A new hypothesis paper speculates that infection of the
vagus nerve itself might be the cause of the ME/CFS.
Given the evidence of the involvement of infectious agents
(virus or bacteria) in ME/CFS, the prevailing view is that its symptoms reflect
an ongoing immune response to infection, possibly because of immune system
dysfunction. However, a recent hypothesis paper (VanElzakker MB, Medical
Hypotheses, 2013) goes much further, speculating that infection of the vagus
nerve itself might be the cause of the illness.
Dr VanElzakker from Tufts University in Massachusetts
postulates that a viral or bacterial infection causes activation of glial cells
(which support and protect nerve cells) somewhere along the vagus, which is a
long, highly branched nerve travelling throughout the visceral organs,
including the gastrointestinal lining, lungs, lymph nodes, spleen, liver and
heart. Glial cell activation then produces inflammatory substances which
bombard the sensory vagus nerve, sending signals to the brain to trigger a
range of involuntary symptoms, including myalgia, fever, fatigue, sleep
architecture changes and cognitive abnormalities. Importantly, when glial cell
activation becomes pathological, as in neuropathic pain, the signals can be
intensified and intractable, leading to chronic illness. According to the
author, variation in ME/CFS between patients could be explained by the location
of infection along the vagus nerve pathway, the severity and duration of the
body’s response, and the type and severity of infection.
One advantage of this theory is that it simplifies the quest
to find specific infectious causes of ME/CFS – since ANY pathogenic infection
of the vagus nerve can trigger the symptoms of the disease. But is the
hypothesis true? Well, only experimentation can answer that question, and
possible strategies include basic biomedical imaging of the vagal nerve pathway
from peripheral to central nervous system, or even functional neuroimaging
studies if these are feasible.
The full paper is available here.