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Chronic fatigue syndrome from vagus nerve infection: A psychoneuroimmunological hypothesis

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By Michael B. VanElzakker • • June 24, 2013

Editor's Comment: The vagus nerve (the 10th cranial nerve) is a very long nerve that wanders from the brain stem to the intestines. It is primarily responsible for receiving sensory input through ganglia (nerve bundles), which is then processed by the brain. Neurotransmitters released through vagus nerve stimulation are parasympathetic; they slow physiological responses. Heart rate and blood pressure drop, neurons in the brain fire less, and so on. For this reason, vagus nerve stimulation is used to control tachycardia (rapid heartbeat) and epilepsy. An overstimulated vagus nerve can cause vasovagal syncope (fainting). VanElzakker's hypothesis states that the symptoms of CFS are caused by infections in vagus nerve ganglia. As an explanation for the cause of this illness, his hypothesis is worth consideration. A vagus nerve infection would affect every organ in the body. It should be mentioned here that the autopsy of Sophia Mirza  found damage in 80% of her dorsal root ganglia, which, like vagal ganglia, are responsible for processing afferent nervous system signals. (Sophia Mirza's symptoms included hypersensitivity to noise, light and touch.) It is possible that CFS/ME subsets may correlate with damage caused by infections in different nervous system ganglia.

By Michael B. VanElzakker 


Chronic fatigue syndrome (CFS) is an often-debilitating condition of unknown origin. There is a general consensus among CFS researchers that the symptoms seem to reflect an ongoing immune response, perhaps due to viral infection. Thus, most CFS research has focused upon trying to uncover that putative immune system dysfunction or specific pathogenic agent. However, no single causative agent has been found.

In this speculative article, I describe a new hypothesis for the etiology of CFS: infection of the vagus nerve. When immune cells of otherwise healthy individuals detect any peripheral infection, they release proinflammatory cytokines. Chemoreceptors of the sensory vagus nerve detect these localized proinflammatory cytokines, and send a signal to the brain to initiate sickness behavior. Sickness behavior is an involuntary response that includes fatigue, fever, myalgia, depression, and other symptoms that overlap with CFS.

The vagus nerve infection hypothesis of CFS contends that CFS symptoms are a pathologically exaggerated version of normal sickness behavior that can occur when sensory vagal ganglia or paraganglia are themselves infected with any virus or bacteria. Drawing upon relevant findings from the neuropathic pain literature, I explain how pathogen-activated glial cells can bombard the sensory vagus nerve with proinflammatory cytokines and other neuroexcitatory substances, initiating an exaggerated and intractable sickness behavior signal.

According to this hypothesis, any pathogenic infection of the vagus nerve can cause CFS, which resolves the ongoing controversy about finding a single pathogen. The vagus nerve infection hypothesis offers testable hypotheses for researchers, animal models, and specific treatment strategies.

SourceMedical Hypotheses. 21 June 2013 (10.1016/j.mehy.2013.05.034). Michael B. VanElzakker 

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