arizona girl

Oh good about the adderall is that a high or low dose? Did you take that article to him? I know a lot of us start with half a pill if it can be split before working up to full dose. I did that with my plaquinel, what you doc say about that? Treatment for SFN is also like pots it depends on the cause of it many things can cause it. The most common cause is diabetic neuropathy, which means treating the diabetes right should help. Mine was autoimmune so we first did plasmapheresis which did improve my autonomic function and help confirm it was autoimmune, I then got an infection and anemia, blood on that showed the cvid/hypogammaglobulinemia and I now infusions to replace those, I also have to treat the companion autoimmune disease. Some forms of sfn may not be reversible that damage from toxic exposure. A good doc will try to figure out the cause and what type of sfn it is mine is more autonomic in nature and for me those symptoms came first. A lot of the research due to the diabetic element believe the periferal neuropathy comes first and don't know that they have that right though. Hope that answers your question.

Yes, I was in extreme pain during my test, had all of those symptoms. Think about how your arm feels if you leave a blood pressure cuff on to long. That is similar to the blood pooling in the lower half of your body like you've got a cuff around your waist and the blood can't move up. I was also wiped for days after the test. My legs and arms were also twitching and spasming contracting involuntarily, my body was trying so hard to compensate and push the blood back up. I did my test with no shoes on, big mistake, I also would have had pants with shorter legs so they could see the change in color of my legs.

mama destiny, If you haven't already get a copy of your full medical record from this doc and make sure it has the documents they made during your tilt table test. It will be a chart showing what happened every few minutes. True pots does not effect the blood pressure it will stay the same even if your hr goes up. Other forms of dysautonomia will show the bp dropping or rising alone with the HR. Dropping usually means you are hypotensive too, rising BP will usually mean you are hyperadrengenic. Those are separte diagnostic findings from pots alone. During your TTT did they check your catechacolines ( epi, norepi, dopamine). Most hypers get elevated norepi, most hypos don't show any rise. On your test did they try to stimulate syncope by give nito or isoperol? If they didn't do that they did not evaluate you for full syncope, as that should be the second part of a ttt, especially if you do get near syncope in real life. That is how I am and my first pass out was on the ttt, but it reduplicated all the symptoms I get in real life when this happens. If they haven't done at least a 24 hour heartrate monitor that is something you might want to ask for because it can reveal more then just pots. Hope this helps. You might posts to see if anyone in your area knows a good doc for you to see. Also have found that Ratemds.com is a good resource to see what other patients experience with their docs. Good luck and take care.

Sorry, this is happening to him, now too! Silver lining at least now he knows how you've been feeling and that you weren't faking it. Tough way to get empathy though. I think this also points to the fact that pots itself is a symptom of most likely some other underlying problem. Many types of illnesses can cause pots and really need to be eliminated, before one can say it is only pots. There are also so many ways dysautonomia presents itself, even the research centers like mayo and grubb are seeing this as the research as evolved. Finding cause can help treat the cause of the symptoms as well as meds that treat symptoms alone. Glad your going to cleveland, inquire that they look into testing for cause. Alot of that is not something a regular doctor or hospital will do. If you search my old posts using phoenix neurology and Todd Levine, I posted all the rare things he tested me for. My skin biopsy found SFN, and then we found immune difiecency and then the autoimmune diseases which I knew were there finally showed antibodies. I treatments for each of them now and there has been some improvement in symptoms, but in my case there is no cure and the best we can do right now is manage it. There is some peace in accepting it is what it is and at this point if I get any great improvement or we are able to keep from getting worse then that is icing. Another thing I've realized is god can still work through you even when your not well and that has been a real blessing and a gift.

