erik

"Just anxiety" has a physiology too... and just the "psyche" can do some amazing things (such as exert influence on autonomic processeeees): http://www.psychosomaticmedicine.org/cgi/c...t/full/63/3/476 I guess the part about the rat's experiencing a rise in temperature from the use of a rectal thermometer (rather than it being caused by the condition trying to be measured in the experiment), is an example of the Tachy's topic of Quantum Entanglement... a case of high level abstract physics. Or maybe the heisendorfer uncertainty principle? I don't know. Some things are more thoroughly understood experientially than objectively. It is similar when physiological processes impinge upon the psyche (and vice versa) is it not? No, no, no... I'm not recommending a novel method of helping doctors understand the distinction yet crossover nuances of conditions that blur psychic & physic... I'm just citing science here. Purely objective.

:) Can you fake a really really good seizure? Just kidding of course.Are barbiturates "just a stronger benzo" or do they have a different quality to them? What about queludes? (Yeah, right they'll lock u up just for asking I suppose Might consider very brief use of Tramadol, as mentioned here it can potentially break through the worst autonomic body traps. Longer term & withdrawal can do opposite... as topics on this board point out and nortryptaline can assist the ween phase. Maybe that makes nortryptaline worth initial consideration too? I see on wikipedia that Tramadol is used by "sugar gliders, wallabies, and kangaroos among others". If you have some of those as mates down there, maybe they could kick you a little on the D.L., as they say Do they say that? I don't know. You'd have to get over a concern of Tramadol & Nortryptaline's SNRI side, amongst their many other characteristics, though

Yeah. Hiding things could be helpful for employment issues. Having the word out there about a "chronic illness" isn't a plus on a resume (including "word of mouth" behind the scenes information). Another sad overtone.

I think EKG = ECG, and the goo thing is an "Echo" as in "Echo-cardiogram". First one/two are electrophysiological and echo is like an ultra-sound, for physical & flow properties (though a "doppler" would be especially for "flow"). Could be wrong, but I think that's how it is.

I get wordy and "loose" from caffeine, like a compensation for inability to "condense" well. I quit for weeks then restarted lately. I had better "densification" of ideas with NuVigil a couple weeks back... more "terseical" yet still "communicable" in the virus-sense (and also better emphasis on absorption and less on excretion, thought-wise... caffeine does loosen the bowels of the mind). Prolly some ADHD in there somewhere. If I can scrounge up the money, I hope to give nuVigil a shot again. Maybe you all can sign a petition to convince my insurance to cover me (to spare yourselves, that is I also love a "loose" cognition as a matter of style (and partial compensation for ignorance of detail). I experience "bland technical things" as though they are rich literature... a synesthete of sorts, perhaps!

"Actually, no they just have to be above 600pmol according to Blair Grubb at Toledo and Robertson, Raj et al at Vandy." Hey, wait a minute! From Raj article: At that time at least, Raj said >600 for any POTS, even higher is associated with H-POTS, just as avidita said.From Grubb article: So in that case, the bar of for H-POTS is just 600... which had been the bar for regular POTS in the Raj (a.k.a. Vandy) article. Are these superseded by new publications? Even if so, probably plenty of GP's & Cardios are going to have varying perspectives, based on what they "happen to read", what fits their general style, how they feel about contravening insurance provider policies or peer scrutiny or liability issues (or FDA scrutiny), blah blah. Not to mention (perhaps last of all), their personal medical opinion on the complexities! "As for SNRIs - ive never heard of Dr Grubb recommending them." Hey again. Note the acknowledgment in prior citation of the NET issue. An autonomic specialist would be aware that overstimulation (with or without compounding NET inhibition and hence extra clearance from cleft) means more spillover (one presumed cause for serum elevations). In that very same Grubb article, in the list of pharma options associated with "H" variety... 3 of the 5 drugs are NRI's+ (including Wellbutrin). The NRI recommendation was not made in ignorance of (nor prior to) the over-stim & under-reuptake issues. Why it was made isn't clear in things I have thusfar managed to find via the web (or my "remote viewing" This fits your situation reasonably well, right fighting4health? Perhaps this jibes with trends of clinical successes that Grubb has observed from his unique vantage point??? One would like to assume this was key when publishing a "clinical guidelines" document. (As always, individual patients vary greatly, particularly in the POTS population) I tend to be encouraged by "diversity of ideas" across experts... I think it is how complex things are resolved by complex systems... a top-down unified policy would shut down research progress (as would too much sheltering from peer scrutiny). Take the "simple case" of prozac. It is an SRI, which means the serotonin is left in the cleft (it's active region) longer giving more umph (an 5-HT "up" regulation of sorts). Over the course of a few weeks, the body counters and down-regulates... which is "coincidentally" when the therapeutic effect comes in... in the resultant "down" regulation, not the initial & continual "up". The initial dosing phase is ironically more associated with aggravation of the targeted symptoms (sometimes even calling for a temporary use of a benzo, or concomitant use of buspirone or who knows what... just extreme patience to bridge this unfortunate gap). It gives a peek at behind the scenes complexity (and enthusiasm for even better future meds though RI's tend to strike the best overall balance, currently). It would make sense that other reuptake inhibitors (of different neurotransmitters and with different selectivity profiles) like NRI's & DRI's (and maybe even loosely similar things like Mestinon... sort of like an acetylcholine-RI, right) could have similar "paradoxical" effect. Some of these things might explain how wellbutrin could help even in light of existing "adrenergic" excitement & spillover (no matter what extent). Your "sleep enhancing" rather than "insomnia inducing" reaction (prompting you to have better result with night dose rather than morning) might be a clue that your body, for whatever reason, is one that enjoys the paradoxical more than the direct. Seems to be "the norm" with POTS in many cases! I don't think I'd be surprised to hear one day that even a vasodilator or a diuretic could be simultaneously helpful somehow... hmm. It is a wild world in the body!

