Orthostatic Intolerance in PwME (POTS?/NMH?) - discussion thread

[Mij]

I did not. My OI symptoms started 10yrs after M.E onset after reactivating EBV and HHV6 from taking immune modulators.

I also wanted to mention that I feel much improved after 5pm. It's the mornings and early afternoon that affects me the most. My CNS is much calmer in the evenings.

 

[Turtle]

Never had OI symptoms before ME. The worst in my case brainfog. I went from a final year uni student to not being able to read a book, immedialtely.

 

[pooriepoor91]

I definitely had POTS or OI for years before I got ME with PEM. I used to work for 12 hours without any issue, and then after a viral infection in college, I could only be upright for a few hours without having a strong urge to sit or lie down and keep my feet up. And when I had to get an ECG before another college admission, my resting heart rate was in the 90s and the doctor asked me why I was anxious about getting an ECG!! And then one thing led to another, and I got ME with PEM after 4-5 years of having OI/POTS.

 

[Ravn]

Do ME/CFS with orthostatic intolerance remember if they had OI symptoms before ME/CFS?

Orthostatic Intolerance can mean many different things. Do ME/CFS patients have more of one type of OI than is expected in the non-ME OI population?

I don't recall any OI symptoms before ME but that was decades ago so memory may not be reliable. However, frequent fainting was the reason I was first taking to the doctor after a bad virus so it must have been a prominent change in my parents' eyes. OI was also one of the only 2 issues that persisted in some form through all remissions and relapses (the other one was PEM)

Interestingly, how my OI manifested changed significantly over time. I suspect all pwME have some sort of underlying OI/bloodflow problem but how - or even if - it shows itself in an individual at a given time then depends on other factors like genetic background, comorbidities, ability to move around, compensatory mechanisms the body has developed over time, etc

The possibility of an asymptomatic underlying bloodflow issue of course means that even if we didn't have any overt OI symptoms before ME the problem may have already been brewing under the surface - which isn't really a helpful thought at all, just makes everything even more complicamated

 

[Evergreen]

Do ME/CFS with orthostatic intolerance remember if they had OI symptoms before ME/CFS?

I did. I didn't know why I felt rotten if I had a bath, or why I definitely needed a seat for the whole train journey in the morning but could stand for a bit in the evening, or why I wound my legs around each other when seated. But I do now!

 

[SNT Gatchaman]

No idea if this is relevant or any good, but someone I follow on Mastodon just posted a link to this with the comment that it's good to see a study taking menstrual cycle into account when looking at POTS. "Abnormalities of Angiotensin Regulation in Postural Tachycardia Syndrome" 2011

I've made a thread for that paper, with accessible link to the PDF here.

 

[SNT Gatchaman]

perhaps a better hypothesis could be that cerebral autoregulation etc is principally aiming to preserve and protect the BBB. If it's damaged that might prompt the brain to use all the tools at its disposal to try and reduce CBF to repair or protect against further damage. That could include the other aspects beyond autoregulation: chemoregulation, neuronal regulation, and endothelium-dependent regulation (reviewed here). Eg why do we seem to have "dysfunctional breathing" — the brainstem could direct hyperventilation, causing hypocapnia leading to cerebral vasoconstriction.

I don't know why hyperventilation is happening but it seems important to find out.

What if ME is a disease of reduced cerebral blood flow that can't be recompensated because of an array of different factors?

Slowing blood flow to the brain generally — perhaps for the benefit of certain regions in particular — might have the consequence of reducing the clearance of metabolic waste. Then you might have a little more waste needing to be cleared via the glymphatic system, which might explain enlarged perivascular spaces that are commonly seen.

In this discussion was the idea that decreased cerebral blood flow would be associated with enlarged perivascular spaces. Now there are a range of possibilities for why that might be the case, but picking up the slack for waste clearance is a theoretical. A preprint today, looking in the context of atherosclerosis and stroke is —

Brain cerebral blood flow with MRI-visible enlarged perivascular space in adults (2024, Preprint: MedRxiv)

Brain CBF decreased with the increasing severity of [Basal Ganglia-Expanded Perivascular Spaces], suggesting that BG-EPVS could serve as an imaging marker for reflecting the changes in brain CBF

 

[Haveyoutriedyoga]

Merged thread

What it Feels Like to have OI (blog)

The feels kinda good, get things done fast until you crash kind of OI / dysautonomia

