flyingsquirrel

I have acephalgic migraines (basically everything but the actual headache). I was already taking monster doses of verapamil for my IST, which happens to be the drug of choice for acephaligic/aura only migraines when I got diagnosed, but I was having significant symptoms anyway. According to my migraine neuro, acephalgic migraines have a different pathophysiology than "regular" migraines and therefor a different treatment. (and since migraine and autonomics are two uncommon subspecialties, it's hard to find someone who does both.) So...since the verapamil clearly wasn't helping me, they started me on topamax. I did have the "dopamax" side effects during the initial taper, but once I was on a stable dose for a week or two (it's a very slow taper up to the target dose) the cognitive side effects completely went away for me. I recently had to increase the dosage and I did have some cognitive side effects for 3-4 days while I was adjusting to the new dose, but now I'm back to normal. (I'm a grad student by the way, I use my brain a lot.) Zap, I understand your hesitation to try something that interferes with any sort of mental activities, but topamax isn't as scary a drug as some people make it out to be. I would encourage you to talk to a good migraine neuro and, if topamax sounds like it will help you, give it a try for a couple months (enough time to get up to a theraputic does and get past the side effects). Worst case scenario, you stop taking it and try something else.

A depressed/absent cardiovagal reflex would mean that your heart rate does not change (much) with deep breathing. This can be present if the parasympathetic side of your autonomic nervous system is depressed. This is one of the problems I have (parasympathetic depression) and I always had minimial heart rate variability. Since I have started taking pyridostigmine (a parasympathomimetic), my heart rate variability has increased tremendously and I have actually developed a healthy respiratory sinus arrythmia.

An increase in heart rate upon inhalation and decrease in heart rate upon exhalation is known as a respiratory sinus arrythmia and is completley normal. It is actually a sign that your cardiovagal reflex is functioning normally. If you ever had formal autonomic testing and you had to take a series of slow deep breaths, this is what they were testing.

I have mild CP and bromelain has been a life saver for me. I don't think I would be able to walk due to muscle spascity without it. Bromelain is a naturally occuring enzyme found in pineapples that, when taken on an empty stomach, acts as an anti-inflamatory. It is sold in most health food stores with digestive supplements. (When you take it on a full stomach it helps digest protein.)

I started at 30 mg 3x day with instructions to increase by 30 mg every three days (up to 120 4x day) as needed. The higher does don't work any better for me than the 30mg TID, so that's what I still take. I had a TON of side effects for the first few weeks, but they leveled off after a few weeks. Good luck.

I've never seen him as a patient (and I know it isn't Boston) but Novak at UMASS in Worcester is very good and his patients seem to like him.

The US system from classifying drugs as safe or not safe for pregnancy is as follows: Class A - definately safe for fetus (shown by studies in pregnant women) Class B - propably safe for fetus (shown by animal studies) Class C - "risk cannot be ruled out" (animal studies show possible fetal risk, but no human studies have been done) Class D - definite fetal risk (shown by human studies or cases) Class X - absolutley contraindicated, fetal risk outweighs any possible benefit Cardioseletive (blocks beta 1): Class B: acebutolol Class C: betaxolol bisprolol esmolol metoprolol nebivolol Class D: atenolol Non-cardioselective (blocks beta-1 and beta-2): Class B: Pindolol Sotalol Class C: all others Now, that being said, labetalol, pindolol, and long-acting metoprolol are usually the prefered drugs in the high-risk OB population. Use of other beta blockers (specifically propranolol, nadolol, and atenolol) at any time during pregnancy is associated with premature labor and neonatal apnea, fetal growth restriction, fetal bradycardia, and hypoglycemia. Additionally, use of these beta blockers EARLY in pregnancy is associated with smaller placental size and low birth weight. The drugs that are safe to take while you are pregnant are not always the ones that are safe to take while you are breast feeding. For example, propranolol, metoprolol, and labetalol are excreted into breastmilk the least and have shown no risk to the infant, while atenolol and acebutolol are excreted into breastmilk at high rates and can therefore put the infant at risk.

