A riff on Dr. Peter Rowe’s presentation at the 2020 Dysautonomia International Conference (note that I expand on many of Rowe’s points; i.e. not all the words are his.)
Dr. Peter Rowe has been around – and has a lot to say. (From the Solve ME Initiative)
Lauren Stiles, the founder of Dysautonomia International, has long believed that the chronic fatigue syndrome (ME/CFS) and dysautonomia fields (POTS, in particular) are way too siloed. It was only natural, then, to bring a researcher and doctor who’s been immersed in both – Dr. Peter Rowe – to talk about ME/CFS at the 2020 Dysautonomia International Zoom Conference.
What you get with Dr. Peter Rowe – who has led the Johns Hopkins Children’s Center Chronic Fatigue Clinic in Baltimore, Maryland, US, since 1996 – is decades of being immersed in ME/CFS/POTS/EDS (and, given his intellectual curiosity, probably other things). In other words, you get a boatload of knowledge. If more people would have just listened to Dr. Rowe, we wouldn’t have had this CBT/GET problem for all these years..
Boy, have I felt like a minority (a forgotten minority) with all the focus on post-infectious illnesses going around. It was good to hear, right off the bat from Dr. Rowe – since I do not have a post-infectious onset – that a gradual, or insidious, onset is found in about 40% of people with chronic fatigue syndrome (ME/CFS).
A Little History
Rowe noted that Peter White, one of the most prominent CBT/GET proponents (and the lead author of the 2011 PACE trial), has asserted that orthostatic intolerance (OI) is only rarely found in ME/CFS. And that UK treatment guidelines or CBT make no mention of testing or treating OI.
Talk about occupying different worlds. While ME/CFS experts regularly test for and treat orthostatic intolerance, the UK government’s official stance is that it basically doesn’t exist in this disease.
Back up – says Rowe – who apparently has an interest in medical history. “Orthostatic tachycardia”; i.e. an alarming rise in heartbeats upon standing (i.e. today’s postural orthostatic tachycardia syndrome [POTS]) was identified back in the 1940s. In fact, with four publications in 4 years, orthostatic tachycardia was kind of a thing. Unfortunately. after its main proponents (Yuskis and Griffiths) stopped publishing on it, the field almost died. For over 30 years, a paper would pop up every now and then (including one on orthostatic tachycardia in chronic Chagas disease – which is caused by a parasite), but that was it.
Coining the term postural orthostatic tachycardia syndrome (POTS) in 1982 didn’t help much either. It was not until the early 1990s that the field started to take off – almost fifty years after the problem had been identified.
Rowe pointed out that the disease actually had even earlier antecedents. Way back in 1924, Dr. William Porter of Roanoke, Virginia in “Effort Syndrome, Its Clinical Course” (you can still get the paper :)) described a disease characterized by shortness of breath, fatigue, palpitations, giddiness and fainting attacks, and a rapid pulse that was accentuated by exertion. Porter noted that earlier manifestations of the disease showed up as “soldier’s heart” and, in perhaps the most precise description, “irritable heart”, during the Civil War.
Various causes (heart diseases, lung problems, tuberculosis, thyroid problems) had been assessed and discarded. In his own study of 80 patients, Porter found, “The relation of acute infection in the production of the initial symptoms of “effort syndrome” appears most striking”. Porter ended up concluding, though, that getting a diagnosis of heart abnormalities after an infection caused the patients to focus too much on their hearts; i.e. they had either a psychoneurosis or anxiety neurosis! (This was after noting that some patients probably did indeed have an “autonomic imbalance”.)
Doctors were interested in blood flows to the brains in the 1890s. It took until 2020, though, to document the widespread reductions in blood flows present in ME/CFS.
By the nineties, though, things were definitely moving fast in a different direction. Rowe’s tilt table studies demonstrated that a drop in blood pressure (neurally mediated hypotension (NMH)) could, at times, be responsible for many of the symptoms some people with ME/CFS experienced during standing. Twenty-five years ago, Rowe’s 1995 journal article demonstrated that the blood volume and pressure enhancer fludrocortisone could be very effective in chronic fatigue syndrome patients with NMH.
Rowe later said that after the publication of that article “We got 5,000 phone calls in the next week. I had never experienced a response like that before—we got a very clear indication there was a huge unmet need in the population.”
Rowe noted that recently our understanding of how prevalent orthostatic intolerance is in ME/CFS (and possibly fibromyalgia) has changed dramatically. In what will surely come to be judged as a seminal paper in the field, Visser, Rowe and van Campen and Verheugt used new technology to demonstrate that virtually everyone with ME/CFS – whether they’ve been diagnosed with POTS or NMH or not – experiences a significant reduction of blood flows to the brain upon standing or sitting; i.e. virtually everyone has some form of orthostatic intolerance. (Even ME/CFS patients without POTS had a 24% reduction in blood flows to the brain.)
Studies indicate that cognition is, not surprisingly, affected when less blood than usual makes it up to the brain. The tilt table test (TTT) where patients are strapped to a table and then tilted (to remove any help from their muscles) has become the orthostatic equivalent of a maximal exercise test. Visser et. al found that a single tilt table test can increase cognitive problems for a week in some individuals.
