What Type Of Pots Might I Have?

[peregrine]

Waiting for my doctor's appointment (9 days to go!) to see a definitive neurologist who has had some satisfied folks here. One thing I'm very curious about is whether we can diagnose which subtype of POTS someone has based on what they respond to? I think this topic has come up on the board before but I couldn't find it via the search.

Here's what's worked and what hasn't for me:

Worked:

walking exercise (I assume due to moving blood) is better than standing

tightening leg muscles/bouncing/twitching/etc while standing

compression stockings - mostly that I'm worse without them (15-20mmHg, knee highs)

atenolol (beta blocker)

Hasn't worked:

drinking enough water (occasionally no water makes it worse, but only when I get below 40 fluid ounces a day)

eating constantly (although skipping meals is bad)

diltiazem (calcium channel blocker) - appeared to make it worse

Cymbalta (SNRI) - appears to make it worse

No effect/other:

flying, despite not drinking enough water

no visible pooling, even during hot showers

flushing with direct contact with hot water during showers

very strong trigger with fewer than 8 hours of sleep

This seems somewhat consistent with the partial dysautonomic (PD) form that Grubb cites in his article "The postural tachycardia syndrome: When to consider it in adolescents," (Family Practice Recertification, Vol 28, No 3, March 2006, worth checking out!) except for the following reasons:

Water intake hasn't helped much

Symptoms originally caused by Cymbalta (which hits norepinephrine really strongly), although they did not go away when we stopped it

No visible pooling

So the Cymbalta origin made me think hyperadrenergic, since it triggers NE so strongly. But it feels like it may be more PD than hyperadrenergic. And I do have hypermobility syndrome, which has been correlated with the PD form of POTS as far as I know.

Thoughts much welcomed, or a lecture for trying to turn you guys into diagnostic tools :^)

[ramakentesh]

Net deficiency could cause a type of hypo POTS in that it can do two things:

1. increase alpha 2 adrenoreceptor action in the CNS, causing a reduction in sympathetic outflow despite peripheral vasoconstriction

2. NET can cause overstimulation of the alpha receptor, bleeding it dry of NE so that you get delayed OI.

If you took a NET blocker and developed POTS then this might be something to consider. I once had a vein biospy of my NET protein.

The original proband with NET deficiency did not have 'hyper' symptoms, she had just basic POTS symptoms that were identical to the majority of patients and even had leg pooling.

Some doctors dont really accept hyperpots as a distinct entity. the hypertension may be a reaction rather than a consequence of the condition. Mayo's recent article suggests that it may be compensatory.

There are so manyt seperate suggested subgroups and its all pretty murky still. And I dont think many docs are treating differently depending on what they think might be the causal mechanism for different patients.

All I know is that there can be pooling in the hands and feet or there can be selective pooling of the stomach which is harder to measure. There may be no pooling and just increased cerebral vasoconstriction although the fact that calcium channel blockers made you worse knocks this one out. Low Flow POTS seems to be all about paleness and intense vasoconstriction when supine.

Grubb's group think its 90% autoimmune, 10% hyper with high NE or postural hypertension as the difference.

Vandy think there is a subgroup of low blood volume, subset of neuropathic, and the hyper can have many different causes including leaky capillories on the stomach circulation that leak out excess plasma when standing. They recently also found a subset with high angiotensin II.

The stewart/Medows group seem to have identified all sorts of different etiological mechanisms so its pretty confusing: neuropathic legs or stomach, parasympathetic withdrawal, increased NO, and low flow (NET or angiotensin II) among the main ones.

Mayo seem to just think they are all autoimmune but that there may be other targets for autoimmune mediated responses (this is also my current theory or one of them).

The Australian group think that NET deficiency is more common than previously suspected.

the chinese group think its all NO or H2S.

[peregrine]

Thanks! Sounds like it's waaaaay more complicated than I imagined. My BP is all over the chart, too - half the time when I get it done (always sitting) it's 140/85 and the other half it's 105/65. Doesn't seem to correlate with exercise, but I do walk to doctor's appointments. So who knows!