Looks like mayo rochester does that right testing at least. This study also reflects what members are posting about their symptoms. That 29% are hyperadrengic which is more then grubbs group and is closer also to what we see posted here. In this study, the Mayo clinic speculates that most POTS types are in fact autoimmune/neuropathic, and that hypovolemic and hyperadrenergic types are compensatory mechanisms: Mayo Clin Proc. 2007 Mar;82(3):308-13. Postural orthostatic tachycardia syndrome: the Mayo clinic experience. Thieben MJ, Sandroni P, Sletten DM, Benrud-Larson LM, Fealey RD, Vernino S, Lennon VA, Shen WK, Low PA. Autonomic Disorders Center, Department of Neurology, Mayo Clinic College of Medicine, Rochester, Minn 55905, USA. Curr Rheumatol Rep. 2007 Dec;9(6):471-2. Abstract OBJECTIVE: To evaluate the prevalence and pathogenetic mechanisms of postural orthostatic tachycardia syndrome (POTS). PATIENTS AND METHODS: We reviewed the medical records of patients with POTS seen at the Mayo Clinic in Rochester, Minn, from January 1, 1993, through December 31, 2003. All patients were required to have had a full autonomic reflex screen. The results of the following additional tests were evaluated: thermoregulatory sweat test, plasma catecholamine measurement, serum ganglionic (a3) acetylcholine receptor antibody detection, and 24-hour urinary sodium measurement. RESULTS: We identified 152 patients (86.8% female; mean +/- SD age, 30.2+/-10.3 years) with a mean duration of symptoms of 4.1 years. The mean orthostatic heart rate increment was 44 beats/min. Half the patients had sudomotor abnormalities (apparent on both the quantitative sudomotor axon reflex test and thermoregulatory sweat test), and 34.9% had significant adrenergic impairment, indicating that at least half of the patients had a neuropathic pattern of POTS. In 13.8% of patients, onset was subacute, and ganglionic acetylcholine receptor antibody was detected in 14.6%, suggesting an autoimmune origin in at least 1 in 7 patients. Hyperadrenergic status was documented in 29.0% of patients (standing plasma norepinephrine level 2600 pg/mL), and at least 28.9% were presumably hypovolemic (24-hour urinary sodium level <100 mEq/24h). The lack of correlation between urinary sodium and standing norepinephrine levels suggests that mechanisms other than hypovolemia accounted for the hyperadrenergic state. CONCLUSION: Our findings suggest a neuropathic basis for at least half the cases of POTS and that a substantial percentage of cases may be autoimmune. Hyperadrenergic and hypovolemic correlates are likely compensatory or exacerbating.

True, but don't forget that was only 4 patients that took the adderall and it looks like they only looked at patient response on 27 patients. Well the percentage for the ss's were better then some treatments but really were closer to 50/50. Really the article was not a lot to go on, but at least it is something. It was just a review of one centers patients. I was told by one doc to do lexapro, but when she found out I went up she suggest effexor, which grubb has used as well. That was early on though and I have been resistant to taking that class of drugs. She also freaked me out by saying if you go up then there are many things that could be wrong with you including a cancer I think that carcinoid kind, you need to go to Mayo and find out what is wrong with you. She was right, but she scared the sssss out of me and I couldn't go to mayo. So, I had to chase down doc's on plan which took me to grubb and vanderbuilt. I got lucky and a local autoimmune neurologist actually figured out the sfn and then the immune defect and got me on the right treatment. He also ran all those scary test the other doc mentioned without me even bringing them up. It has been a long journey and I still am not where I want to be. I want to know what normal feels like. I'm in accepting mode now, cause at this point it probably ain't going away. I think as the research progresses management will get better. That will happen because patients are better informed and can know push the doctors into new direction and understanding. As my doc said "What you have though considered rare, I don't think is rare at all!" I laughed and said yes, just rarely diagnosed. He nodded yes!

Anoj, I posted a 2011 study from Dr. Gubb on the forum yesterday, where he shows the response hypers had to certain meds. All the ones you are talking about are there. Go to my post and take a look at the article, it might be something you want to take to your doc. Interesting though only 4 took it they all rated adderall at 100%

Yes, this happens with a lot of us. Mine could hit those lows usually while sleeping and would show on my waking bp/hr. I'd have low bp at times along with the low hr. However, if you do get syncope or presyncope after you've been upright, then there are usually symptoms also, for me it is a sign I'm about to faint. Your TTT test did not take you syncope? Also you don't say what happened with your blood pressure. That is important to know to. Beta blockers can be tricky it would be good to know which one and how much. Have they done any investigation into the cause of why you are having pots?

Yea, I know not a lot when you consider the informal polls and posts here reflect about half us are presenting hyper. I would have been one of those patients, but I never sent my cat test result to them showing I went from 400 to 1100. So, maybe they have patients they missed, who didn't come back. In my medical record he wrote hyperadrengenic. What I think is interesting is where patients had more symptoms and not all were hypertensive, but still considered hyper. In the meds area the only med that was 100% was the adderall though only 4 out of 27 had used it, but 4 for 4 had effective results I also wonder what meds are considered neri. I was not able to take clonidin though it appears to be the second most successful. My body started acting like it was a drug addict to it, requiring more and more to keep my bp/hr down, for me coming off was awful and scary. I don't have that problem with labetalol which is both alpha/beta and I can take as needed, it also though isn't always effective. Also what happens if you are both hyper and autoimmune? While I didn't do the mayo panel. I have all kinds of positive antibodies for thyroid, rheumatic and biopsies showing an autoimmune respose to nerves and tissue, also have an immune deficit. All of these are being treated with their own appropriate treatment. But my cardio said all the immune stuff is like a circle and when one goes off then others are bound to follow, which reflects what has happened with me. So is there a way to treat autoimmune hyper? I don't know that they are there yet.

