and metabolic abnormalities of chronic fatigue syndrome can be explained by endotoxin tolerance, thus completing the model.

2 Review Examining clinical similarities between myalgic encephalomyelitis/chronic fatigue syndrome and D-lactic acidosis: a systematic review. 2017

Wallis, Amy / Ball, Michelle / McKechnie, Sandra / Butt, Henry / Lewis, Donald P / Bruck, Dorothy. ·Psychology Department, College of Health and Biomedicine, Victoria University, PO Box 14428, Melbourne, VIC, 8001, Australia. amy.wallis@vu.edu.au. · Psychology Department, College of Health and Biomedicine, Victoria University, PO Box 14428, Melbourne, VIC, 8001, Australia. · College of Engineering & Science, Victoria University, Melbourne, VIC, Australia. · Bioscreen Yarraville (Aust) Pty Ltd, Melbourne, VIC, Australia. · CFS Discovery Clinic, Melbourne, VIC, Australia. ·J Transl Med · Pubmed #28592308.

ABSTRACT: BACKGROUND: The pursuit for clarity in diagnostic and treatment pathways for the complex, chronic condition of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) continues. This systematic review raises a novel question to explore possible overlapping aetiology in two distinct conditions. Similar neurocognitive symptoms and evidence of D-lactate producing bacteria in ME/CFS raise questions about shared mechanisms with the acute condition of D-lactic acidosis (D-la). METHODS: D-la case reports published between 1965 and March 2016 were reviewed for episodes describing both neurological symptoms and high D-lactate levels. Fifty-nine D-la episodes were included in the qualitative synthesis comparing D-la symptoms with ME/CFS diagnostic criteria. A narrative review of D-la mechanisms and relevance for ME/CFS was provided. RESULTS: The majority of neurological disturbances reported in D-la episodes overlapped with ME/CFS symptoms. Of these, the most frequently reported D-la symptoms were motor disturbances that appear more prominent during severe presentations of ME/CFS. Both patient groups shared a history of gastrointestinal abnormalities and evidence of bacterial dysbiosis, although only preliminary evidence supported the role of lactate-producing bacteria in ME/CFS. LIMITATIONS: Interpretation of results are constrained by both the breadth of symptoms included in ME/CFS diagnostic criteria and the conservative methodology used for D-la symptom classification. Several pathophysiological mechanisms in ME/CFS were not examined. CONCLUSIONS: Shared symptomatology and underlying microbiota-gut-brain interactions raise the possibility of a continuum of acute (D-la) versus chronic (ME/CFS) presentations related to D-lactate absorption. Measurement of D-lactate in ME/CFS is needed to effectively evaluate whether subclinical D-lactate levels affect neurological symptoms in this clinical population.

3 Review Nitrosative Stress, Hypernitrosylation, and Autoimmune Responses to Nitrosylated Proteins: New Pathways in Neuroprogressive Disorders Including Depression and Chronic Fatigue Syndrome. 2017

Morris, Gerwyn / Berk, Michael / Klein, Hans / Walder, Ken / Galecki, Piotr / Maes, Michael. ·Tir Na Nog, Bryn Road seaside 87, Llanelli, SA152LW, Wales, UK. · IMPACT Strategic Research Centre, School of Medicine, Deakin University, P.O. Box 291, Geelong, 3220, Australia. · Orygen Youth Health Research Centre and the Centre of Youth Mental Health, Poplar Road 35, Parkville, 3052, Australia. · The Florey Institute for Neuroscience and Mental Health, University of Melbourne, Kenneth Myer Building, Royal Parade 30, Parkville, 3052, Australia. · Department of Psychiatry, Royal Melbourne Hospital, University of Melbourne, Level 1 North, Main Block, Parkville, 3052, Australia. · Department of Psychiatry, University of Groningen, UMCG, Groningen, The Netherlands. · Metabolic Research Unit, School of Medicine, Deakin University, Waurn Ponds, Australia. · Department of Adult Psychiatry, Medical University of Lodz, Łódź, Poland. · Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. dr.michaelmaes@hotmail.com. · Department of Psychiatry, Faculty of Medicine, State University of Londrina, Londrina, Brazil. dr.michaelmaes@hotmail.com. · Department of Psychiatry, Medical University Plovdiv, Plovdiv, Bulgaria. dr.michaelmaes@hotmail.com. · Revitalis, Waalre, The Netherlands. dr.michaelmaes@hotmail.com. · IMPACT Strategic Research Center, Barwon Health, Deakin University, Geelong, VIC, Australia. dr.michaelmaes@hotmail.com. ·Mol Neurobiol · Pubmed #27339878.

