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http://www.ncbi.nlm....les/PMC3055735/ There have been a variety of articles I've read on the brain's own internal RAAS, and it seems that angiotensin ii has many different effects within the brain, with emphasis on autonomic control and cerebrovascular and baroreflex activity. I've since gone back on losartan at a higher dose (50mg/d) and combining this with florinef. I've been getting periods of near remission, and certainly I notice a decrease in symptom intensity. It's looking like losartan might be an effective way to ameliorate brain inflammation, boost cerebral blood flow, and regulate autonomic activity. It's been two weeks since I've been on both, but I'm likely going to try to titrate up my florinef dose from .1 to .2/d.

Thank you all for the well wishes, I have some idea of what I want to specialize in and certainly dysautonomia is going to be a large part of my practice. However, I'm also interested in advancing medical science in other areas such as autologous stem cells and biological treatments.

I received my first acceptance to medical school. It's going to be a long journey, but it seems like I've already come a long way through it all. I hope I can serve as inspiration for others that it is still possible to achieve whatever you set your mind to. Fight POTS any step you can. Needless to say, I am both very excited and very aware of the amount of debt I'm about to go into!

I don't know about y'all, but my presyncope is constant. I also get time periods (especially under stress) where my presyncope ramps up and very nearly turns into syncope. I'm currently taking .1 mg florinef 20 mg propanolol and 25 mg losartan. This drug regiment has helped my presyncope somewhat, but I still have the tachycardia. Probably will be doing some further dose adjustments. I've had the presyncope even when I'm lying down and my HR is normal. It's likely due to norepinephrine throwing off the proper autoregulation of the blood vessels. I notice that after a long run, my presyncope is helped a lot even though my tachycardia is actually increased. This study probably explains why: http://circ.ahajournals.org/content/100/11/1194.short

I don't believe you will find patients who have tried Rituximab for POTS. There have been some patients who've done IVIG, with varying levels of success. However, there was a study about Rituximab working very well for CFS patients, and POTS is known to occur in a significant percentage of CFS patients. It's not unreasonable to suspect that some of the patients in the CFS study also had POTS and benefited from this drug. Rituximab is dangerous and you should talk with your doctor about the risks before pursuing such a treatment. I'm surprised your doctor mentioned it as a potential treatment, it must be doctors are catching up on the research. Autoantibodies are implicated in POTS.

They said biofeedback can treat Raynaud's however, RCT's showed this not to be the case. Take that for whatever it's worth.

Some POTS patients are trying Ivabradine - it's not a beta blocker, so it doesn't operate on the nervous system, however it has met with a lot of success over in Europe for POTS and IST patients. It directly lowers the heart rate without lowering blood pressure like BB's do. Fatigue is a listed side effect of propanolol. I'm currently taking 20 mg of it and I'm not getting side effects, however I'm not getting much benefit either. Trying to get on ivabradine.

Yes, for whatever reason - be it that POTS isn't seen as serious compared to other disorders, which honestly it isn't. (If you compare POTS to other disorders doctors regularly see, such as Parkinson's, Alzheimers, heart failure, cancer, etc. etc.) or that doctors just don't understand POTS and vent their frustration as our own psychological problems - it doesn't matter. We deserve the respect and dignity that we're under hardship and need help, and really you shouldn't go to doctors who treat you otherwise. Unfortunately I'm in the zone of doctors who acknowledge POTS as a physical illness but have no time or interest in pursuing treating it.

I'm feeling better on propanolol, still have my symptoms but they're alleviated somewhat. Currently on 20 mg BID.

It has been shown in some studies that patients with TBI (traumatic brain injury) can develop POTS. It has also been shown that patients with multiple sclerosis have a high incidence of POTS. Whether that's attributed to a triggered inflammatory response or a central disruption in autonomic control is uncertain. Interesting to note that in the reported incidences of TBI induced POTS, the onset was insidious arguing against a central nervous system origin and more towards a triggered inflammatory response. (If brain damage to the autonomic region of the brain was the cause of the POTS, one would expect the POTS to be nearly instantaneously produced.)

I haven't had a concussion, but I have read about using EEG's to diagnose post concussion symptoms. If the symptoms are new it would be more likely attributed to the concussion. Did they discuss using a prolonged EEG or EEG in general?

http://www.ncbi.nlm.nih.gov/pubmed/22772053 Well according to this study Ivabradine had statistically significant results over metoprolol in treating IST, which is similar to POTS. Other studies have suggested Ivabradine is able to treat patients unresponsive to beta blockers. It will be interesting to see.

Lightheadedness

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I haven't read about this surgery in a while, when I left of it a little over a year ago I remember Canada approved testing of the procedure on the basis of preliminary evidence for MS efficacy. It's an interesting theory, with some data to support it. I did read several studies documenting a higher than average incidence of CCSVI. However, nothing close to the extremely positive findings by Zamboni. Review studies from what I recall that excluded Zamboni's paper showed non statistically significant difference in MS and controls with respect to this phenomenon. Additionally the diagnostic criteria of CCSVI is not so clear. One hopes that this or something like this would actually work, as MS is a terrible disease.

