2019
DOI: 10.3389/fneur.2019.00316
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Corrigendum: Neuroinflammation and Cytokines in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): A Critical Review of Research Methods

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Cited by 9 publications
(7 citation statements)
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“…Limitations to this study include the need to correct for motion artefacts related to cardiac and respiratory pulsations ( Linnman et al , 2012 ; Buhle et al , 2013 ; Terem et al , 2018 ; VanElzakker et al , 2019 ). Future studies should include heart rate and respiratory rate monitors and processing to reduce the motion artefacts induced by arterial pulsations in the Circle of Willis and vertebrobasal arteries, and changes in venous engorgement related to the positive and negative intrapulmonary pressures during breathing.…”
Section: Discussionmentioning
confidence: 99%
“…Limitations to this study include the need to correct for motion artefacts related to cardiac and respiratory pulsations ( Linnman et al , 2012 ; Buhle et al , 2013 ; Terem et al , 2018 ; VanElzakker et al , 2019 ). Future studies should include heart rate and respiratory rate monitors and processing to reduce the motion artefacts induced by arterial pulsations in the Circle of Willis and vertebrobasal arteries, and changes in venous engorgement related to the positive and negative intrapulmonary pressures during breathing.…”
Section: Discussionmentioning
confidence: 99%
“…Supporting the frequency specificity of this effect, relative to healthy controls, patients with myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) exhibit reduced SWA in the SO frequency range and increased SWA in the delta frequency range, particularly over prefrontal cortex (Le Bon et al, 2012). This is notable, because central inflammation is a core component of ME/CFS (VanElzakker et al, 2019) and this frequency effect on SWA is highly consistent with the reported effects of Aβ (Mander et al, 2015;Winer et al, 2019). Regardless of the mechanism or the direction of causality, what is clear is that Aβ burden is associated with local disruptions in frontal slow waves, even prior to MCI diagnosis both crosssectionally (Mander et al, 2015;Varga et al, 2016b;Winer et al, 2019) and longitudinally (Winer et al, 2020 in press).…”
Section: β-Amyloid and Local Expression Of Slow Wave Activity (A)mentioning
confidence: 95%
“…121 Although several brain anomalies are associated with ME/ CFS, 122 brainstem abnormalities have been the most consistently documented. 108,[122][123][124] The brainstem, a central hub in inflammation neurocircuitry, 125 is implicated in sickness behaviors such as malaise, lassitude, fatigue, numbness, coldness, muscle and joint aches, and reduced appetite. 126 Like ME/ CFS, both long-COVID/PASC 22,127 and GWI 37,128 have been linked to brainstem anomalies.…”
Section: Antigen Persistence and Chronic Conditionsmentioning
confidence: 99%
“…Similarly to GWI and long-COVID, ME/CFS is associated with immune system disruption 103 including systemic inflammation 104,105 and neuroinflammation. 106-108 Numerous infectious agents including several human herpes viruses (eg, EBV, HHV6, CMV) have long been suspected in the pathogenesis of ME/CFS 109-113 ; indeed, CFS was historically known as “chronic Epstein-Barr virus syndrome.” 114 Several lines of research suggest that viral reactivation or viral persistence underlies ME/CFS, 98,112 including evidence of HHV-6 antigen in peripheral blood mononuclear cells in patients with CFS, 115 evidence of active and latent HHV-6/HHV-7 infection in plasma samples of CFS patients, 116 and deficient EBV-specific B- and T-cell memory response indicative of impaired ability to control early steps involved in EBV reactivation in CFS patients. 117 ME/CFS is also associated with autoimmunity, 118,119 and recent evidence suggest that molecular mimicry between viral and human proteins may contribute to the condition.…”
Section: The Persistent Antigen Hypothesismentioning
confidence: 99%