Check out the VanElzakker interview on Simmaron Rising
Michael VanElzakker’s hypothesis that infections of the vagus nerve cause ME/CFS has generated an enormous interest. Now the Tufts neuroscientist talks about how he got interested in ME/CFS, how he’s trying to test his hypothesis, why he believes it may be able to explain post-exertional malaise and more in a Simmaron Rising blog
I’ve had CFS for 42 years, since I was 21. The symptoms are a little less severe by now, but I still get killer headaches with fluid pressure and get very strung out. I exercise hard a few days in a row, then ease up as the symptoms build. I have always worked, though the illness has held me back from my full capacity. I once was diagnosed by David Bell – nice guy.
I find VNIH compelling given my symptoms, especially the cardiac arrhythmia – I know the vagus nerve regulates heart rate. I also like the infection hypothesis, since this started as a flu-like illness, and also infected a couple of my college classmates, though they eventually recovered after a few months. In some ways it seems analogous to shingles, which also infects a cranial nerve and has a period of activity and dormancy.
I’m encouraged to read that there’s a company close to getting a powerful anti-viral drug approved. Maybe I can be cured before I die.
Shingles is a great analogy. I don’t know a lot about it, but I believe VanElzakker is proposing a similar scenario. I agree that the connection with the vagus nerve which sends signals regarding both infection and things like heart rate, blood flows, etc. is very compelling!
Ditto the vagus nerve connection; I’ve a life long history of elevated sed rates, constant herpes zoster, low grade unexplained fevers since I was five ( I missed part of kindergarten.). In high school I began to simply pass out with no prodrome. I would just hit the ground like a marionette whose strings had been cut. Upon regaining consciousness I thought onlookers were joking about what they’d seen. Afterall I was ‘still’ standing, and I had no memory of the events. I did however feel near death. But docs dealt with the inexplicable then as they do now. They simply ignored it. Dysautonomia was dx’d later in life ( I became disabled at 11:30 a.m. Feb. 3rd 1993 post major life stresses and (ta daa) a smallpox vaccination. I sat down and never really got back up ) . But oddly ( to me) dysautonomia was not then and is not now treated by my docs as particularly significant, even worthy of mentioning. This is frustrating to say the least. I believe it is integral to the entity called M.E. of CFIDS which I suffer now. I often wonder if some memo was sent out that diagnosticians deliberately invalidate the suffering of this patient population. Our struggle is a nightmare that…never ends. And yes, ‘shingles’ resonates, seems analogous to aspects of, and to the bature/type / extreme degree.. of suffering.
This theory makes the most sense of any I have heard of. Would this also account for the ganglionitis found during the autopsies of Sophie Mirza and Lynn (forgot her last name — she committed suicide.)
My guess is that it would exactly account for that.
Its a good model but I’m a little concerned that it centres on ongoing infection and in a location that’s hard to access.
The same effects can be triggered in other ways. For example the very similar systemic symptoms of complex regional pain syndrome that are out of proportion with the scale and location of the initial injury and persist after the injury ‘should have’ healed.
A spreading neuroinflammation model of CRPS suggests that neuroinflammation can propagate from the periphery to the central nervous system resulting in self sustaining microglial activation/neuroinflammation which disrupts many brain functions including the autonomic nervous system. A chronic non-ongoing infection could have the same effect as can stress in vulnerable individuals.
In the context of Lipkin’s proposed microbiome study, dysbiosis could also trigger neuroinflammation via the enteric and vagal nerves.
Given the admitted difficulties in confirming ongoing infection in the vagal nerve perhaps a broader more downstream (or upstream?) approach would be a good starting point. PET scanning of radiolabelled ligands of microglial activation in the brain might confirm neuroinflammation (regardless of the driver) and one study (poster session only) appears to confirm CNS microglial activation in ME/CFS.
Small scale ‘proof of concept) trials using glial attenuators such as Ibudolast, low dose naltraxone or Minocycline might support an improvement in symptoms even without identifying the source of the inflammation (with the caveat that attenuating microglia has to approached carefully if an active infection is suspected – but not impossible).
Otherwise the danger is that it remains a nice hypothesis that’s currently very difficult to prove or disprove of current technology can’t detect such localised infection in the vagal nerve.
Start at the top (sic) and work down?
As I have been harping on the topic of Herpes Simplex viruses (predominately because of where it takes up residence — neurons in the ganglia and even in the brain), I am curious if Dr. VanElzakker has a side motive for his theory, namely seeing the Vegus Nerve theory as a microcosm for any and all other infections that involve neuronal beginning points leading to organ control. A different way of putting this is: if the effect of HSV, or VZV on the heart, and any other organ tied to the Vegus Nerve lead to X, Y, and Z effect, do these effects also pertain to just about every other organ-to-ganglion relationship?
If the assumption that all other ganglion-to-organ relationship can suffer the same problems as the Vegas Nerve-to-heart relationship, then perhaps there are easier connections to study, e.g. Dorsal Root Ganglion-to-bladder relationship (I believe the bladder is connected to this nerve hub).