I tend to get it from physical or just anxiety situations alike. It can be odd to notice lights or fans turned on or off, know that I must have done it a few minutes prior, but not recall doing it. Then later being able to remember... like the traces were layed down but short term recall was blocked. I have "a friend" who once drove to another city with only blips of memory for the event (during a period of great duress)... hmm. Is that in the realm of POTS explainable... or more like simple partial seizure, electrolyte imbalance, real dissociative disorder, somebody drugged them, or what??? I've heard of that for seizures, but maybe other things can do that too? Is POTS that potent?

Toasting with a tall drink (of water)... happy b-day.

Oh man. PP of 19 is no fun indeed. That sounds like a really solid explanation and place to start.

Unless you wish to keep it totally "top secret" kind of thing, telling a stranger or someone that is a more distant friend/associate can be a cathartic thing and kind of safer feeling since if they react weird it doesn't matter much. I told a fellow I used to do athletic stuff with a little about it and felt pretty safe doing so... he kindly came up with a rather cool suggestion on helping weird hydration things beyond just electrolytes and such (insight from his athlete side... a Hammer Nutrition product). If instead he had reacted less helpful (or if he now has some private doubts about me) it doesn't affect me... but it felt nice to go ahead and mention it. If it causes too much distress though, some tactful bending of the truth seems allowable to me... like offering something sort of similar that someone can digest easier, like "migraine" complications, a mild hormone deficiency that is tough to treat, being placed under house arrest for insider trading violations... you know, the common stuff people can relate to better.

Good luck to you! Fingers crossed.

I'm baffled by how the head elevation is supposed to help, but somehow it does assist me, especially during phases of weird night anxiety like stuff (I used a lazee boy). When I'm practicing good overall POTS hygiene (solid steady hydration, gluco-steady diet, sparse caffeine, sparse alcohol, etc.) and fludro I tend to get away with sleeping flat... but like toddm I feel overpressured in the head often when fully supine (even if BP isn't outrageous).

It is an interesting point of contention between experts (if that's what's going on, I'm not really sure). Using my "dissociative skills" as a tool rather than a deficit, and projecting myself to an out-of-body experience (an extreme derealized state)... I can place myself carefully as a fly-on-the-wall in Dr. Raj's lab and perhaps even read the minds of the Vandy folks (a little "remote viewing" a. la. staring at goats). I am doing this now and this is what I hear them saying: An I'm getting the "vibe" that this makes them leery of prescribing anything that can induce in "healthy" what is already present in a patient... on assumption that it will exacerbate it.I also hear them saying something about regular pots being plasma NE >600 and Hyperadrenergic being >1200 or so... As I fly through space & time and eavesdrop on the Cleveland folks, it seems they're saying H-POTS is indicated by NE >600 (hmm, a different definition it seems), urinary urge from prolonged standing, significant tremor, anxiety, cold sweaty hands, and such. And that after being so bold as to still try NRIish meds (after all, most POTS meds are paradoxical or mixed-result sort anyway) actually found success with them. This latter conclusion about clinical success is mostly my mind-reading, which quite error prone to say the least... whereas the former just happens to coincide with some references (Raj and Grubb basics) also available via the internet... which sadly put me and my "remote viewing" skills to the redundancy-bin some years back. Oh well.

