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, the hypothesis paper 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 (abstract) 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.