Invest in ME Conference 12: First Class in Every Way
OverTheHills wraps up our series of articles on this year's 12th Invest in ME International Conference (IIMEC12) in London with some reflections on her experience as a patient attending the conference for the first time.
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The Neuroinflammatory Etiopathology of ME/CFS

Discussion in 'Latest ME/CFS Research' started by Kati, Mar 8, 2017.

  1. Kati

    Kati Patient in training

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    Front Physiol. 2017 Feb 17;8:88. doi: 10.3389/fphys.2017.00088. eCollection 2017.
    The Neuroinflammatory Etiopathology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)
    Glassford JA1.
    Author information
    1Independent Health Researcher and Consultant Shrewsbury, UK.


    Abstract

    Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a debilitating multi-systemic chronic illness of unknown etiology, classified as a neurological disorder by the World Health Organization (WHO).

    The symptomatology of the condition appears to emanate from a variety of sources of chronic neurological disturbance and associated distortions, and chronicity, in noxious sensory signaling and neuroimmune activation.

    This article incorporates a summary review and discussion of biomedical research considered relevant to this essential conception perspective.

    It is intended to provide stakeholders with a concise, integrated outline disease model in order to help demystify this major public health problem.

    The primary etiopathological factors presented are: (A) Postural/biomechanical pain signaling, affecting adverse neuroexcitation, in the context of compression, constriction, strain, or damage of vertebral-regional bone and neuromuscular tissues; (B) Immune mediated inflammatory sequelae, in the context of prolonged immunotropic neurotrophic infection-with lymphotropic/gliotropic/glio-toxic varieties implicated in particular; (C) A combination of factors A and B.

    Sustained glial activation under such conditions is associated with oxidative and nitrosative stress, neuroinflammation, and neural sensitivity.

    These processes collectively enhance the potential for multi-systemic disarray involving endocrine pathway aberration, immune and mitochondrial dysfunction, and neurodegeneration, and tend toward still more intractable synergistic neuro-glial dysfunction (gliopathy), autoimmunity, and central neuronal sensitization.
     
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  2. valentinelynx

    valentinelynx Senior Member

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    Tucson
    Weird. Written by an "Independent Health Researcher and Consultant," whose degree is a bachelor's in economics. Focuses on neuroinflammation as the etiology of ME/CFS.

    The main topic is: "The central focus of this work is the proposition that ME/CFS constitutes the symptomatic manifestation of enhanced nervous sensitivity attributable to a neuroinflammatory etiopathology associated with abnormal nociceptive and neuroimmune activity. The article reviews, highlights, and interconnects numerous relevant disease features, processes, and concepts from the biomedical literature, the ultimate aim of which is to provide stakeholders with an instructive pathophysiological conceptual framework."

    Some of the paper is a fairly useful review of some of the literature. Other parts are a very odd mishmash of ideas, e.g. "Core intensive/high neuro-dynamic intensity physical activity increases the risk of encumbrance-linked health problems, particularly during spinal development. Related risk factors also include acute neuromuscular strains, neuropathies,* and peri-neural adhesions, as well as relatively indirect processes such as the evolution of connective tissue, hypermobility, and inflammatory disorders. Such issues may be underpinned by genetic vulnerability concerning/the epigenetic impact of psychological trauma (Heim et al., 2009) and psychosocial stress (Prins et al., 2008), together with a broader array of neurotoxic (Giordano and Costa, 2012)/immunotoxic stressors (Dietert, 2014), on the development and functioning of (neuro)anatomic, (neuro)endocrine, and (neuro)immune systems."

    [Sorry, but I don't follow... and I think, if I did follow, I wouldn't agree...]

    This article could have used intensive editing and peer review. IMO. :D
     
  3. adreno

    adreno PR activist

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    Babble.
     
    merylg, valentinelynx and Hutan like this.
  4. Snow Leopard

    Snow Leopard Hibernating

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    South Australia
    Lacking in specific testable hypotheses. :(

    There is also a lack of evidence for the cytokines mentioned, in causation of this illness.
     
    merylg likes this.

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