It is neat (in a very geeky way) that the 3 stages of beta-adrenergic vasodilation are covered nicely by various responses here! The nitrates trigger a NOS release via mitochondrial enzymatic action... the NO/NOS cascades to induce cAMP increase (who's reuptake is the target of the PDE inhibitors like Viagra)... and the cAMP adjusts the calcium-ion channels that come later and sort of do the "work" (and the calcium channel blocker meds tamper with that gently, like norvasc and the like)! It seems like the "collective wisdom" of the board has nice breadth & symmetry! Anyway, enough geeking out! I came across this which might be another option if the nitrates peter out or docs get uncomfortable (there are always pro's & con's with meds, of course). I assume I snagged & bookmarked it from firewatcher's post a while back: Symptom improvement in postural orthostatic tachycardia syndrome with the sinus node blocker ivabradine Anyway, ivabradine is potentially used for angina pectoris. Might be a study a doc could comment on if they haven't already noted it... assuming it applies to your situation. One could bend the notion of "stable angina pectoris" and say that the POTS vascular dysregulation is a substitute/explanation for an "exercise trigger" for example. But it would be important for a doctor to make that judgment call as to whether you have "stable" form or if something else is happening, of course. I'm still fixated on the vein vs. artery thing, personally. If there were an imbalance sensitizing veins more than arteries, couldn't a totally normal vasoconstrictive signal sent out in response to orthostatic stress (as normal folks do within seconds of standing) turn into an overpressurization in the vascular bed, leaking & pooling via osmotic/oncotic disturbance, lack of return to heart, localized messenger attempts at counter-regulation (kinins, histamines, et. al.) with their side-effects, etc.? In a normal person, the arteries should constrict, which results in simple healthy redirection of blood, without the other side effects. Isn't this a semi-workable POTS hypothesis for some cases?

Wellbutrin, a dopamine-norepinephrine reuptake inhibitor (DNRI) is on one of Grubb's published lists associated with H-POTS (Table 2 in here)... along with two SNRI's. I heard indirectly of one of his patients being incredibly improved by an SNRI plus aripiprazole (a neuroleptic but also used to augment anti-depressant effects). It is surprising on the surface for sure. One might speculate that more global reuptake inhibition could prompt counter-regulations that mitigate even an existing inhibited reuptake (as with NET deficiency)... for example, down-regulation of calcium-ion channels that just as critical to neural signals as the neurotransmitters. Some say that prolonged elevation of neurotransmitter presence (activity in the synaptic cleft) can result in long term reduction or antagonization of the receptors that the neurotransmitter binds with (a very direct counter regulation). Maybe whatever makes that happen (if it does) is triggered more centrally rather than in peripheral sympathetic nervous system synapses. Another way they could theoretically help is by applying a consistent pervasive "pressor" response... perhaps lessening the need for the "overreaction" during orthostatic stress in the first place. Or just as mysteriously as the SSRI's, they might just kind of "shift the regulation" of the autonomic system to partly correct it's misresponse. If one has partial denervation involved in their POTS, maybe they are helped with strengthening the signals in remaining nerves... even at the cost of overexciting some others (but I don't know if the denervation POTS causes would typically give a hyper-adrenergic presentation or not???). Also, many of these meds effects are shaped by their variable affinity for specific receptors. "Selective" is the first "S" in SSRI... and NRI or DRI or DNRI should be called SNRI, SDRI, SDNRI respectively except for the fact that it would then get confused with SNRI where "S" is seretonin (which should be SSNRI). I'm just trying to say that they tend to be "Selective"... like some beta-blockers are cardio-selective (leaving lungs & brain alone) whereas others are non-selective (and give anxiolytic effect in brain and can aggrivate asthma and such). I don't know how much this selectivity affects wellbutrin and the like, but it is another way they could have this paradoxical benefit amid an already goofed NET situation. Just some speculations... my pseudo-science... I wouldn't know which, if any, are plausible in reality (or substantiated by much research). This study might be informative too: Norepinephrine Transporter Blockade With Atomoxetine Induces Hypertension in Patients With Impaired Autonomic Function So theoretically, if the patients' existing disorder involves a NET deficiency specific to beta receptors (which is a finding in some research I think)... an NRI (or DNRI) that also inhibits NET in other adrenergic receptors (or centrally) could arguably bring "balance" even while also mildly exacerbating the original problem.