There are some beta blockers that are safe to take while you are pregnant or trying to get pregnant. Atenolol is not one of them. Please talk to your cardiologist as soon as possible and get switched to a beta blocker that is safe for pregnancy. I'm in the same boat that you are. I can't function without the meds. I've talked to my cardiologist about getting pregnant and she is fine with it as long as I switch to medications that are safe BEFORE I try to get pregnant. Then I will need to see her on a regular basis (for my health) and a high-risk obstetrician (for the baby).

How soon after standing are you taking the first measurement? If you don't wait one minute, you will get unreliable numbers. EVERYONE has a jump in heart rate and blood pressure when they first stand up, then it settles down. Your 2 and 3 minute heart rates and blood pressures are heading back to your baseline (rather than heart rate increasing further) so without knowing anything more about whether or not you were symptomatic, I would say that your second test looks completley nomal.

Eating a high-fat meal makes me tachy for hours on end. Also, even in non-dysautonomia people, high fat-meals take longer to be digested than "regular" meals. My gut feeling (no pun intended) is that the food you ate is "stuck" in your stomach because of normal mechanisms. Extra blood is probably being diverted there to aid in digestion, hence the tachycardia...at least that's how I explain it in me. Now if someone could explain why I go into a second degree heart block when I eat a high carbohydrate meal...

BG = blood glucose (blood sugar)

I hope it helps!

Are the speech problems caused by muscle weakness or is more of a 'higher brain function' problem? High doeses of pyridostigmine can cause muscle weakness, but it is not supposed to affect the brain. (Drugs in the same class that are also not supposed to cross the blood-brain barrier have been shown to do so in states of extreme physiological stress.) Other symptoms that would be expected with this kind of "overdose" would be increased sweating, increased salivation, diarrhea, and constricted pupils. Basically any part of the body that can increase fluid production, does. There is no harm in calling your neuro and asking what to do. If they can have you adjust your dose now, then check you when you go in, you will have a much more productive appt.

I found that I got used to the fatigue in a couple of weeks. If you don't, you might try switching to a long acting beta blocker like nadolol and taking it at night. That way, by the time you wake up, the worst of the fatigue will have passed.

I'm a tough stick too, especially when I'm sick so I can sympathize. It sounds like you did this, but tell them you are a tough stick so they start with someone good. Make sure they put the tourniquet on nice and tight (if it is over your shirt sleeve it won't pinch as much). Keep track of where your successful IVs are placed and have them try there first the next time. Not every hospital lets their nurses do this, but ULTRASOUND GUIDED IV...if you can see the vein on the screen, you can put a needle in it. I know this isn't always possible, but if you know you need an IV, try to drink a bunch of water and hour or two before...full veins are easier to hit.

Nausea after eating can be gastroesophegeal reflux (GERD)...and GERD can be worsened by beta blockers. Severe GERD can sometimes cause wheezing, but that doesn't sound like what you are describing. If the shortness of breath is more mild it might be irritation to the diaphram (from the GERD).

You're right about beta blockers decreasing renin secretion (I had completley forgotten about that). However I've never heard of florinef increasing renin levels, nor has a quick check of my favorite references yielded anything to that effect. Do you have any resouces that support this?

brethor... what do you mean beta blockers and florinef cancel each other out? Florinef aproximates the function of aldosterone and causes the retention of sodium and therefore water. This increases (or prevents the loss of) blood plasma volume. Beta blockers prevent the activation of beta receptors by epinephrine (and to a lesser extent norepinephrine) which leads to a decrease in heart rate and blood pressure.

I can't give you any advice on that one...only sympathy with the bad med experiences. I just got put back on the same drug that sent me to the ED in respiratory failure multiple times because it is the ONLY thing that is FDA approved that can keep my heart rate down.

The effect of clonidine on renin (and therefore on aldosterone) is MINOR compared to its effects on alpha-2 receptors. Also, keep in mind I'm explaining how it works in non-POTS physiology...things could be different for you.

issie... You bring up an interesting point with clonidine and fatigue. In addition to all the reasons you mentioned, alpha-2 receptors are involved in consciousness. As a centrally acting alpha-2 agonist, it makes sense that you would feel some of these effects. In fact, there is a 'hot new' ICU sedation drug (dexmedetomidine) that is also an alpha-2 agonist. As for your question, you might say that I have a "bit" of medical training. I would be happy to answer in more detail if you want to PM me. McBlonde... I won't dare to challenge the great Dr. Grubb, (and correct me if I'm wrong) but isn't the problem with hyperadrenergic POTS too much norepinephrine? Clonidine increases alpha-2 activity which helps bring down levels of norepinephrine.

