“Investigating ME/CFS at the intersection of the nervous and immune systems.” Speaker: Dr. Michael VanElzakker Oct 26 2019

For anyone who is in the same position as me and only gets a blue bird silhouette instead of a tweet message:

https://www.massmecfs.org/news/30-news/730-annual-event-10-26-2019-dr-michael-vanelzakker

Dr. VanElzakker will discuss some challenges and opportunities in using brain scans to study communication between the immune and nervous systems. He will describe two ongoing studies that seek to elucidate autonomic dysfunction and possible neuroinflammation in ME/CFS. He will also give an update on the OMF-funded Harvard ME/CFS Collaboration.
 
Anna H said:
Available on their YouTube channel now.
Very interesting talk!



Q&A:
Click to expand...

Fascinating!

Especially, I thought, the bit about his fMRI study on post-exertion symptom provocation with iCPET starting about 24:00, first video.

There are some brain scans (28:50, unpublished data) of patients & healthy controls at rest and while holding their breath (autonomic challenge). The difference is astounding.

As I understood it the idea behind the test is that holding your breath changes the level of CO2 in your blood and therefore should trigger a response by the blood vessels and cause them to dilate. What's happening in the vasculature in the brain and in the body should be closely correlated - and is so in the healthy control but not in the 6 patients, especially during PEM [ETA: not actually sure if the scans are during PEM or not; they're definitely showing the difference between resting state and breath holding state].

Of course very small numbers and no disease controls in the very preliminary data but this will be a very interesting study.
 
Last edited:
Interesting that at 16:22 in the Q&A video he mentions a site in the brainstem called the "nucleus ambiguus," which is apparently important in voluntary breathing (according to a "lesion study"). I know that myself and some others have mentioned the sensation of "having to remember to breath" after the onset of ME. For me, this was something I experienced only during a brief period of weeks immediately after onset (although I was much later diagnosed with intermittent episodes of central sleep apnea). I'm pretty sure that those to whom I mentioned "having to remember to breath" at the time just wrote it off as anxiety, and that might have been the case, but it's interesting to hear about a region of the brainstem that can affect voluntary breathing in the context of the brainstem's possible connection to ME.

[Yes, it is spelled "ambiguus."]
 
Last edited:
The video of the brain 'moving' in response to heart beats was pretty cool - I did know that was happening - it is at 23 mins of the first video.

I also like how he says (28 mins, second video) that it may not be prudent to tell a new doctor you have ME because they won't investigate further and may be missing things.
 
ScottTriGuy said:
The video of the brain 'moving' in response to heart beats was pretty cool - I did know that was happening - it is at 23 mins of the first video.

I also like how he says (28 mins, second video) that it may not be prudent to tell a new doctor you have ME because they won't investigate further and may be missing things.
Click to expand...

Agree. Describing major symptoms will get you a referral to a specialist much quicker.
 
Ravn said:
There are some brain scans (28:50, unpublished data) of patients & healthy controls at rest and while holding their breath (autonomic challenge). The difference is astounding.
Click to expand...
That really stood out to me too!

In the second Q&A video he discusses how they are making sure to have well qualified patients in their studies. They are funnelling patients through one doctor only so that they are properly diagnosed, and pipelining the patients through the different studies. All patients will be tested for Small Fiber Neuropathy with a biopsy. The core collaborative team meet every other week via video to coordinate and continue to build on what they are doing.

In his recent talks Ron Davis has also mentioned the importance of having a well defined patient group to study in the Stanford work. If I remember right the nanoneedle testing required CCC + a local ME experienced doctor to validate the diagnosis.

In the recent OMF announcement about a genorous annonymous donor that will fund Proteomic and Metabolic Plasma iCPET Studies, the cohort has been narrowed further to "the high-flow PLF ME/CFS patients". They do seem to be taking patient selection very seriously.
https://www.omf.ngo/2019/12/02/trip...-study/?utm_source=twitter&utm_medium=organic

EDIT : Mike mentioned in the Q&A that his funding so far for project and wages is from private donors. I think it is an incredibly important source of funding. People who want to fund the research individually in a relatively large amount want to choose which projects they fund.
 
Last edited:
Interesting. A lot of ppl with Cfs have a bad skin perfusion and are very pale. Seems like its not just a centralization from the body, more like a bad perfusion in the whole body. Including brain and organs. Holding the breath is a strong parasympathetic trigger. But it seems its totally missing in the Cfs crowd. Dysautonomia.
 
Speaking to my daughter last night/ this morning. She has headaches and facial pain ( seems related to very tight muscles - she feels though as if someone has taken a baseball bat to specific parts of her head) .
This also induces nausea , almost like being in shock, and puts her on " alert" so she can't sleep.

Her description of it is interesting relative to this thread. She describes it as having the effects of holding your breath, without holding your breath.

Anyone else have the same experience?
 
Badpack said:
Interesting. A lot of ppl with Cfs have a bad skin perfusion and are very pale. Seems like its not just a centralization from the body, more like a bad perfusion in the whole body. Including brain and organs. Holding the breath is a strong parasympathetic trigger.
Click to expand...

Isn't it primarily a sympathetic trigger?

"Apnea-Induced Cortical BOLD-fMRI and Peripheral Sympathoneural Firing Response Patterns of Awake Healthy Humans"
https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0082525

"Effect of repetitive end-inspiration breath holding on very short-term heart rate variability in healthy humans"
https://iopscience.iop.org/article/10.1088/0967-3334/35/12/2429/meta
HRV changes may indicate sympathetic activation during breath holding and parasympathetic activation during recovery after breath holding.
Click to expand...

Neural sites involved in the sustained increase in muscle sympathetic nerve activity induced by inspiratory capacity apnea: a fMRI study
https://www.physiology.org/doi/full/10.1152/japplphysiol.00588.2005

An inspiratory capacity apnea causes a sustained and pronounced increase in MSNA (20). It has been suggested that this increase results from unloading of the low-pressure (cardiopulmonary) baroreceptors [...] Low-pressure baroreceptors are located in the atria and pulmonary veins and respond to low-level changes in absolute venous pressure. They detect changes in right atrial filling and, as a result, are almost certainly responsible for producing the changes in sympathetic activity that accompany conditions such as congestive heart failure [...] Like the arterial baroreceptors, cardiopulmonary baroreceptors are unloaded by falls in pressure and project via the vagus nerve to the nucleus of the solitary tract (NTS). This is consistent with the signal intensity changes in this study, as cardiopulmonary baroreceptor unloading evoked a decrease in signal intensity in the region encompassing the NTS. Despite these similarities, the cardiopulmonary reflex circuit does not appear to be the same as the arterial baroreflex circuit, i.e., the well-described NTS-caudal ventrolateral medulla (CVLM)-rostral ventrolateral medulla (RVLM) pathway. [...] Therefore, it is likely that, during an inspiratory capacity apnea, cardiac unloading results in decreased NTS activity, which in turn produces an increase in drive onto PVN (paraventricular nucleus of the hypothalamus) neurons. This increase in PVN activity may then directly activate RVLM premotor neurons, producing an increased muscle sympathetic drive.
Click to expand...

A key point is that the brain changes should be related to adaptive responses to the challenge - increased activity in parts of the brain that are trying to compensate for the hypercapnia for example.
 
Last edited:
You must log in or register to reply here.
Back
Top Bottom