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peregrine

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Everything posted by peregrine

  1. So far nothing like you describe, but it's only been a week on 0.1mg twice daily. Maybe some minor constipation is all; unusual, since I usually get GI side effects!
  2. Also not able to sing here - I used to sing while walking pre-POTS and now when I try I get pretty lightheaded. Same issue using my peak flow meter for asthma. The way I think about it is this - did you ever do a Valsalva while getting tested for POTS? The Valsalva made me really lightheaded, as does any type of controlled breathing (under exercise, or at the doctor's, etc), and we know that most folks with POTS have an abnormal Valsalva response. So it makes some sense that any time of controlled breathing - especially any type of forced exhalation like a Valsalva, peak flow, or singing for that matter! - would trigger similar issues.
  3. As soon as my spaciness started back in the spring of 2011 (the first sign of my dysautonomia beginning to be an issue), I stopped driving. I didn't drive on a daily basis anyways - we don't own a car, we get Zipcars - so less of an issue for me. I did drive a few times in September of this year after the methylphenidate (Ritalin) made me much less spacey while sitting down, but always drove with another person, and I couldn't do it for more than about 30-40 minutes at a time. Since starting the clonidine, I'm less spacey, but so sleepy that I fall asleep at my desk sitting up and almost doze off while talking to people, doing stuff at work, etc, so obviously driving is absolutely contraindicated again. This is all self-monitoring; I still have my license, mostly because my doctors trust my judgment. (folks who can't drive and need to run errands, etc might look into various community transport programs for folks with disabilities - things like Access Transport or whatever your local community has; they can sometimes help you run errands and the like. I walk and take the bus.)
  4. Pretty much everyone has a brief spike in heart rate when they stand - the difference between folks without POTS-type issues and those with them is that most folks without POTS, etc don't sustain the high heart rate; it goes down back towards their baseline after a brief period (I would say less than "a few minutes" but I don't have hard numbers for you) once their body has adjusted to being upright. The rest of us, of course, don't adjust so well, so we stay high while upright, give or take. Sustaining 150 for several minutes does seem abnormal to me even if you do drop back to 115 (though I'm not a doc, of course).
  5. Batik - don't recall from other posts here, but do you have issues (more severe symptoms etc) after meals normally? I know some folks have issues with large meals and drops in blood pressure/abdominal pooling during those times, and it seems like your blood pressure (and pulse pressure!) might be tied with eating?
  6. The pyridostigmine is... well, mostly meh. I think it helps with fatigue some, but it's hard to say; days when I don't take it I'm generally a bit more tired, but it's hard to separate out from the day-to-day variation due to both POTS variation and how my schedule, sleep, etc changes. Thanks for the additional info on the paresthesias - that's good to know. It does feel annoying, but knowing that it's not a sign of tissue damage/structural problems per se (like carpel tunnel) means I'm at least a little less afraid (both for the future and also afraid of damaging my hands), which is very helpful - thank you for the clarifications and explanation!
  7. Neat stuff! My only concern with hypermobility/EDS issues is how correctable they are in an adult - once the collagen is produced, it's pretty much inert tissue, so it's not clear that fixing collagen production or the collagen genes themselves would improve things for someone whose collagen has already been formed, although it would help for things like scar tissue. But for kids, babies, etc - that would definitely be a neat advance! I still can't believe folks are trying to ignore the connections between these different illnesses - it's so obvious after a while, but some docs seem to only focus on one part of the body and pretend that it doesn't affect anything else. Silly.
  8. I wasn't allowed to talk during my TTT, other than while she set up and in between tests - otherwise only at times that the technician would ask me how something felt ("now that the tilt is done, how do you feel? how did you feel over the course of the test?" etc). I assume they worry it would affect blood pressure and heart rate (forced breathing due to speech production, getting animated during a conversation), but I'm really not sure.
  9. Gah - I didn't see the replies for this (no emails sent) - sorry! But thanks all for the responses - good to know, especially that other folks have had it in similar spots. I'm seeing a pulmonologist next month; we'll see what they say about the breathing after my neurologist weighs in. It started fairly suddenly, so I don't know if it's a continuing response to a particular issue (breathing in dust during one particular day) or something else. I do have a history of asthma, so it could be a combination of POTS-related and asthma-related. Ugh. Glad to get all the info from you guys! Strangely, the paresthesia has mostly gone away; no idea why. I expect it'll come back eventually, though I'm glad to hear that it's probably more general POTS stuff rather than something specifically wrong with my hands (especially since it's so different from my usual pain and hypermobility). I don't know about my BP during the time - I should take it next time, since I swing widely in both directions. E Soskis - you mentioned the parasympathetic system causing paresthesias - due to failure or overactivation? It sounds like failure? I'm on pyridostigmine, but if you're describing it due to failure, I guess that's less relevant. Thanks again!
  10. Also not an expert, but it does sound like they didn't monitor your blood pressure at all. During my TTT (which included Valsalva) they had a finger BP monitor (funky but awesome) and also the usual electrodes. I don't think (but not certain) that they can get blood pressure just with electrodes.