ABSTRACT: Nitric oxide plays an indispensable role in modulating cellular signaling and redox pathways. This role is mainly effected by the readily reversible nitrosylation of selective protein cysteine thiols. The reversibility and sophistication of this signaling system is enabled and regulated by a number of enzymes which form part of the thioredoxin, glutathione, and pyridoxine antioxidant systems. Increases in nitric oxide levels initially lead to a defensive increase in the number of nitrosylated proteins in an effort to preserve their function. However, in an environment of chronic oxidative and nitrosative stress (O&NS), nitrosylation of crucial cysteine groups within key enzymes of the thioredoxin, glutathione, and pyridoxine systems leads to their inactivation thereby disabling denitrosylation and transnitrosylation and subsequently a state described as "hypernitrosylation." This state leads to the development of pathology in multiple domains such as the inhibition of enzymes of the electron transport chain, decreased mitochondrial function, and altered conformation of proteins and amino acids leading to loss of immune tolerance and development of autoimmunity. Hypernitrosylation also leads to altered function or inactivation of proteins involved in the regulation of apoptosis, autophagy, proteomic degradation, transcription factor activity, immune-inflammatory pathways, energy production, and neural function and survival. Hypernitrosylation, as a consequence of chronically elevated O&NS and activated immune-inflammatory pathways, can explain many characteristic abnormalities observed in neuroprogressive disease including major depression and chronic fatigue syndrome/myalgic encephalomyelitis. In those disorders, increased bacterial translocation may drive hypernitrosylation and autoimmune responses against nitrosylated proteins.

4 Review The Neuro-Immune Pathophysiology of Central and Peripheral Fatigue in Systemic Immune-Inflammatory and Neuro-Immune Diseases. 2016

Morris, Gerwyn / Berk, Michael / Galecki, Piotr / Walder, Ken / Maes, Michael. ·Tir Na Nog, Bryn Road seaside 87, Llanelli, SA152LW, Wales, UK. · IMPACT Strategic Research Centre, School of Medicine, Deakin University, P.O. Box 291, Geelong, 3220, Australia. · Orygen Youth Health Research Centre and the Centre of Youth Mental Health, Poplar Road 35, Parkville, 3052, Australia. · The Florey Institute for Neuroscience and Mental Health, University of Melbourne, Kenneth Myer Building, Royal Parade 30, Parkville, 3052, Australia. · Department of Psychiatry, University of Melbourne, Level 1 North, Main Block, Royal Melbourne Hospital, Parkville, 3052, Australia. · Department of Adult Psychiatry, Medical University of Lodz, Lodz, Poland. · Metabolic Research Unit, Deakin University, Geelong, Australia. · IMPACT Strategic Research Centre, School of Medicine, Deakin University, P.O. Box 291, Geelong, 3220, Australia. dr.michaelmaes@hotmail.com. · Department of Psychiatry, Faculty of Medicine, Chulalongkorn University, Bangkok, Thailand. dr.michaelmaes@hotmail.com. · Health Sciences Graduate Program, Health Sciences Center, State University of Londrina, Londrina, Brazil. dr.michaelmaes@hotmail.com. · Impact Strategic Research Center, Deakin University, Geelong, Australia. dr.michaelmaes@hotmail.com. ·Mol Neurobiol · Pubmed #25598355.

ABSTRACT: Many patients with systemic immune-inflammatory and neuro-inflammatory disorders, including depression, rheumatoid arthritis, systemic lupus erythematosus, Sjögren's disease, cancer, cardiovascular disorder, Parkinson's disease, multiple sclerosis, stroke, and chronic fatigue syndrome/myalgic encephalomyelitis, endure pathological levels of fatigue. The aim of this narrative review is to delineate the wide array of pathways that may underpin the incapacitating fatigue occurring in systemic and neuro-inflammatory disorders. A wide array of immune, inflammatory, oxidative and nitrosative stress (O&NS), bioenergetic, and neurophysiological abnormalities are involved in the etiopathology of these disease states and may underpin the incapacitating fatigue that accompanies these disorders. This range of abnormalities comprises: increased levels of pro-inflammatory cytokines, e.g., interleukin-1 (IL-1), IL-6, tumor necrosis factor (TNF) α and interferon (IFN) α; O&NS-induced muscle fatigue; activation of the Toll-Like Receptor Cycle through pathogen-associated (PAMPs) and damage-associated (DAMPs) molecular patterns, including heat shock proteins; altered glutaminergic and dopaminergic neurotransmission; mitochondrial dysfunctions; and O&NS-induced defects in the sodium-potassium pump. Fatigue is also associated with altered activities in specific brain regions and muscle pathology, such as reductions in maximum voluntary muscle force, downregulation of the mitochondrial biogenesis master gene peroxisome proliferator-activated receptor gamma coactivator 1-alpha, a shift to glycolysis and buildup of toxic metabolites within myocytes. As such, both mental and physical fatigue, which frequently accompany immune-inflammatory and neuro-inflammatory disorders, are the consequence of interactions between multiple systemic and central pathways.

