Chronic Fatigue from Inflammation

Dr. Weeks’ Comment:  Not just chronic fatigue syndrome and fibromyalgia are driven by inflammation but autism and ADHD and all psychiatric illnesses are made worse with inflammation – like driving in a snowstorm with poor functioning windshield wipers at night… neuroinflammatory cytokines disrupt cognitive process and function – so stop putting that cell phone up to your head and drink anti-inflammatory seed oils and see and think clearly.  And get OUT of pain!




A precautionary approach may be considered sensible with respect to additional factors that could conceivably complicate pathophysiological processes outlined in this article. These may include: Exposure to toxicants e.g., chemical pesticides (Dietert, 2014)/heavy metals (Giordano and Costa, 2012), mold (Aikawa and Suzuki, 1985), and both low frequency (ELF) (Rowland et al., 1998) and high frequency RFR (Pall, 2016) EMFs/EMR, as well as psychological stress (Prins et al., 2008), dehydration (Rowe et al., 1999), and exhaustion (Blaylock and Maroon, 2012).”


Front. Physiol., 17 February 2017 |

The Neuroinflammatory Etiopathology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)

  • Independent Health Researcher and Consultant, Shrewsbury, UK

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.


Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is an idiopathic, heterogeneous condition involving distortion of homeostasis across multiple organ systems. It is chiefly characterized by myalgia, fatigue, neurocognitive dysfunction, and, critically, delayed muscle recovery (Paul et al., 1999) and the intensification of symptoms following physical exertion: “Post Exertional Malaise” (PEM), or “Post Exertional Neuroimmune Exhaustion” (PENE) (VanNess et al., 2010).

This highly intrusive disease involves varying degrees of physical disability and cognitive deficits, associated psychosocial difficulties, and significantly reduced quality of life (Winger et al., 2015) and life expectancy (Jason et al., 2006), across a patient population numbering in the millions worldwide. Complete/spontaneous recovery is extremely rare and conventional treatment strategies rarely deliver even modest direct, objective and, sustained symptomatic improvement. Thus, ME/CFS constitutes a particularly enigmatic, debilitating, and costly major public health issue, and the advancement of our understanding of its essence, hence, a pressing area of biomedical enquiry (Arroll, 2014).

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.


Neuroanatomical Input

Postural and biomechanically induced neuroexcitatory neuroinflammation has been posited as a partial explanation for PEM/PENE (Rowe et al., 2013), and sustained muscle activity and associated cortical excitability have been observed in ME/CFS (Brouwer and Packer, 1994).

A number of clinical and physical therapy researchers have, over the course of recent decades, variously formed associations between ME/CFS, orthostatic intolerance, and Ehlers-Danlos syndrome (Rowe et al., 1999), ME/CFS and joint hypermobility (Barron et al., 2002), and ME/CFS and innate (flat thoracic spine), osteochondritis, or trauma-linked vertebral defects (Perrin, 2007). These issues, along with other connective tissue disorders, fractures, and other factors that reduce range of motion (ROM), a physical impediment common among ME/CFS patients (Rowe et al., 2014), plus lengthy periods of reduced movement of neuromuscular tissues, may be associated with diminished neural motility and increased neuromuscular tension/strain. Both during and 24 h following strain-inducing experimental physical maneuvers, ME/CFS patients report significantly greater symptom intensity elevation than do sham exposed patient and healthy control cohorts (Rowe et al., 2016). Along with neuropathies and peri-neural adhesions, these issues represent potential ongoing sources of nociceptive input and glial activation, resulting in enhanced peripheral and central nervous sensitivity (Rowe et al., 2013). Peri-neural adhesions are fibrous bonds proximal to nerve tissues, often formed during post-operative/injury healing.

Any residual central sensitivity may, in turn, effect heightened sensitivity of relevant portions of the peripheral nervous system (PNS) to further input (Rowe et al., 2014). Furthermore, neurons may continue to fire after the initiating stimulation has ceased (Löscher and Ebert, 1996): a phenomenon observed in relation to persistent, relatively low threshold stimulation, colloquially referred to as “kindling” (Jason et al., 2011). Thus, the potential exists for the emergence of an insidious peripheral-central neurogenic sensitization loop, which would conceivably have the power to modulate the impact of symptom worsening events in ME/CFS. Hypothesized pathological products of these processes include increased resting muscle tone, affected by enhanced tension in/stimulation from proximal peri-neural fibers subject to sensitization, and aggravation of vascular and autonomic tone (Rowe et al., 2013).

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