  11. Same; they can also error out if they fail to detect your pulse, which can happen with low blood pressure or other reasons - some folks seem more prone to it than others.
  12. Starting yesterday I've had problems with numbness/paresthesia (tingling) in my left hand. I was using the computer in a less-than-good way for a few hours and noticed my left hand feeling odd - particularly the outer fingers (pinky, ring) and outer part of the hand (so not carpal tunnel). It didn't improve with sleep (and I avoided the computer all evening). This morning it returned, and now my right hand is also having the same issues to a lesser degree. Every time they tingle badly, I get a sudden rush of sympathetic stuff - sudden cold sweat, feeling of doom, some nausea, a bit more lightheaded. I do have a cervical rib on the right side, which has caused numbness when I wake up in the past, but this is different (hand and wrist only) and on both sides. I also have a small amount of (probable) autonomic neuropathy in my left arm (QSART only, no biopsy) but not (if I recall correctly) in my right. Hard to tell if the issue is nerves or blood vessels. Flexing the backs of my hands back towards my wrist does help somewhat. I know some folks here have long-running paresthesia - anyone have anything like this, especially with the sympathetic activation? I'm kind of anxious here (unusually), since I use my hands for a fair bit of computer work in my career. mmm - edited, I've been having increased breathing difficulty for about a month now. I'm seeing a pulmonologist next month (now that we know it's not a pulmonary embolism and it's not responding well to asthma treatment). I've read that breathing issues can cause hand numbness, so figured I'd mention it. (also, if anyone knows anything about being short of breath and POTS, I'd love to hear it; I know there's some stuff out there, but haven't read up on any of it yet)
  13. No problem! It's really cool when someone like him who does basic research (as opposed to directly-medical research) finds out such cool stuff. Nice guy, too - he was super-shy and said he hadn't spoken in front of 500 people before :^)
  14. If you can get in touch with her beforehand (sounds like yes), you could ask her if there's something else to try in the meantime. I've been doing this with my neurologist - that way I go there and we discuss how the new medication is doing rather than just agreeing to prescribe something else - it speeds things along a bit as long as we're both comfortable with me starting it without him seeing me weekly or something like that. Worth a shot!
  15. Obviously not a doctor, but I agree - the warnings are usually targeted to people taking much higher doses for longer, but it's always a fine thing to check with your doctor or even a pharmacist. One thing you might consider trying with your doctor's help - if you're up for it - is trying a selective beta blocker - something like atenolol. They are a little more "clean" in terms of how your body sees them - they bind specifically to one receptor but avoid binding to the others that propranolol does, so they don't affect things like breathing. I'm not sure if this would avoid your sugar, parasthesia, etc issues that you had on propranolol, but it might be worth a shot? Other folks have found selective betas like atenolol to be less useful; for me they're better than propranolol, mostly because they don't interfere with my breathing.
  16. So... the guy who won the prize (well, one of the two) just gave a talk here at my university, so I stopped in. Lots of really high-level stuff (I would have been lost in seconds without having a lot of background), but some directly relevant stuff too! If folks want more information about the general topic (rather than just the stuff he did at the end), message me.The The one really applicable part to us is the end, where he talked about the way that G protein-coupled receptors (these receptors that bind things like epinephrine, but also bind things like beta blockers) are specific as to what binds to them. They have two levels (kind of like two floors in a house) of the "pocket" that holds the drug or molecule. The first level - the highest one - determines what molecule can bind - the "specificity" of the receptor; the molecule has to pass through here to be effective. Some of these receptors are more picky than others - it depends on how wide their pocket is. The second level - the lower one, and the one where the molecule actually sits - determines how active the receptor is once that molecule sits there - basically, its "efficacy" - how strongly it responds to the drug or molecule. Specific beta blockers like atenolol and specific other drugs like albuterol sit in the second level, but many of them extend a "tail" up to the first level, so they are specific even when they are past the part of the pocket that is more picky. This is why albuterol only hits beta-2 receptors and not beta-1 receptors. Other nonselective beta blockers like propranolol and other drugs don't stick out into the first level when they're sitting in the second level, so as long as they can sneak into the receptor past the picky part of the pocket, they're good. This is why propranolol affects things like breathing - it hits both the beta-1 receptors (which deal with the heart rate, etc) and the beta-2 receptors (which is why it's bad for breathing). Sometimes other types of receptors - like muscarinic receptors - make the molecule or drug "float" around for a bit, so even if it doesn't have the magic tail extending into the picky part of the receptor, the receptor still has a chance to say "nope, wrong molecule" even though these receptors are generally more generalized. He also said a bit during the Q+A at the end - something about epinephrine and norepinephrine-binding G protein-coupled receptors being nonselective - they bind anything that looks like epinephrine or norepinephrine and target a wide variety of downstream effects? And that vasopressin receptors are more selective - they only target a certain set of cellular machinery. Anyways, fun talk!