Correlation isn't causation but causation has already been established with NET. Blocking NET with reboxetine produces POTS in healthy volunteers and when the reboxetine is metabolized out of the system the POTS also disappears. It's not about knowing anything with certainty, which is impossible, but rather what's more likely and less likely. Autoantibodies and NET transcription aren't regulated by CNS activity. Blood volume, sympathetic activity, and parasympathetic activity do have connection with CNS activity, but might also arise from a peripheral problem. That would be the only conceivable means of implicating the CNS in POTS that I can think of. However, more likely to me is the NET transcription defects which might be explicable by autoimmune illness hence the autoantibodies. The studies themselves can only be wrong if there was methodological error, as their findings are data. Given the quality of scientific researchers involved with the studies, I don't think the data is wrong.

This is an interesting discussion to have. I think in the preliminary years of POTS research there was this huge rush towards optimism. I recall reading in several reviews that 90% of POTS patients respond to therapy. Now the articles coming out are starting to ask questions as to why we're not getting better, why we're difficult to treat etc. etc. It was the same thing with beta blockers, some early studies were boasting near 100% treatment response, and now other studies are saying actually few POTS patients tolerate beta blockers in appreciable dosages. There has been a long term follow up study which I posted (somewhere?) that showed that about 33% of POTS patients after 6 years considered themselves remitted, and something like 60% (including the remitters) considered themselves improved. The old study on soldier's heart (probably POTS) patients showed that about 20% improved over the years with the remaining 80% being symptomatic. So yes it does seem possible to "outgrow" or I guess have a remission from POTS, and you'll find stories of that here. However, I don't know how accurate it is to think that everyone will outgrow POTS. I developed POTS when I was 17, I'm now 24 and still symptomatic. What has changed since then? Well admittedly my gastrointestional symptoms such as early morning vomiting and vomiting in general has relented. My adrenal surges have calmed and my presyncope is not as intense as it used to be. So I would rate myself as improved. I suspect an average exists, some people will have better results than me, some worse. The research however is starting to suggest that POTS is immune mediated which has circumstantial as well as biomarker evidence for it. Autoimmune disorders are difficult to predict, some are chronic, a lot are relapse/remitting, and still others can disappear after time. The prognosis depends heavily on the underlying cause of the POTS and probably is the best deterministic variable as to whether one will improve or not by itself.

CFS is associated with autoantibodies from the ritixumab trials. POTS is associated with ACHR autoantibodies, and probably others as well as NET dysfunction. Neither of these things have an origin of the CNS. I hope it works to help your symptoms though.

You're welcome! I was hoping for some discussion on these topics. Most interesting was the woman who started the therapy and had a remission only to go back to POTS after ceasing the medication. This provides firm evidence that there is a chronic underlying physical mechanism involved with POTS. I know we've had a few members here on ivabradine, some with success others without, does anyone have any further experience?

Yes, I have seen these studies, and maybe in time the prevailing opinion of the medical community will change with respect to fibromyalgia sufferers. However, in this case I highly doubt that POTS is a central nervous system sensitization as this article argues. The primary evidence being drugs that don't have anything to do with the central nervous system such as ivabradine, fludrocortisone, midodrine etc. have been effective. Additionally autoantibodies to peripheral nerves as well as the heart have been identified in POTS patients not to mention the loss of NET activity.

Two published case studies: http://www.ncbi.nlm....les/PMC2995161/ http://europace.oxfo.../9/12/1202.long As well as a single center publication on 20 patients: http://europace.oxfo...t/13/3/427.long It seems to help ~60% of patients. Not just their tachycardia, but other symptoms of POTS as well.

It seems like this paper is trying to set the stage for making POTS the fibromyalgia of neurology, and I mean that with no disrespect to fibromyalgia sufferers, to whom I have no doubt is a physical condition outside their control. But one can't deny that fibromyalgia has become designated as psychosomatic illness and therefore the research is almost non existant when it comes to trying to find biological origins of the illness. We can't allow this to happen, if we get stigmatized like this it will virtually end any respectable effort to find the cause and possibly the treatment of POTS. This year has been very productive, new autoantibodies have been discovered and the NET dysfunction has been found. This is not the time to back track and fall back into this quagmire of pseudoillness. And I have to believe that the psychosomatic sentiment is stemming from a foundational frustration at not being able to find an effective treatment. The logic is, "Oh, we throw fludrocortisone, midodrine, and beta blockers at it, if those don't work then we've tried all these medications and obviously the person is just messed up in the head." ... HELLO! Fludrocortisone was originally approved for something far different than POTS. In fact, none of these treatments are FDA approved to be effective for POTS. There's all these research articles coming out about autoantibodies - well none of these drugs with the exception of possibly fludrocortisone have any immunomodulatory effects. Don't give up the fight. But I feel we have a strong need for advocacy, because this psychosomatic view needs to be put out like fire.

I don't like this article at all, several times it repeats the "somatic hypervigiliance" line. Doesn't even comment on the autoantibodies found in various studies nor the loss of transcriptional function of the norepinephrine transporter. POTS is not psychosomatic that's just ignorant and quite frankly insulting.

I've been noticing lately that I've been slurring words, especially when I'm lightheaded and on the job.

Excellent, I forwarded the research to my neurologist, I'll await her reply.