Amen, KayJay, I was very athletic in college when it first became very obvious there was a problem and I was collapsing during aeorbic class. You made me laugh about the cardio work out taking a shower, brushing teeth or hair for that matter. Try washing a window or a mirror or stirring a thick pot of something, even just digging a small hole for a plant in my yard and I'm in full cardio. In arizona sometimes it happens just walking to your car in the heat. I guess I know it's not going to go away. I'm just want to do enough that I don't end up in a wheel chair. Which has concerned some of my doctors.

The title of the abstract only says POTS and the abstract didn't identify any subgroup that I can see. So don't know!

I don't know but I'm going to ask them that when I go there. I let you know what they say.

Another center review of Pyridostigmine when used to treat pots, they don't say exactly with the improvement was in bp/hr so I don't know if they meant it helped patients who BP went up or down. Rama, what do you think? Pacing Clin Electrophysiol. 2011 Mar 16. doi: 10.1111/j.1540-8159.2011.03047.x. Pyridostigmine in the Treatment of Postural Orthostatic Tachycardia: A Single-Center Experience Kanjwal K, Karabin B, Sheikh M, Elmer L, Kanjwal Y, Saeed B, Grubb BP Electrophysiology Section, Division of Cardiology, Department of Medicine, The University of Toledo, Toledo, Ohio Department of Neurology, The University of Toledo College of Medicine, Health Science Campus, Toledo, Ohio] The long-term efficacy of pyridostigmine, a reversible acetyl cholinesterase inhibitor, in the treatment of postural orthostatic tachycardia syndrome (POTS) patients remains unclear. We report our retrospective, single-center, long-term experience regarding the efficacy and adverse effect profile of pyridostigmine in the treatment of POTS patients. Methods: This retrospective study included an extensive review of electronic charts and data collection in regards to patient demographics, orthostatic parameters, side-effect profile, subjective response to therapy, as well as laboratory studies recorded at each follow-up visit to our institution's Syncope and Autonomic Disorders Center. The response to pyridostigmine therapy was considered successful if patient had both symptom relief in addition to an objective response in orthostatic hemodynamic parameters (heart rate and blood pressure). Three hundred patients with POTS were screened for evaluation in this study. Of these 300, 203 patients with POTS who received pyridostigmine therapy were reviewed. Of these 203 patients, 168 were able to tolerate the medication after careful dose titration. The mean follow-up duration in this group of patients was 12 ± 3 (9-15) months. Pyridostigmine improved symptoms of orthostatic intolerance in 88 of 203 (43%) of total patients or 88 of 172 (51%) who were able to tolerate the drug. The symptoms that improved the most included fatigue (55%), palpitations (60%), presyncope (60%), and syncope (48%). Symptom reduction correlated with a statistically significant improvement in upright HR and diastolic blood pressure after treatment with pyridostigmine as compared to their baseline hemodynamic parameters (standing HR 94 ± 19 vs 82 ± 16, P < 0.003, standing diastolic blood pressure 71 ± 11 vs 74 ± 12, P < 0.02). Gastrointestinal problems were the most common adverse effects (n = 39, 19%) reported. The overall efficacy of pyridostigmine in our study was seen in 42% of total patients or 52% of patients who could tolerate taking the drug. Conclusion: The subgroup of POTS patients who can tolerate oral pyridostigmine may demonstrate improvement in their standing HR, standing diastolic blood pressure, and clinical symptoms of orthostatic intolerance ©2011, The Authors. Journal compilation ©2011 Wiley Periodicals, Inc]

Do you only get it when you lie down at night, especially if you've been on your feet a lot? Does it feel like your legs and feet are vibrating, tingling or burning? Or is there numb spots? That can be a sign of peripheral neuropathy. The test is a skin biopsy for small fiber neuropathy. I have an autoimmune version of it and I also have cvid and I am on IVIG to replace the immunoglobulins. This is one of my symptoms that has almost completely subsided since I started IVIG, that and my pms symptoms are a lot better, I've also had improvement in my hr/bp, that has not completely corrected yet. I had forgotten I used to have this until your post.