5 Review Revisiting adverse reactions to vaccines: A critical appraisal of Autoimmune Syndrome Induced by Adjuvants (ASIA). 2015

Hawkes, David / Benhamu, Joanne / Sidwell, Tom / Miles, Rhianna / Dunlop, Rachael A. ·Department of Pharmacology and Therapeutics, The University of Melbourne, Victoria, Australia; Friends of Science in Medicine, Melbourne, Victoria, Australia. Electronic address: dhawkes@unimelb.edu.au. · Friends of Science in Medicine, Melbourne, Victoria, Australia. · Department of Molecular Immunology, The Walter and Eliza Hall Institute of Medical Research, Victoria, Australia. · Greenslopes Clinical School of Medicine, University of Queensland, Greenslopes, Queensland, Australia; Department of Renal Medicine, Greenslopes Private Hospital, Greenslopes, Queensland, Australia. · Australian School of Advanced Medicine, Macquarie Park, NSW, Australia. ·J Autoimmun · Pubmed #25794485.

ABSTRACT: In 2011 Shoenfeld and Agmon-Levin proposed a new syndrome as a way of grouping together a range of emerging autoimmune diseases with possible adjuvant-associated causes, Autoimmune/Auto-inflammatory Syndrome Induced by Adjuvants (ASIA). At present, there is no evidence to suggest that ASIA syndrome is a viable explanation for unusual autoimmune diseases. Since the initial paper, over 80 publications have discussed ASIA. This systematic review examines the research that has been done to investigate whether ASIA is a broad umbrella term with little clinical significance, or whether there is some underlying mechanism which could be utilised to reduce the occurrence of adjuvant mediated disease. Twenty-seven animal, epidemiological and case studies were reviewed. Unfortunately, a robust animal model of ASIA using biologically relevant doses of adjuvants has yet to be defined. It is also apparent that the broadness of the current ASIA criteria lack stringency and, as a result, very few cases of autoimmune disease could be excluded from a diagnosis of ASIA. The current studies involving human cases are so diverse, in both external stimuli and in resulting conditions, that there is currently a lack of reproducible evidence for any consistent relationship between adjuvant and autoimmune condition. The addition of a mandatory criterion requiring temporal association and clinically relevant adjuvant dose would allow better definition of what constitutes a diagnosis of ASIA.

6 Review Sleep Disturbances in Pediatric Chronic Fatigue Syndrome: A Review of Current Research. 2015

Snodgrass, Kelli / Harvey, Adrienne / Scheinberg, Adam / Knight, Sarah. ·Clinical Sciences, Murdoch Childrens Research Institute. · Department of Paediatrics, The University of Melbourne. · Victorian Paediatric Rehabilitation Service, The Royal Children's Hospital. · Faculty of Medicine, Monash University, Melbourne, Victoria, Australia. · Victorian Paediatric Rehabilitation Service, Monash Children's, Parkville, Victoria, Australia. ·J Clin Sleep Med · Pubmed #25766714.

ABSTRACT: OBJECTIVE: Children and adolescents with chronic fatigue syndrome (CFS) frequently report sleep disturbances. However, little is known about the nature and severity of sleep disturbance and factors associated with sleep problems in pediatric CFS. The purpose of this review was to synthesize and critically appraise existing literature relating to sleep disturbances in pediatric CFS. METHODS: Embase, CINAHL, PsychINFO, PubMed. and Medline databases were searched to retrieve all studies that included an assessment of sleep in pediatric CFS. Two reviewers independently assessed eligibility, extracted data, and systematically assessed reporting quality. RESULTS: Six studies were included and these were mostly case-controlled designs. Findings varied across studies; however, most studies found that children and adolescents with CFS had significantly more sleep disturbances when compared to healthy controls. Significant methodological variations and limitations were apparent. CONCLUSIONS: This review suggests that children and adolescents with CFS experience sleep disturbances. However, results need to be interpreted cautiously given the limited evidence available and its overall low quality. More research is required to elucidate the nature and extent of sleep disturbance in pediatric CFS and should focus on (1) identifying the specific types, causes, and severity of sleep disturbances; (2) the specific consequences of sleep disturbances; and (3) the most effective interventions for sleep problems in this population.