The collapsing within, withdrawing, fading out kind of OI / dysautonomia

some interesting descriptions of orthostatic intolerance with a bit of theory.
LINK

 

[Haveyoutriedyoga]

I am interested in knowing whether this is true

These feelings are commonly described by people with NMH, neurally mediated hypotension. It is also known as DELAYED orthostatic hypotension. There is a sudden and short-lived (difficult to capture even on a tilt table test) drop in blood pressure that is like what would happen in a faint, but not that severe. It is like getting half way there and then staying conscious but not quite being about to snap out of it and reset. It is not the same as a drop in blood pressure that happens immediately upon becoming upright. It can take up to 45 minutes of pure standing still to develop.

Doctors and nurses often think we are referring to the short, no delay kind called plain orthostatic hypotension when we try to explain about orthostatic intolerance or NMH

 

[Hutan]

From an article that New Scientist emailed me the first bit of:

Per Borghammer’s “aha” moment came nearly 20 years ago. The neuroscientist was reading a paper from researchers who were examining whether REM sleep behaviour disorder (RBD), a condition that causes people to act out their dreams and is often found in people who later develop Parkinson’s disease, could be an early form of the neurological condition.

Rather than starting with the brain, however, the team instead looked for nerve cell loss in the heart. Though Parkinson’s is historically associated with nerve cell depletion in the brain, it also affects neurons in the heart that manage autonomic functions such as heart rate and blood pressure. And, says Borghammer, “In all of these patients, the heart is invisible; it is gone.”

Not literally, of course. But in these people, the neurons that produce the neurotransmitter norepinephrine, which helps control heart rate, were so depleted that their hearts didn’t show up on scans using radioactive tracers. This kind of neuron loss is associated with Parkinson’s, but at the time, none of the people had been diagnosed with the disease and their brain scans seemed normal.

There is mention of the loss of neurons in the heart that produce norepinephrine (adrenalin), as something that happens in Parkinson's, potentially early in the disease for a subset of people. It notes that the norepinephrine helps control heart rate.

I wonder if something like that might be happening in ME/CFS too? Could the heart neurons be failing in their job when there is demand on them, such as being upright?

We've talked about how sometimes, when there is a demanding/important situation, we can actually perform ok for a while, but at the expense of a 'wired but tired' feeling afterwards. Could it be that adrenalin produced in the adrenal gland/brain can help us get through the demanding situation, help the heart to function, covering for the reduced performance of the heart neurons? Or is the adrenalin produced by heart neurons a much more site specific/momentary thing?

 

[Jonathan Edwards]

I wonder if something like that might be happening in ME/CFS too?

Norepinephrine speeds the heart up if I remember right. So POT seems to be the opposite of the Parkinson situation - the norepinephrine cells are working overtime, or at least responding to demand. But if there are people with ME/CFS who when they stand up do not get any tachycardia (a small amount is normal) they might feel faint because the heart is too slow. I don't think we have evidence for that though.

 

[Hutan]

Yes, I'm not sure that it hangs together.

But, I hadn't heard of heart neurons producing adrenalin before. I wonder if it could be something like:
the heart neurons produce adrenalin in a way that finely tunes the response and acts primarily locally on the heart. But, if those neurons aren't functioning properly, then we are more reliant on the adrenal gland to respond to a physiologically stressful situation and it sort of swamps the body with adrenalin, resulting in systems over-shooting and not responding appropriately?

It just seemed to fit with an idea of peripheral nerves not functioning properly/diffuse demyelination that we have been tossing around.

 

[Jonathan Edwards]

I hadn't heard of heart neurons producing adrenalin before. I wonder if it could be something like:
the heart neurons produce adrenalin in a way that finely tunes the response and acts primarily locally on the heart. But, if those neurons aren't functioning properly, then we are more reliant on the adrenal gland to respond to a physiologically stressful situation and it sort of swamps the body with adrenalin, resulting in systems over-shooting and not responding appropriately?

As far as I know the immediate palpitation response to fear or pain is mediated by adrenergic nerves to the heart. Google says: "Sympathetic efferent nerves are distributed throughout the atria, ventricles (including the conduction system), and myocytes within the heart. " Those are the heart neurons that make adrenaline, driven from the CNS or baroreceptor reflexes in the neck or whatever. They speed up the Sino-atrial node and also increase the force of ventricular contraction, presumably by recruitment of cardiac muscle cells.