Rich I don't have weakness in my chest muscles. I'm sure my abdominal muscles are weak and pool as well. If im standing still or on my feet to long even if walking my body aches from the waist down. I do though get delayed post exercise fatigue, that is worse then the fatigue I always have. I will actually be getting pool therapy exercise this time. The PT felt it would be more effective for me then land exercise with gravity and there is less impact. When I know what the exercises are I will let you know. The hospital where I'm being referred hasn't contacted me yet. But the PT thinks highly of their pool therapy program. My only concern is picking up bugs because I'm prone to infection. I don't know what to think about Levine's program. I know I don't have a small heart, which is his criteria for inclusion I think. I know I don't do well with standing upright exercise. So I'm hopefully, I also hope I loose some weight. Between meds, pcos and hashimoto I'm up to 150, but I was a tiny girl so that is easily 25 pounds to much for me. I long for the day I can go shopping in my closet, I have so many like new clothes I can't get into. I'll keep you all posted!

Just found this don't know if it's been posted yet. Really breaks us down into groups/symptoms and treatments. http://stars-us.com/files/file/Clinical%20papers/110819-tl-Hyper-POTS%20Proof%20copy.pdf

Hey Kayla, kept you in my prayers while your were in the hospital. You said you bleed a lot with your periods. Did your doctors do a through evaluation for anemia? Heavy bleeding can cause anemia and it doesn't alway show on a cbc. I had it and it didn't show until I got really bad. Some forms of anemia can be hidden too. I think a hematologist is the doc to see for that. Anemia can cause a high heart rate too! If they stop the bleeding with the depo shot, maybe you will start to improve after a few months. It can take anemia a while to correct and sometimes iron infusions are needed. That was what I had to do. I also was always more symptomatic before my period. My pots is autoimmune and since being on IVIG my pms has gone away.

Yup, flying is one of my triggers too! I now fly with a handicapped tag on my ticket, if I'm flying alone. You can request that if the plane is not full to leave the middle seat open I can then sit sideways with my feet with socks on in the middle seat. They do reserve seats now near the bulkhead and front of the plane for handicapped. The bulkhead is tricky if the wall is close enough you can put your feet up on it, that keeps you legs elevated, if not then your in trouble because the bulkhead seats are separate by the tv tray and you can't put the arm rest up to give you more room if the middle seat is open. I now tell the flight attendants that I might need to lay down, if my blood pressure drops and if I faint to make sure my head is down and my feet up. I don't say any of this though if my husband is with me. It also doesn't always happen. Seems like if the plane gets shaky it happens. That happened on the way back from seeing Dr. Grubb, I got so ill I had to have a wheel chair and lay down in the terminal as well. That has only happened once thank goodness. I prepare better now. I always have a barf bag with me too!

Oh good article!! I had gi and feeding problems in infancy. I remember when my baby sister was born sneaking the baby bottle and putting juice in it so I could drink laying down. I still prefer to drink reclined using straws, seems there is less resistance. When i drink or eat sitting straight up I always seem to get full faster and can't eat or dring as much and my stomach will feel the pain you get with distension. I know this was done in children but if you have that issue as a child you could still have it as an adult. Wonder if there are any adult studies?