7 Clinical Trial Open-label pilot for treatment targeting gut dysbiosis in myalgic encephalomyelitis/chronic fatigue syndrome: neuropsychological symptoms and sex comparisons. 2018

Wallis, Amy / Ball, Michelle / Butt, Henry / Lewis, Donald P / McKechnie, Sandra / Paull, Phillip / Jaa-Kwee, Amber / Bruck, Dorothy. ·Psychology Department, College of Health and Biomedicine, Victoria University, Melbourne, Australia. Amy.Wallis@vu.edu.au. · Psychology Department, College of Health and Biomedicine, Victoria University, Melbourne, Australia. · Bioscreen (Aust) Pty Ltd., Melbourne, Australia. · CFS Discovery Clinic, Donvale, Melbourne, Australia. · College of Engineering and Science, Victoria University, Melbourne, Australia. ·J Transl Med · Pubmed #29409505.

ABSTRACT: BACKGROUND: Preliminary evidence suggests that the enteric microbiota may play a role in the expression of neurological symptoms in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). Overlapping symptoms with the acute presentation of D-lactic acidosis has prompted the use of antibiotic treatment to target the overgrowth of species within the Streptococcus genus found in commensal enteric microbiota as a possible treatment for neurological symptoms in ME/CFS. METHODS: An open-label, repeated measures design was used to examine treatment efficacy and enable sex comparisons. Participants included 44 adult ME/CFS patients (27 females) from one specialist medical clinic with Streptococcus viable counts above 3.00 × 10 RESULTS: Large treatment effects were observed for the intention-to-treat sample with a reduction in Streptococcus viable count and improvement on several clinical outcomes including total symptoms, some sleep (less awakenings, greater efficiency and quality) and cognitive symptoms (attention, processing speed, cognitive flexibility, story memory and verbal fluency). Mood, fatigue and urine D:L lactate ratio remained similar across time. Ancillary results infer that shifts in microbiota were associated with more of the variance in clinical changes for males compared with females. CONCLUSIONS: Results support the notion that specific microorganisms interact with some ME/CFS symptoms and offer promise for the therapeutic potential of targeting gut dysbiosis in this population. Streptococcus spp. are not the primary or sole producers of D-lactate. Further investigation of lactate concentrations are needed to elucidate any role of D-lactate in this population. Concurrent microbial shifts that may be associated with clinical improvement (i.e., increased Bacteroides and Bifidobacterium or decreased Clostridium in males) invite enquiry into alternative strategies for individualised treatment. Trial Registration Australian and New Zealand Clinical Trial Registry (ACTRN12614001077651) 9th October 2014. https://www.anzctr.org.au/Trial/Registration/TrialReview.aspx?id=366933&isReview=true.

8 Article Rethinking ME/CFS Diagnostic Reference Intervals via Machine Learning, and the Utility of Activin B for Defining Symptom Severity. 2019

Lidbury, Brett A / Kita, Badia / Richardson, Alice M / Lewis, Donald P / Privitera, Edwina / Hayward, Susan / de Kretser, David / Hedger, Mark. ·National Centre for Epidemiology and Population Health, RSPH, College of Health and Medicine, The Australian National University, Canberra, ACT 2601, Australia. brett.lidbury@anu.edu.au. · Paranta Biosciences Limited, Suite 549, 1 Queens Rd, Melbourne, VIC 3004, Australia. · National Centre for Epidemiology and Population Health, RSPH, College of Health and Medicine, The Australian National University, Canberra, ACT 2601, Australia. · CFS Discovery, Donvale Specialist Medical Centre, Donvale, VIC 3111, Australia. · Centre for Reproductive Health, Hudson Institute of Medical Research, Clayton, VIC 3168, Australia. · Department of Anatomy and Developmental Biology, School of Biomedical Sciences, Monash University, Clayton, VIC 3800, Australia. ·Diagnostics (Basel) · Pubmed #31331036.