  17. It definitely depends on the place. In most cases I've run into, you don't have to pay for records being sent to another doctor, but have to pay for personal use, and they often will take up to a month to get things settled. You also often have to sign paperwork authorizing the information release (including to you as the patient!), which often has to be done in person or by mail/fax, which can be a pain. I've gotten into the habit of just getting copies of my records after each practice as I've gone through life.
  18. I eat salt straight - pour some (usually 1tsp = ~6g of salt) on my palm, lick a portion of it up, then put some water in my mouth, swish, and swallow. I've always loved to eat salt straight, though, so this definitely doesn't work for some. Eating salt on a full stomach is definitely better for me. (also, I'm not a doc, but the method of ingestion of salt shouldn't matter)
  19. Only on a pretty basic level... basically, G protein coupled receptors (GPCRs) are involved in cell-to-cell signaling - the receptor receives a signal (perhaps a hormone or a neurotransmitter, for example, though there are others too), then triggers a cascade of reactions via the G protein coupled complex. This cascade changes something in the cell - perhaps gene regulation (which RNA is produced from DNA) or translation (how proteins are made from RNA). They're a very broad class of receptors with a lot of different purposes. They are (apparently, though I hadn't known this) the target of ~40% of pharmaceuticals, so understanding their basic structure and function is very important for medicine. (edited to add - the Nobel is usually for something fundamentally basic and important like this, rather than direct applications, though those exist too - like stuff involving insulin. From a fight/flight/ANS point of view, GPCRs are involved in things like hormone/neurotransmitter reception, so they probably are involved in our sympathetic nervous system regulation via their reception of things like norepinephrine. If this is totally unclear, let me know; sometimes it's hard for me to take my "biology grad student" hat off :^)
  20. I've been taking very low dose Seroquel (an antipsychotic, though at very low doses it acts as a sedative) for many years now. It does help me fall asleep when I have mild nausea, but if the nausea is particularly bad, or I wake up with bad nausea, I find it doesn't make me fall back asleep, so I'm awake and nauseous. Strangely, what helps me (especially when woken in the middle of the night by severe nausea) is eating goldfish (my gold standard for antinausea snacks, amusingly), reading a comforting book, and snuggling up in my bathrobe, pillow, and blanket... on the bathroom floor. For some reason the change of environment (plus easy access to the toilet for vomiting!) helps me fall asleep again.
  21. As a hopefully humorous example... I do recumbent biking and swimming at the gym at my school. With the bike set on Level 9 (resistance, no clue what that translates to), my RPM is 85 and my HR is 80. The concept of RPM being greater than HR is hilarious to me! When I upped it to Level 10 (I have to keep it low due to my joint wonkiness), my HR got up to 115 and I got the muscle lactic acid mild burn, which is good in my book. The atenolol (and earlier the propranolol) are to blame, but my ANS neuro told me to not pay attention to the numbers and just pay attention to how I feel (though not everyone should use that advice, of course; see what your doc says).
  22. I found that moving from 15-20/knee highs to 30-40/thigh highs made somewhat of a difference, but I'm currently trialing a period without them. I don't have much noticeable pooling myself, so someone with more pooling "experience" (so to speak) may have more useful input. In my experience they do start wearing out after about 6-8 months; the opaque type (rather than sheer) are more durable. Compared to raising meds, they are often lower risk and less burdensome, although the higher compression can be a pain to put on.
  23. I get some benefit (maaaybe) from pyridostigmine (Mestinon) - barely enough to notice, and I can't take more since it causes speech inhibition and confusion at higher doses. The neurologist prescribed methylphenidate (Ritalin) to help with the spaciness; it hasn't helped with that symptom in particular, but I do have more energy and less "brain fog" while trying to read journal articles at work, which the neurologist is pleased by. Downside for me is the appetite suppression, which synergizes with nausea in all sorts of unfortunate ways. I'm mixed on whether to continue taking it, but in the short term the decrease in fatigue is helpful. Also, sadly, getting >9 hours of sleep a night, though I can't always manage that.
  24. I go back and forth between acceptance and depression; it depends on the day and how well I'm doing. It helps that pre-POTS I already had some serious body issues (constant joint pain, fatigue, bipolar), so I was used to moderating my activities, saying "no" when I needed to, etc. The difficult thing with the POTS is that it's harder to (1) predict at the start of the day how bad things will get and (2) I go from okay to nonfunctional with very little warning sometimes. Those days are the ones where I typically get depressed because I just don't have the ability to plan ahead when things go from okay to bad so fast.
  25. My tachycardia is pretty controlled on my beta blocker, but I do still get severe fatigue (which the Ritalin is helping with to a degree, amusingly) even on days when I don't have presyncope. So - yeah - fatigue appears to be pretty common for us. Remember that even if you don't have presyncope or tachycardia, your autonomic system is out of whack in other ways that cause fatigue. Tachycardia is just the most easily measured (and classified) one, but pretty much everyone with POTS has more than just tachycardia (hence "syndrome").
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