Posted the article since the link didn't work. I don't think ivabradine is available in the USA yet. Is that right anyone? As far as the subtypes go the research that is being done on treatments for symptoms is now starting to define the different ways orthostatic intolerance presents. If you've been reading on the forum you will see all these types presenting differently in the forum members. So, how you treat someone who gets hypotensive on standing may be different then someone who becomes hypertensive on standing, or someone who only gets a high heart rate. This article discribes perfectly what happens to me when vasovagel collapse happens, I am super high in hr/bp and then I suddenly tank when my body can't take it any more or there is an additional stressor added in, then a collapse and can't get up. So these treaments as you see from the article may or may not help. It is important to note that this is treatment for symptoms only and does not go to defining what may have caused the orthostatic intolerance to begin with. I hope that is clearer. I think I've got that part right. If not please chime in! Richard Sutton& and Tushar Salukha - Ivabradine in the treatment of orthostatic intolerance Author Affiliations International Centre for Circulatory Health, Imperial College and Imperial College Healthcare NHS Trust, 59-61 North Wharf Road, London W2 1LA, UK *Corresponding author: Tel: +44 207 935 1011, Fax: +44 207 935 6718, Email: r.sutton@imperial.ac.uk This editorial refers to ‘Single centre experience of ivabradine in postural orthostatic tachycardia syndrome’ by C. McDonald et al., on page 427. Attention was drawn to postural orthostatic tachycardia syndrome (POTS) in 1993 by Philip Low's team at Mayo Clinic.1 Postural orthostatic tachycardia syndrome has remained difficult to treat despite almost 2 decades of expanding research and recognition. The typical patient is a young female, 15–40 years of age, whose symptoms are usually multiple. In combination, the symptoms are very debilitating and those most common are fatigue, orthostatic intolerance, palpitation manifest as sinus tachycardia, oedema and discolouration of the lower limbs, and occasionally syncope. Two sub-types of POTS have been described. In the first of these, a primary neurological defect is present, possibly triggered by a viral infection. This defect takes the form of a partial autonomic denervation leading to excessive venous pooling in the legs and, sometimes, additional affection of the renal innervation resulting in a reduced plasma renin activity. The second sub-type is considered to have central sympathetic activation, termed the hyperadrenergic type.2,3 In 2005, a possible third sub-type was described that clinically presents facial and/or upper thoracic flushing, in some triggered by exercise, together with the typical symptoms noted above.4The explanation of the finding is postulated to be the release of a vasodilator from activated mast cells, supported by a raised urinary methylhistamine.4 These patients, as might be expected, may be worsened by beta-blockers but may respond to H1 and H2 histamine blockers with or without alpha-methyldopa. This third sub-type of POTS may present raised blood pressure at times in association with flushing and offer a differential diagnosis from phaeochromocytoma. This sub-type may only be a small percentage of those with POTS but, for them, there may be a specific therapy, anti-histamines not beta-blockade. For the majority, therapy remains incompletely effective. Contemporary therapy includes increased fluids and salt, support stockings, counter-pressure manoeuvres,5 exercise, fludrocortisone, beta-blockers, midodrine, pyridostigmine, octreotide, erythropoietin, and the inspiratory impedance valve.6 These have been well described in a recent review in the Journal.7 Combinations of these measures frequently offer a greater response. McDonald et al.8 implied the benefit in symptomatic terms for POTS patients from the use of ivabradine and may thus be pointing us a new direction. Ivabradine9 is a novel If channel inhibitor which slows phase 4 sinus node diastolic depolarization directly promoting bradycardia. The drug is approved in many countries for treatment of angina on an evidence base10 but, in the UK, it is currently not licensed for the POTS indication. By reducing or preventing the symptomatic sinus tachycardia, McDonald et al. have shown, in a retrospective case series, that control of one symptom is not only valuable in itself but might also contribute to resolution of others in this complex syndrome. In addition to the reported benefit in POTS, there may be some in vasovagal syncope from ivabradine therapy. In the original VASIS classification of vasovagal collapse patterns, an exception to the standard ones (mixed, cardioinhibitory, and vasodepressor) was excessive heart rate response, where the heart rate was >130 bpm just prior to collapse, in a few per cent of tilt-positive patients.11 At our centre, we see 1000 patients per year with orthostatic intolerance and currently have 20 patients on ivabradine therapy (10 with vasovagal syncope and excessive heart rate response and 10 with POTS). We use 5 mg twice daily in the majority and have found help in combination with midodrine in a few. Two patients have abandoned therapy because of lack of benefit, and side-effects have been minimal without serious visual disturbances. The remaining 18 patients continue therapy, with a maximum duration, to date, of 18 months. All have notable benefits in terms of palpitation and others of their symptoms. Now seems an appropriate time to consider a randomized controlled trial so as to provide, if possible, a firm evidence base for the use of ivabradine in POTS.