ABSTRACT: Biomarker discovery applied to myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), a disabling disease of inconclusive aetiology, has identified several cytokines to potentially fulfil a role as a quantitative blood/serum marker for laboratory diagnosis, with activin B a recent addition. We explored further the potential of serum activin B as a ME/CFS biomarker, alone and in combination with a range of routine test results obtained from pathology laboratories. Previous pilot study results showed that activin B was significantly elevated for the ME/CFS participants compared to healthy (control) participants. All the participants were recruited via CFS Discovery and assessed via the Canadian/International Consensus Criteria. A significant difference for serum activin B was also detected for ME/CFS and control cohorts recruited for this study, but median levels were significantly lower for the ME/CFS cohort. Random Forest (RF) modelling identified five routine pathology blood test markers that collectively predicted ME/CFS at ≥62% when compared via weighted standing time (WST) severity classes. A closer analysis revealed that the inclusion of activin B to the panel of pathology markers improved the prediction of mild to moderate ME/CFS cases. Applying correct WST class prediction from RFA modelling, new reference intervals were calculated for activin B and associated pathology markers, where 24-h urinary creatinine clearance, serum urea and serum activin B showed the best potential as diagnostic markers. While the serum activin B results remained statistically significant for the new participant cohorts, activin B was found to also have utility in enhancing the prediction of symptom severity, as represented by WST class.

9 Article Epidemiology of paediatric chronic fatigue syndrome in Australia. 2019

Knight, Sarah / Elders, Shane / Rodda, Jill / Harvey, Adrienne / Lubitz, Lionel / Rowe, Kathy / Reveley, Colette / Hennel, Sabine / Towns, Susan / Kozlowska, Kasia / Payne, Donald N / Marshall-Gradisnik, Sonya / Scheinberg, Adam. ·Neurodisability and Rehabilitation, Murdoch Children's Research Institute, Melbourne, Australia. · Victorian Paediatric Rehabilitation Service, Royal Children's Hospital Melbourne, Melbourne, Victoria, Australia. · Paediatrics, The University of Melbourne, Parkville, Victoria, Australia. · Royal Children's Hospital Melbourne, Parkville, Victoria, Australia. · General Medicine, Royal Children's Hospital Melbourne, Parkville, Victoria, Australia. · Victorian Paediatric Rehabilitation, Monash Children's Hospital, Clayton, Victoria, Australia. · Sydney Children's Hospitals Network Randwick and Westmead, Westmead, New South Wales, Australia. · Adolescent Medicine, Princess Margaret Hospital, Perth, Western Australia, Australia. · SPACH, UWA, Perth, Western Australia, Australia. · Griffith University-Gold Coast Campus, Southport, Queensland, Australia. ·Arch Dis Child · Pubmed #30798255.

ABSTRACT: OBJECTIVE: To estimate the paediatrician-diagnosed incidence of chronic fatigue syndrome (CFS) in Australia, and describe demographic and clinical features, as well as approaches to diagnosis and management. METHODS: The Australian Paediatric Surveillance Unit facilitates monthly national surveillance of uncommon conditions seen by paediatricians. Data from young people aged <18 years diagnosed with CFS were collected. Incidence was estimated based on new cases reported from April 2015 to April 2016. RESULTS: A total of 164 cases of newly diagnosed CFS in young people aged 4-17 years were identified for inclusion. The estimated national incidence for children aged 4-9 years was 0.25 per 100 000 per annum. In children aged 10-17 years, the estimated incidence of paediatrician-diagnosed cases for Victoria (17.48 per 100 000) was substantially greater than other Australian states (range 1.31-5.51 per 100 000). Most cases were female and Caucasian, most commonly presenting after an infectious illness with symptoms gradual in onset. The majority were diagnosed at least 13 months after symptom onset. Symptoms, associations, investigations and management strategies were highly variable. CONCLUSIONS: Current findings suggest that, consistent with other countries, the Australian incidence of CFS in children aged <10 years is very low. In contrast, the national incidence of CFS in older children and adolescents (aged 10-17 years) is more unclear, with marked variability between geographical regions apparent. This may be due to variation in service accessibility and clinician understanding of CFS. Accordingly, national initiatives to improve equity of care for children with CFS may be required.