No tattoo yet. I'm waiting on the results of the DI-NET logo contest first.

I went through a slow "molting" phase my first time on fludrocortisone. I think I see that in your signature lines. I've heard of rash responses to that. Is that a possibility? It seems like some of these dysautonomia meds can have skin side effects, like making the skin extra sensitive... so maybe a really mild scratch (like just from some clothing) could have turned into something looking worse. I know one med I took warned of extra sun sensitivity too. If there are ghosts, they are not necessarily bad or hurtful. Just be at peace with yourself and a ghost cannot harm you. Focus on good things and friends and how much of a blessing it is to be granted the gift of life. Acknowledging that miracle is very warming to the soul.

One anecdotal thing is that when I exercise regularly at the same time of day, usually the evenings to avoid heat, I tend to feel my body rev up at that time of day on it's own. It's like it is anticipating the exercise. In that case, it is harmless or helpful. I might have noticed this with my sleep disturbance phases too. Like having a "real" disturbance one night... then "echoes" on subsequent nights. Not sure how much of that is in my head, but maybe the body does that. I don't know. I can say that my body gets into "same time of day" episodes of several sorts somehow, so you're not alone in that!

I personally "disconnect" in order to avoid anxiety & pain. I am calmer for doing it. I am uber-calm outside when anxious, but messed up inside. Sometimes this works out, like facing certain situations without going fully dysfunctional or enduring lousy stuff (often longer than I should)... but sometimes it bites back like in a "relationship" (when did they invent that torturous word anyway . Then again, perhaps I truly am just a cold hearted sonofa-gun (or "monster" as one gf called me when I made mistake of actually sharing my feelings honestly with her... guy's, don't fall for that one... it's a trap) that also just happens to also be disconnected & distant??? Anyway, I figure if "pervasive fatigue" can happen from POTS (which is mostly characterized by specific orthostatic challenges)... pervasive anxiety is fair game to be lumped in... and even a need to "down-regulate" emotional response due to chronic assault by one's own body (physiological stress/anxiety responses). This is "numbing out". It is reportedly the predominant state of PTSD for many, though of course the aggro side get's the fan-fare. And PTSD is technically an "anxiety disorder" but probably more akin to a "dissociative disorder" in terms of how it disables folks. I guess I've gone full circle again, from saying it is just POTS physiological to saying how identical it is to psychological stuff. Maybe I have "DID" multiple personalities??? ...or is that just from POTS too

This is a little off topic, since you're wondering more about "when is it urgent", but I had one or two urgent care/ER visits that were total wastes of time, at the time. That is, until years later when I can now piece them into my puzzle (for example appearing "dehydrated" despite normal electrolytes & urinating adequately). I now wish I had some of my older "useless" stuff. So it's a small point, but sometimes a useless visit can have some nominal use later in documenting patterns (like the elusive ones). If you've got a solid diagnosis and non-progressive disease, I guess that's of limited use... but you never know.