Hi, because of your daughters age she falls into the classic age group of patients being first diagnosed with pots, there is more research in this age group and it states that many in this age group recover. I hope that for your daughter. I also presented even younger then your daughter, though no one knew at the time, because I didn't tell anyone. I am now 55 and the cause of my pots symptoms are autoimmune and a defective immune system. So, it really depends on what may be causing it. Are her symptoms only a rise in heart rate on standing or does she have other seemingly unrelated symptoms that are governed by the autonomic nervous system. Like digestion issues, or sweating issues, or moisture issues, eye problems. You get the idea anything the autonomic nervous system does automatically for us. These are questions I would put to your doctor. Have they looked for any type of cause or done any type of testing to rule out other conditions that might be contributing. A real easy one that causes high heart rate is anemia, correct the anemia and the heart rate settles down. So the treatment depends on the cause. Many doctors right now are only treating symptoms, which is also good too, to calm them down. However if the cause is from something like mast cell, or autoimmune, etc, treating only symptoms means that the primary cause is not being addressed and the body will continue to decline, which is what happened with me. Only in the last 5 years have they been able to diagnosis and start treating me properly. What I have is chronic and not going away, but it can be managed. Also there are no perfect medicines out there many have unwanted side effects. So you have decided what you will tolerate and what you won't. Some on the forum have decided to live with it as is, because they couldn't tolerate the meds. I tolerate most of my meds pretty well now, after a lot of trial and error. Everyone reacts to meds differently, so the only way to know is to try. I think sometimes we may give up on a med to soon, as sometimes the symptoms will dissapate as the body gets used to it. But if after a fair run like 3 months and side effects still aren't tolerable, I'd talk to my doctor and try something else. Though there are some side effects where you should stop the drug immediately, you need to ask your doc and pharmacist about them. Hope this is helpful and this is just my opinion.

Thanks futurehope for the heads up. I have trouble with my knees when stepping down. Where I have trouble probably due to car accident injuries is my right hip and si joint going into spasm and the bone where my neck meets my shoulders the big one sliding out and causing my whole neck an shoulder into spasm. Yes, sue I agree that there may be something else causing those specific muscles to be weak, since the others in spite of no exercise are still pretty strong. I do have hashimoto, hypo thyroid, but my endo said that it was hyperthyroid that causes that type of weakness. With sfn though I also wonder if this may be some large fiber damage. I've never had emg on those muscle groups. I do to have cushing like symptoms as a result of PCOS/metabolic syndrome caused by high insulin. My cortisol is normal and cushings was supposedly ruled out, though I did have a stim test that pointed to addison's the follow-up tests were normal. I don't know that the parathyroid has been tested for or ruled out yet, I will have to talk with my endo about that. I guess I'll have to wait and see how I respond and if the weakness improves to figure out if it is decondtioning or something else. I'll post the stuff that helps down the road.

I know we shouldn't be happy when something comes back abnormal, but we know we aren't right even when tests come back normal. So I'm so happy for you that you've found another piece of the puzzle which may lead to effective treatments. I think as the research evolves they are going to find that all this different autoimmune diseases have more in common then they don't and that they effect many more body systems then previously realized. I think there is a mast cell doctor up in your area somewhere. Members if you know one let julie know.

That was beautifully said futurehope! Dr.Grubb prescribed exercise for 20 min 3 x a week for me. The main reason being that strengthing the muscle pumps in the body is a back up system to get blood to the brain. Keeping the muscles strong provides some added assistance. I think that is why when I was younger I was able to function better then today. I had always been in gymnastics or dance. However knees up exercise like in aerobics or stepping uphill would trigger those dramatic episodes where I would collapse. I have not been able to accomplish an exercise program in recent year there were a few attempts with PT's who didn't understand what I had and caused muscle spasm and flare ups, so I gave up. How ever my neuro said lets try again and sent me to his to his PT that specializes in neuro diseases. I had my evaluation this week and low and behold I was weak exactly where I thought in the top mid part of my thighs and the same location in my upper arms. I was very strong though in my other muscles groups. So the muscles you use to climb stairs and stir a pot or clean the windows. Because of the orthostatic issues he is sending me to pool therapy with specific exercises to strengthen me where I am weak. I will mention Levine's program next time I see him. I'll let you know how it goes and what the exercises are once I find out. I'm not ready to give into this yet either. I may be 55 now, but I still feel like a girl in many ways and long for my dancing days.

I might have been tested for one of those but not the mayo panel. There is no doubt that my pots is a result of autoimmune defects.I had a very high ana many times many years ago was the first marker, went neg for awhile but became positive with the onset of hashimoto. With ana's today they don't just look at the number ratio they also look a type of pattern. The patterns will point to different autoimmune disease states. I am getting immune modulation in the form of ivig, but there are other biologics now, say for lupus as an example. This area of treatment is really starting to evolve and hopefully will only improve with time. That is good news for the younger ones among us. Northwestern is actually doing stem cell transplants with several autoimmune disease. I know one nurse who's wife got rapid onset schleroderma and last I heard after the treatment it still hasn't come back. Another patient with polyneuropathy was accepted, but insurance issues got in the way. I do think there is hope for the future.