10 Article Weighting of orthostatic intolerance time measurements with standing difficulty score stratifies ME/CFS symptom severity and analyte detection. 2018

Richardson, Alice M / Lewis, Don P / Kita, Badia / Ludlow, Helen / Groome, Nigel P / Hedger, Mark P / de Kretser, David M / Lidbury, Brett A. ·National Centre for Epidemiology and Public Health, Research School of Population Health, ANU, Acton, ACT, 2601, Australia. alice.richardson@anu.edu.au. · CFS Discovery, Donvale Medical Specialist Centre, Donvale, VIC, 3111, Australia. · Paranta Biosciences Limited, Melbourne, VIC, 3004, Australia. · School of Life Sciences, Oxford Brookes University, Headington, Oxford, OX3 0BP, UK. · The Hudson Medical Research Institute, Monash University, Clayton, VIC, 3168, Australia. · Department of Anatomy and Developmental Biology, Monash University, Clayton, VIC, 3168, Australia. · National Centre for Epidemiology and Public Health, Research School of Population Health, ANU, Acton, ACT, 2601, Australia. ·J Transl Med · Pubmed #29650052.

ABSTRACT: BACKGROUND: Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is clinically defined and characterised by persistent disabling tiredness and exertional malaise, leading to functional impairment. METHODS: This study introduces the weighted standing time (WST) as a proxy for ME/CFS severity, and investigates its behaviour in an Australian cohort. WST was calculated from standing time and subjective standing difficulty data, collected via orthostatic intolerance assessments. The distribution of WST for healthy controls and ME/CFS patients was correlated with the clinical criteria, as well as pathology and cytokine markers. Included in the WST cytokine analyses were activins A and B, cytokines causally linked to inflammation, and previously demonstrated to separate ME/CFS from healthy controls. Forty-five ME/CFS patients were recruited from the CFS Discovery Clinic (Victoria) between 2011 and 2013. Seventeen healthy controls were recruited concurrently and identically assessed. RESULTS: WST distribution was significantly different between ME/CFS participants and controls, with six diagnostic criteria, five analytes and one cytokine also significantly different when comparing severity via WST. On direct comparison of ME/CFS to study controls, only serum activin B was significantly elevated, with no significant variation observed for a broad range of serum and urine markers, or other serum cytokines. CONCLUSIONS: The enhanced understanding of standing test behaviour to reflect orthostatic intolerance as a ME/CFS symptom, and the subsequent calculation of WST, will encourage the greater implementation of this simple test as a measure of ME/CFS diagnosis, and symptom severity, to the benefit of improved diagnosis and guidance for potential treatments.

11 Article The many roads to mitochondrial dysfunction in neuroimmune and neuropsychiatric disorders. 2015

Morris, Gerwyn / Berk, Michael. ·Tir Na Nog, Bryn Road seaside 87, Llanelli, Cardiff, Wales, SA152LW, UK. activatedmicroglia@gmail.com. · IMPACT Strategic Research Centre, School of Medicine, Deakin University, PO Box 291, Geelong, 3220, Australia. mikebe@barwonhealth.org.au. · Orygen Youth Health Research Centre and the Centre of Youth Mental Health, Poplar Road 35, Parkville, 3052, Australia. mikebe@barwonhealth.org.au. · The Florey Institute for Neuroscience and Mental Health, University of Melbourne, Kenneth Myer Building, Royal Parade 30, Parkville, 3052, Australia. mikebe@barwonhealth.org.au. · Department of Psychiatry, University of Melbourne, Level 1 North, Main Block, Royal Melbourne Hospital, Parkville, 3052, Australia. mikebe@barwonhealth.org.au. ·BMC Med · Pubmed #25889215.

ABSTRACT: BACKGROUND: Mitochondrial dysfunction and defects in oxidative metabolism are a characteristic feature of many chronic illnesses not currently classified as mitochondrial diseases. Examples of such illnesses include bipolar disorder, multiple sclerosis, Parkinson's disease, schizophrenia, depression, autism, and chronic fatigue syndrome. DISCUSSION: While the majority of patients with multiple sclerosis appear to have widespread mitochondrial dysfunction and impaired ATP production, the findings in patients diagnosed with Parkinson's disease, autism, depression, bipolar disorder schizophrenia and chronic fatigue syndrome are less consistent, likely reflecting the fact that these diagnoses do not represent a disease with a unitary pathogenesis and pathophysiology. However, investigations have revealed the presence of chronic oxidative stress to be an almost invariant finding in study cohorts of patients afforded each diagnosis. This state is characterized by elevated reactive oxygen and nitrogen species and/or reduced levels of glutathione, and goes hand in hand with chronic systemic inflammation with elevated levels of pro-inflammatory cytokines. SUMMARY: This paper details mechanisms by which elevated levels of reactive oxygen and nitrogen species together with elevated pro-inflammatory cytokines could conspire to pave a major road to the development of mitochondrial dysfunction and impaired oxidative metabolism seen in many patients diagnosed with these disorders.