Rowe noted that the orthostatic intolerance was there all the time, but we just didn’t know how to look for it. (Here’s hoping that an enterprising researcher starts looking for it in fibromyalgia.) Peter White, in other words, couldn’t have been more wrong.
The Exercise Conundrum
Exercise has always been a tricky subject in OI because a lack of activity can exacerbate it or even cause it. It’s taken quite a while to show that while physical inactivity certainly does exacerbate the OI in ME/CFS, it doesn’t – as White and others in the CBT/GET field have believed – cause it. The Visser/van Campen/Rowe team showed that low blood flows to the brain are present in ME/CFS whether patients were deconditioned or not.
Everyone, of course, wants to exercise! Prior to ME/CFS/FM, I used to flog myself physically several times a week and felt great doing it.
Lauren Stiles asked given the very different prescriptions for exercise that show up in the POTS community and the ME/CFS community what does Dr. Rowe recommend for people with both ME/CFS and POTS.
My apologies to Lauren for getting her question wrong in an earlier version of this blog.
Dr. Rowe believes that improving your orthostatic intolerance should improve your ability to tolerate exercise.
Before we get to Rowe’s answer, let’s look at ME/CFS. There’s a reason that the term post-exertional malaise (PEM) was coined in ME/CFS and not POTS or fibromyalgia (or any other disease). There’s a reason why so many more exercise studies have been done in ME/CFS than POTS or FM. There’s a reason why the two-day exercise test protocol showed up in ME/CFS. There’s a reason why Workwell and Nancy Klimas have both developed heart rate-based exercise programs in ME/CFS. All the evidence suggests that the exercise intolerance found in ME/CFS is simply more extreme than in these other conditions.
There’s also a reason why Dysautonomia International conferences are populated by a very different group (predominantly young women) than you see in ME/CFS conferences. While there is overlap, the two conditions have some real differences.
Rowe stated that there’s been such a reaction to CBT/GET protocols which had you get out and push, push, push has left some people believing that exercise of any sort is bad for you, and he believes that is a bit counterproductive. Noting that we have to be very sensitive to how people are doing Rowe noted that “we have to support their circulation and allow them to be more active.”
But how to do it, though, in this supremely exercise-challenged disorder? Rowe Rowe has a general prescription – if you can find a way to improve your orthostatic intolerance, your ability to exercise may increase. (The obvious adverse to that not being able to improve your orthostatic intolerance is a different story.) The goal then is improve your orthostatic intolerance, and he gave several examples of how that’s helped with his patients.
Drugs
One of his patients who was feeling better on fludrocortisone and atenolol started doing just 3 minutes on a reclining exercise bike – the only thing that didn’t make her lightheaded and flare her symptoms.) Showing great discipline, she slowly increased her time and within 2 months, she was up to half an hour a day. Both Rowe and Stiles emphasized starting very slow.
One 22-year-old’s heart rate boomed to 180 bpm when she tried to exercise (setting off a migraine to boot). Even her resting heart rate (104-140 bpm) was quite high. The ticket for her was Ivabradine – a drug that’s made quite a splash in the POTS community. After Ivabradine, she was able to hit the elliptical trainer for 30-40 minutes and hike for ten miles. Rowe emphasized that without ivabradine she simply could not exercise – she had to have her medical problems addressed first.
At the 2018 Dysautonomia International Conference, Dr. Blair Grubb was effusive about the effectiveness of Ivabradine (or Corlanor) in POTS, stating that it worked in 75% of POTS patients. Since then, several Ivabradine studies have been published. Health Rising will have an update on this intriguing drug soon.
Resolving Movement Restrictions
Dr. Rowe discovered that resolving muscle and tendon constrictions was “incredibly helpful” and “a good bridge” to tolerating more activity. In a 2014 interview, Rowe reported that:
“In the clinical care of those with ME/CFS, we have observed that the manual forms of physical therapy have been quite helpful for improving overall function, especially when people had not done well with exercise-based therapies alone. The exercise ended up being “too much, too soon.”
“After the areas of restricted movement have been treated, people find that they can tolerate gradual increases in exercise without as much post-exertional worsening of symptoms. This then allows them to obtain some of the expected benefits of regular exercise.”
He suggested that the original inciting factor – infectious mononucleosis, or other problems – might create “adverse neural tension” which could lead to “increased noxious input to the nervous system”; i.e. increased pain signals slamming the nervous system. He suggested that “neuromuscular strain would be expected to lead to … altered pain signaling, fatigue, and autonomic nervous system changes.”
Connective tissue problems which create lax ligaments may play a role. The connective tissue problems seen in joint hypermobility, Ehlers Danlos Syndrome (EDS) and sometimes ME/CFS may be putting pressure on the nerves causing them to act up. At the same time, they may causing the tendons to tighten up in order to compensate.
Given the possibility that the nerves in ME/CFS/FM/POTS may be under increased “load”, it’s interesting that BDNF – a nerve growth factor implicated in chronic pain – has been found in both ME/CFS and fibromyalgia.