It seems like the list of potential (probable?) psychological mis-diagnoses is pretty long for dysautonomias: anxiety, depression (or uni or bipolar), dissociative disorders... since hypoglycemia can mimic schizophrenia it seems a severe autonomic disruption could even put one in that ballpark. Plus seizure/migraine mimicking & crossover. If electrolytes go wild, compounded with "extra sensitivity" to electrolytes, dehydration & glucose flux, some crazy things can happen in the mind! Kind of sad/scary prospects. +++ Oh yeah, ADHD is associated too! Plus this study claims to distinguish "anxiety" by the Beck score (a question & rating system I guess) as opposed to focus on physical signs of anxiety perhaps? +++ I also heartily agree it is really important to consider concurrent conditions and physiological crossover issues (some rather theoretical but some pretty solid). The NET (norepinephrine reuptake) discovery (correlation with both POTS & panic disorder) is hard to ignore along with physiological responses being so similar. The general direction of mental health is away from considering almost anything to be "neurosis" and toward everything having as yet pinned down multiple physiological causes... at least within reason and after making best efforts with behavioral factors. I don't really like saying "my anxiety is physiological, unlike those other folks" or "I've got POTS, not CFS... so I've got a physical sign... ne ner ne ner!" Bottom line though, even for pure physiological problems, there is almost always something a patient can do behaviorally to better their prospects. That's what it is about in the end, IMHO. For example, with POTS I don't personally care all that much if my heart rate doubles or triples (for me it still isn't into a painful or scary rate) but I care greatly about how it makes me "feel" and how it somehow translates to persistent symptoms that really interfere with my life... most of which basically cross psychological bounds (like central fatigue, feeling panic at times, etc.) or otherwise cascade to real downers! So for what I care about in life, first and foremost, I can't escape psychological things. If my heart rate changed oddly but didn't make me feel lousy... who gives a hoot! If there is some silly behavioral change I can make, even if my problem is "just physiological"... I'm going to do it! I don't really care about the science even... except that it *might* help me manage the results better (or give me a helpful "illusion of control" . Not to be too "contrarian" but the theories on depression are still rather unresolved. Tianeptine is a working clinical example that counters a simplistic "seratonin" or "monoamine shortage hypothesis" to depression. It's a serotonin reuptake *enhancer*, exact opposite of an SSRI... yet is an anti-depressant. Some opioids and even NMDA-antagonists also end up being anti-depressants. There apparently are even theories that NOS (yes, Rama, nitric oxide! is important to the disorder... as well as BNDF stimulation... etc. Despite how much research goes in to it, and how successful monoamine therapies are, there is more to the story (maybe even future treatments that will work out better and more direct). This doesn't discredit current best therapies, just acknowledges extra complexity behind their workings.

This is a slight tangent to this thread, but related by being another reason to consider some protein supplementation. It is also a partial argument against strict carb restriction, notably the observation that proteins & carbs together prevent catabolism better than either alone. This tends to be used in exercise enthusiast regimes. If concerned with carb effects, it can translate into a compromise such as general carb restriction (generalized use of slow-carbs), with strategic timing of carbs (even fast ones) during post-exertion (and/or during exertion) in combination with essential proteins. This can help with dieting where one is cycling between loss & build phases (it is generally difficult to lose fat & build/keep muscle so cycling between is needed for many). Can apply to those with limited ability to exercise. http://dinet.ipbhost.com/index.php?showtop...%20Amino%20Acid (the endojournal link being key)

Good to watch blood sugar for sure. It appears one can have hypoglycemia symptoms without hypoglycemia too, via relative drops in blood glucose as well as so called "Adrenergic Postprandial Syndrome", which may or may not be a useful perspective on it. It may be difficult to know which came first, though, since ANS response and glucose/insulin/glucagon/et. al. kind of push back & forth on eachother (parasympathetic ANS is also quite key to insulin). Anything that follows a regular rhythm gets pretty fascinating. Aside from unnoticed external or behavioral causes (good to screen for), the body's clocks have some interesting quirks. I've not found the original study I recall reading, but essentially even an adrenal gland cut off from normal external synchronization (like that stimulated indirectly by light received in the eyes) can end up keeping a very regular clock cycle! This overview article on the Adrenal Clock has some similar (and contradictory) citations. It is probably accurate to say that the adrenals have their own clock that is "fine tuned" based on the signals from higher-up regulation. This makes me wonder what that adrenal clock will end up doing if the higher-up signal is dysregulated and confusing... like a 'garbage in-garbage out' circumstance to a little analog 'computer/clock' of sorts. It seems like lots of circadian dysregulations could result... and since the adrenals are central to so much, this could mess with a lot of endocrine regulation elsewhere and set the body up to respond poorly to otherwise normal circumstances. It is also said that properly regulated sleep cycles tend to have two sleepiness peaks, the nighttime hours and also a second mini-peak a bit after noon time. So perhaps even giving in to a noonish nap/relaxation thing might come in handy (even if you don't particularly feel like it), on the wild theory that your body is over-countering this tendency with sympathetic flood, like we tend to do urgently against orthostatic stress. Just throwing out some speculative thoughts for you to adapt to your more informed personal circumstances & insights.

There is also lissey's post here, which may apply too?

That's a great point. Odd feelings like that can be migraine or seizure aura or effects. Worth considering for sure.