jangle

I had a brain MRI in 2005 when this all started w and w/o contrast, that showed no lesions. I had a repeat MRI 6 years later w and w/o contrast that also showed no lesions. So take that for what it's worth.

I think I've hit 210 before. Doesn't feel so good. Nowadays I've been able to keep it below 190. I did 24 mins on the stairmaster and think I maxed at 187. Ultimately id like to get it below 170. Im incorporating a lot more heart exercises like rows and squats together with endurance jogging and the stairmaster

I too have/had severe anxiety before and after POTS. POTS likely involves a reduced expression of norepinephrine transporter - a protein which removes norepinephrine from your sympathetic nervous system (SNS). It being deficient means norepinephrine is staying longer in your SNS and thus overactivating it. In terms of treating it, you could ask about clonidine which is something that would reduce your norepinephrine output. Not really sure how effective that would be as it would also reduce your blood pressure which may or may not exacerbate POTS symptoms. Endurance exercise will tend to reduce your serum norepinephrine levels, that might be a better alternative as it could work on your POTS symptoms as well. Psychotherapy can be effective, but it depends largely on the relationship you develop with the therapist and it can be a long process. I would personally avoid any kind of brain surgery as that can lead to lasting permanent deficits.

Probably beta blocker

Chaos the reason for studying recovered pots patients is because it would be necessary to assess the question of damage to the brain. If you study pots patients while they're sick and find they have cognitive impairment one has to ask how much of that is due to just being sick or how much of that is due to damage. Studying recuperated individuals allows one to isolate the question on actual damage. Yes the question of subgroups and oh is of particular interest.

There's no argument that POTS diminishes cognitive ability. The question of brain damage is a much more complex issue and might necessarily be open ended. What we do know is that researchers who've followed POTS patients for decades have not noted a transition to MCI or Dementia that an illness that caused brain damage would tend to illicit. Additionally patients with POTS aren't shown to develop typical neurological signs of physical brain damage, and there's not been any real mention of brain MRI abnormalities - no shrinking or notable atrophy of the brain. Even in neurodegenerative illnesses that evade MRI, such as chronic traumatic encephalopathy - associated with tau deposition and neuronal death, one will typically see symptoms suggestive of neurodegeneration, which again has not really been noted in POTS patients. One would tend to want to look at patients who recover from their POTS and see if they're cognitively normal to controls, and follow them up in the long term. The message I've gotten from researchers about POTS and IST patients is that the prognosis is benign in the sense of bringing out further complications, but that they are functionally debilitated.

I assume your talking about people who have pots with no blood pressure fluctuations? Since many people experience fluctuations in blood pressure along with tachycardia, the lines are obviously blurred. In these cases, one is not speculating if there is hypoperfusion? So these people dont have pots? By what standards? Nothing personal, I just think it is dangerous to make a assertion based on a strict interpretation on something that is not so clear cut? Typically the brain can maintain perfusion up to around 85 mmHg or less systolic pressure. Whether there is a shift towards higher blood pressure values before fall in cerebral profusion in POTS patients is uncertain. The study I'm referring to is this one: http://jap.physiology.org/content/99/3/828.full Additionally I had correspondence with a Mayo autonomic researcher who also confirmed that perfusion is typically maintained in POTS. I'm sure that researcher is basing their opinion on more than just that one study (probably having seen and SPECT tested many POTS patients over the years) as they have actually published articles on POTS. Yes, one typically talks of POTS in the absence of appreciable orthostatic hypotension. There can be no argument that with OH, cerebral perfusion can be compromised past a certain threshold.

I've had pots lightheadedness for 7 years and om in medical school. Some doctors will argue that pots patients actually don't have hypoperfusion. There have been a few studies showing pots patients with lightheadedness actually maintain perfusion. Where the symptoms of lightheadedness come from then is uncertain. One can speculate that damage is occurring, but the evidence just isn't there. There are people who've had pots for decades and they don't show signs of neurodegenerative disorder. Now of course when one considers complications or confounding factors such as hitting ones head from passing out, having severe untreated sleep apnea, or depression from chronic pain - all these things can influence cognitive function.

How old is your grandmother? Keep in mind age and high blood pressure are significant risk factors for stroke and mini strokes. As for other issues- there hasn't really been an association between inappropriate sinus tachycardia, POTS, or dysautonomia and stroke. If you have hypertension you should definitely focus on reducing blood pressure and also make sure you don't have sleep apnea or disorders as are often found in dysautonomia conditions

Likely low aldosterone levels. Why that is, is still a question. Also the sympathetic nervous system does regulate your blood volume, so there could be a mechanism at play with a faulty SNS.

