Jesse2233
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At the end of his seminal vagus nerve infection hypothesis paper, Dr VanElzakker puts forward a potential treatment protocol (1). I was wondering if anyone here has deliberately followed it, especially with all treatments done concurrently.
Note: Dr VanElzakker is a researcher not a clinician. He makes clear that both his hypothesis and treatment proposal are theoretical.
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Less accessible options...
Note: Dr VanElzakker is a researcher not a clinician. He makes clear that both his hypothesis and treatment proposal are theoretical.
- Famvir - Rodent studies have shown that the antiviral Famvir (famciclovir) penetrates peripheral nerve ganglia better than other antivirals, which makes it an attractive option if symptoms are driven by latent or active herpesvirus infection of peripheral vagus ganglia.
- lbudilast - An anti-inflammatory drug used mainly in Japan for asthma, stroke, and treatment of neuropathic pain as an adjunct with opioids. Ibudilast crosses the blood-brain barrier and suppresses glial cell activation.
- Vagus nerve stimulation (VNS) - involves delivering electrical impulses to the vagus nerve via a medical device. Use is currently reserved as an adjunctive treatment for certain types of intractable epilepsy and treatment-resistant depression. Vagus nerve stimulation promotes the anti-inflammatory effects of the motor (efferent) vagus nerve. In the case of the vagus nerve infection hypothesis, it may also regulate exaggerated sensory (afferent) signaling.
- Mestinon (Pyridostigmine) - a drug that blocks the enzymatic breakdown of acetylcholine, which is the primary neurotransmitter of the vagus nerve, especially the parasympathetic/ motor/ efferent branch. Mestinon is frequently prescribed for POTS, especially to improve tachycardia, and can work synergistically with vagus nerve stimulation.
- Celebrex - Celebrex is a COX2 inhibitor, which blocks an enzyme that is part of the production of prostaglandins. When glial cells become activated, they produce neuroexcitatory mediators - molecules that turn on nerve cells. According to the vagus nerve infection hypothesis, infection of vagus nerve ganglia causes activation of associated glial cells, which in turn overly-excite the vagus nerve via these mediators. Prostaglandins are one of these neuroexcitatory mediators, along with proinflammatory cytokines, nitric oxide, reactive oxygen species, glutamate, and nerve growth factor. Beside the antiinflammatory mechanism of COX2 inhibition, herpesviruses upregulate COX2 to aid with its own replication.
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Less accessible options...
- Ampligen - a drug that stimulates the production of natural interferon
- Anesthetization of the vagus nerve - to temporarily disrupt cytokine signaling and microglial brain inflammation
- Vagotomy - severing of the vagus nerve to permanently disrupt cytokine signaling and microglial brain inflammation