True, but it isn't all wikipedia's fault. When new drugs are studied for use in humans they go through a specific series of clinical trials. Part of these clinical trials is recording the "adverse effects" or side effects of the drugs. However it is nearly impossible to parse out what symptoms are caused by the drug, what symptoms would have happened anyway (even in placebo controled trials), and what symptoms are due to underlying medical conditions. Parts of the transparency regulations stipulate that EVERY adverse effect experienced during a clinical trial must be recorded and must be atributed to the drug being tested unless it can be definitively proven otherwise (something that is rarely attempted and almost never successful). This is why, if you read the package insert, pretty much every drug has "headache" and "nausea" and "sinusitis" listed as side effects. It's not that the drug caused headaches, nausea, and sinusitis, it's just that over the course of a multi-month clinical trial several people were bound to get headaches, feel nauseated, and get sinus infections...and the FDA mandates that these be reported as "adverse events." The validity of this method can be argued in another forum. I have my issues with the FDA, but this is not one of them...my problem is how this information gets misinterpreted and mis-applied. Sometimes drugs, especially ones that are prescribed "off label" are given not for their primary effect, but for a specific side effect. Take pyridostigmine (mestinon) for example. The primary effect of pyridostigmine is decreased muscle weakness (primarily prescribed to people with myasthenia gravis), however a significant side effect is bradycardia. I don't have any problems with muscle weakness. I do however have a big problem with tachycardia. I was prescribed pyridostigmine to try to bring my heart rate down, therefore I take this drug for the side effect. I think (and I have no evidence of this) that this was the thought process of whomever listed clonidine as a volume expander: They might have seen "sodium and water retention" listed as a side effect (see above as to how it got listed as a side effect) and without thinking about the mechanism of action of the drug, misinterpreted this data, decided that this must be a common side effect and therefore clonidine could be given for the purposes of eliciting that side effect.

This is not really accurate. Clonidine is an centrally acting alpha-2 agonist which means that it decreases the amount of circulating norepinephrine, thereby reducing blood pressure and, to a lesser degree, heart rate. Without going into the intricacies of renal physiology, clonidine, at normal dosages should not have any significant effect on kidney function. There will be a SLIGHT reduction of blood pressure within the kidneys due to the decreased levels of norepinephrine, however the kidneys have much more sophisticated ways of regulating renal blood flow and these systems are not affected by clonidine. Clonidine also inhibits renin secretion. This has two important consequences. The first is that a lack of renin inhibits the conversion of angiotensinogen to angiotensin, thereby (further) decreasing blood pressure. The second is that without angiotensin, aldosterone is not secreted (remember florinef=aldosterone) and sodium and water are lost, thereby DECREASING blood volume. Now, when used for extended periods of time, people who had problems with sodium (and water) retention can develop a "tolerance" to clonidine and (re)develop symptoms of sodium and water retention. There is nothing in the primary literature to suggest that this is an effect of the drug itself.

My partner is a paramedic...they WILL look at them if they can find them (they aren't going to go hunting for a wallet card or a notebook). Mainly they are interested in medications, allergies, and medical conditions (and name and date of birth) if you can't tell them that information at the time.

Take a look at RoadID. They are made for runners/endurance athletes but they have two lines that can be customized (name and date of birth) then they have a phone number, website and PIN # that link to your medical info that you can keep continually updated. I think it's only $10/year which is much less than similar "medical" services I have looked at and you have constant access to your info. EMS/ER can either call the phone number (they have multiple international numbers) or logon to the website with your PIN and get access to all the info that you have entered. I have the basics...demographic info, insurance, emergency contact, doctors' names and contact info, medications (and why I take them), allergies (and the reaction), medical conditions...and I also have a one paragraph description of IST and one line descriptions of the different treatment needed for three common conditions (because of the IST/meds). I also keep my current immunizations and glasses prescription in there for the sake of completness and for when I'm out of the country.