For the past month I've been ramping up exercise again. This time around I'm incorporating other things into my workout regiment, namely weight lifting to try to boost vagal output and the stairmaster. There have been numerous studies which documented reduced stroke volume in POTS patients, but there have also been studies which showed that even with normalization of stroke volume, symptoms persist - arguing against stroke volume as being the cause of the symptoms. The stairmaster seems like a great exercise to reduce standing heart rate, it works the thigh muscles where most of the blood volume occurs in the legs (your legs hold a substantial percentage of your overall blood volume). So boosting that muscle pump will aid in blood flow back to the heart. Additionally it seems to target the heart and cardiovascular system well, which hopefully will lead to enlargement of the heart. One of the things I notice however, with exercise - and this may be individual. But so far all exercise does is delay the time my tachycardia sets in. For example, without exercise my standing HR will go from 70s to 120s in about a minute. With exercise it still goes near the 120s (I think I maxed at 117) but now it takes 5 minutes. I guess that's improvement, but ultimately one wants to get the absolute standing HR permanently down. I was wondering if this has been other's experience with exercise? I know from several of the papers people were able to get reduction in symptoms of their POTS without much reduction in heart rate values - and honestly I think the tachycardia is loosely correlated to symptom intensity. I believe the tachycardia is just an artifact of reduced NET proteins, and stems from being flooded with norepinephrine rather than as compensatory mechanism.

I wish they'd just straight up do a RCT on CBT or therapy and see its effect on standing HR.

Neither SSRI's nor benzodiazepines helped my lightheadedness which is my only symptom. I got the most relief from florinef.

POTS doesn't have to rule your life. Is it painful? Yes, undoubtedly the headaches and lightheadedness are significantly debilitating. POTS is a spectrum of disease however, for me, it does present a significant challenge but it is not disabling. One thing that must be emphasized is that it is possible to achieve symptom reduction through treatment. Fludrocortisone helped my lightheadedness to a noticeable degree. Endurance exercise if done long enough and hard enough will also make a noticeable and significant impact on your symptom intensity. The way I rationalize POTS is to think about ways and things I can do to get better. Treatments do exist, you just have to find what works for you.

Foggy, Arizona girl has some very good ideas. Have you had any small fiber neuropathy testing? If not I unfortunately can't assist you about who to go to as I myself am in the boonies. The progressive nature suggests several things but the sporadic location and duration lends me to think of underlying autoimmune process at play. In the end something like half of sfn cases are labelled idiopathic and get ivig thrown at them. Don't be discouraged by dismissive docs, they re just in denial of how little is actually known in this field. Have you had a QSART?

Bebe is correct and something I've thought of a lot myself. Anxiety is autonomically mediated and so if you have dysfunction of the autonomic nervous system it would make sense that there would be dysfunction in anxiety. With a lot of research pointing out hyperadrenergic states, vagal hypoactivity, and higher than levels of noreoinephrine - wouldn't it make sense that anxiety fits in there somewhere? Anxiety therefore can be a symptom of a physiological system gone haywire but it is not likely a psychological cause as Vanderbilt showed. (Which by the way I find kind of sad that they had to do a research study to confirm we're not crazy -how many other chronic diseases conditions get treated that way?)

Go on to the next doctor. No point in trying to convince them otherwise. When they ignore scientific evidence, they're not subject to reason.

Exercise has many different mechanisms that could improve POTS symptoms. It improves your skeletal muscle pump's strength, aiding blood flow throughout the body. It regulates nitric oxide which also assists in blood flow. It strengthens venuous return which reduces tachycardia. Which is an important characteristic. Even in normal athletes, resting heart rates decrease with endurance exercise. It is possible to modify one's tachycardia through exercise alone. In addition, exercise boosts parasympathetic control of the heart, so it directly affects the autonomic nervous system. It also has regulatory roles on the Renin-angiotensin-aldosterone system. It also lowers serum norepinephrine levels and raises blood volume. In short, exercise is probably the best treatment for POTS there is.

Ivabradine or beta blockers should in theory increase exercise tolerance. I noticed on low dose propanolol I don't get as winded and can run longer and faster. 10k I believe is roughly 6.5 miles. If you can run one of those (and have regularly trained to do so) your POTS will probably be significantly diminished.

Neuronal loss is unlikely cause given that POTS can begin and end spontaneously. Links to MS probably more akin to inflammation or possible autoantibody involvement.

Interesting report of the 13 year old girl. It is very likely that there are yet to be discovered antibodies involved with autonomic dysfunction and POTS in particular.

Keep in mind that POTS patients tend to have reduced NET (Norepinephrine Transporter) function, which leads to a situation where you have norepinephrine staying in your sympathetic nerves for longer periods of time. This in and of itself can cause anxiety. Anxiety can cause a heightened sense of symptoms, but it is incorrect to say that anxiety is the primary cause of POTS. It can be a symptom, but it is not the cause.

Same experience as Rama, even then it took >5 weeks and I'm still feeling improvements now 3 months into it. For reference I'm on .1 mg fludrocortisone

Yes it is possible to improve. Time alone works for some, for me exercise and medications such as losartan and fludrocortisone as well as volume loading have helped a great deal. I still get relapses but I also have periods of much improvement.

Ssris made my tachycardia worse...take that for what its worth?