ramakentesh

That it interesting because nearly all the evidence over the last 12 years or so has suggested that pots has a peripheral or non-brain origin

Lots of what you are describing may not necessarily be pots. if her spinal fluid pressure was elevated she may have intracranial hypertension which can cause headache and postural symptoms. most pots patients will improve for a short period after low or staggered amounts of caffeine. Too much can cause worsening tachycardia or rebound crashed

Those with sfn as part of their pots may find this if interest: http://www.ncbi.nlm.nih.gov/pubmed/25484269

Yepp. Lots of autoantibodies implicated in CRPS as well - some if which are being investigated in cfs and pots

Story of my pots: Had a complete remission between feb 2006 and dec 2008. Had milder remissions from 2010-2012, and now days my crashes ate shorter but more intense and in between im pretty good. sonetimes its overdoing it, sonetimes it just comes back. For me the quicker i recommence treatment (florinef and alpha agonists) the quicker i respond and improve.

I found betas worsened by oi and increased fatigue. I respond better to alpha agonists and volume expanders

Or it could just be a symptom of POTS...

Wow interesting

When essential hypertension patients are given too much antihypertensive medication they often experience 'adrenalin surges' as when the body interprets reductions in cerebral or reduced stroke volume it tries to compensate by activating beta receptors (increased heart rate but beta 2 receptors actually increase thoratic vasodilation which is probably not helpful). These adrenalin surges seem a part of POTS whether its a compensatory mechanism or just part of the problem. Researchers are looking at autoantibodies to beta receptors as well as antagonist ones to alpha 1 receptors. Perhaps variations in these aabs causes these strange symptoms but who knows. beta hypersensitivity is common in POTS.

Should I update the options here or leave it. its missing a few and clearly some havent had many hits.

Its interesting how some POTSies do so well on exercise programs yet some even with amazing effort show absolutely no change.

I dont think its that easy to figure out. Because if it was GABA then xanax would do the same and it doesnt. GABA may play a role but alcohol has numerous effects including changes in endothelial function, aldosterone activity, and there is a sustained increase in BP the next day after even acute rare use according to several papers that is not explained by increased adrenergic or angiotensin ii mediated vasoconstriction. My take is its an immunosuppressive as well as it also knocks my ank spond on the head occasionally. Volume loading with cold drinks is also helpful at the time. But the danger of saying definitively why it helps is that an assumption can obscure an important clue.

I also get this symptom. cant really explain it - it seems an inflammatory response of some sort.

The reason for your brain fog may be reduced cerebral hypoperfusion. The only way to improve it is to increase venous return although some docs are commencing studies on modafinil and losartan for brain fog.

Altitude changing symptoms is probably more patient reports than anything with a scientific basis. It seems everyone is very different,

The most likely reason you are experiencing these symptoms is because you have reduced blood flow to your brain meaning there is limited glucose and oxygen metabolism in your brain. In fact there are studies by Dr Medow and Stewart that suggest that POTs patients dont experience cerebral vasodilation in response to cognitive challenges.

It is possible that you had a bad reaction to midodrine because your alpha 1 receptors were super sensitive from reduction reception of norepinephrine like a depression patient finds when they start an SSRI - acute worsening of symptoms until the receptors normalise. Just a thought.

Dihydroergotamine has the added bonus of activating serotonin receptors only in the veins therefore bypassing and avoiding the adrenergic system completely (although some studies do suggest that it activates alpha 1 receptors like midodrine and phenylephrine) You may or not be aware but the best med for my POTS in terms of improvement of symptoms and reliability of action is Pseudoephedrine but obviously high tachy POTSies should avoid.

Some other docs are now trialling Northera for POTS. But Id tend to think Dr Raj is right on this (as always).

Phenylephrine is used for POTS/OI in Australia. I am told it is less bioactive than midodrine and requires a larger dose as a consequence. I took it for a while and it worked well but the half life was tiny (2-3 hours on a good day). It also has central effects which seemed to help me but not every body. Increasing norepinephrine synthesis in POTS may or may not work very well. In australia they refuse to include POTS patients in the Northera study out of concern it may worsen tachycardia.

Nearly all your symptoms are probably a coping mechanism or consequence of disordered postural blood flow.

The view now days from some of the researchers is that small fiber neuropathy might be a manifestation rather than cause of POTS. That being said SFN patients tend to be dizzy patients but some have hyper presentations. I have mild SFN and a fluctuating course of relapses and remissions. And i get insane itching

I can only speak for myself but pots arrived overnight and I was normal before then

Methyldopa basically does the opposite of what adhd meds do for central blood pressure medication. Assuming it wont effect central dopamine but who knows

Results still pending