Rowe said he worked hand in hand with his physical therapist (PT), Rick Violand. As Rowe addresses orthostatic intolerance with drugs, Violand works on the movement restrictions found. Together they produce more than the sum of their parts.
Rowe noted that PTs trained in manual techniques, osteopaths who perform mostly manual therapy, and others should be able to help ease movement restrictions and restore normal movement. The manual treatment techniques they’ve found to be most helpful include using combinations of neural mobilization, positional release, myofascial release, and cranial work.
Rowe noted that some of the manipulations – including ways to release myofascial trigger points – can be done at home. Check out how a myofascial trigger point therapist addresses the pain and fatigue in ME/CFS and FM below.
Stimulants and vasoconstrictors that help with cerebral blood flows can be useful as well.
Rowe noted other factors that need to be assessed including mast cell activation syndrome (MCAS), protein hypersensitivity, movement restrictions, anxiety, depression, neuroanatomic factors and others.
Dairy Watch
About that protein hypersensitivity. Rowes found that about 30% of pediatric patients have milk protein intolerance. It appears that the mono that often set off their ME/CFS/FM/POTS reverts patients’ immune systems back to a childhood state when they had colic. The impact of dairy is so powerful that Rowe has found that if that isn’t treated, none of his other treatments will work.
Neuroanatomic Factors
We’re most acquainted with craniocervical instability (CCI), but in a report that Rowe worked up for publication, he showed that spinal stenosis, too, can at times mimic all the symptoms of ME/CFS/FM. Fixing that problem in one patient returned her to health – she’s now rock climbing. Doctors, Rowe, asserted must do careful neurological exams.
ME/CFS, OI and the COVID-19 Long Haulers
Then it was on to post-COVID-19. Rowe described a 30-year-old scientist who, two days after being infected with the coronavirus, was lightheaded. On the 5th day, he lost his ability to taste and smell, and was experiencing tremendous fatigue. By day ten, this scientist couldn’t make sense of the numbers on his bank statement.
Upon testing him after five months of rest, Rowe found that his heart rate went up 77 beats per minute (bpm) upon standing and hit 160. Anyone with severe fatigue after COVID-19 needs, Dr. Rowe asserted, to be assessed for orthostatic intolerance.
One young man who was running was 60-70 miles a week, now has trouble standing.
The Gist
- In an attempt to bridge the often too-wide gap between ME/CFS and dysautonomia research, Dr. Peter Rowe spoke at the Dysautonomia International Zoom Conference this year on ME/CFS.
- He noted that Dr. Peter White apparently asserted at one point that there was no orthostatic intolerance in ME/CFS.
- That was rather confusing to Rowe who’s been treating OI in ME/CFS since the mid-1990s.
- Rowe noted that references to an ME/CFS-like POTS condition actually date all the way back to the Civil War and in the 1920s to “Effort Syndrome”. POTS was first clearly described in the 1940s, and named in the 1980s, but it was not until the mid-199’s that research started to take off.
- In the mid-1990s, Rowe noted that in some cases the symptoms of people with ME/CFS and orthostatic intolerance could be completely resolved using drug therapy.
- The biggest orthostatic discovery of all occurred this year. Using new technology, Rowe, Visser and van Campen found that the reduced blood flows to the brain upon standing (and therefore orthostatic intolerance) are present in virtually everyone with ME/CFS.
- Rowe proposed that one way to enhance one’s ability to exercise is to treat their orthostatic intolerance. He provided reports where drugs like Florinef and Ivabradine, spinal treatments that resolved spinal stenosis, and certain physical therapy techniques that are able to resolve movement restrictions, have all dramatically enhanced ME/CFS patients’ ability to exercise.
- Rowe also reported on several post-COVID-19 cases where formerly healthy people quickly developed orthostatic intolerance. He asserted that every post-COVID-19 case should be assessed for OI.
Conclusion
Drawing on years of knowledge and first-hand experience, Dr. Rowe reported that, contrary to the opinions of some biopsychosocially oriented researchers and doctors, orthostatic intolerance is not just common, but is likely the most common condition found in ME/CFS.
The road to uncovering that was a long one. One could argue the pieces were present in the 1920s with “Effort Syndrome” which was dismissed in an overview as a kind of anxiety disorder. In 1948, POTS first showed up in the scientific literature in the form of orthostatic tachycardia but interest was intermittent until the mid-1990s.
Studies in the mid-1990s demonstrated that orthostatic intolerance was present in ME/CFS, and at times, could be treated quite successfully. Just this year the Visser/van Campen/Rowe research team used new technology to dramatically redefine our understanding of orthostatic intolerance in ME/CFS. They showed that orthostatic intolerance – in its most basic of terms (reduced blood flows to the brain) – was present in virtually every person with ME/CFS.
How to safely exercise is a huge but important issue in ME/CFS, in particular given the circulatory boost it provides, and the many bad things that being inactive exacerbates. But how to exercise in a disease which is defined in great part by issues with exertion?
After noting that most patients given exercise programs have tried to go too far too fast, Dr. Rowe asserts one’s ability to exercise may be able to be enhanced if one can successfully tackle, or at least partially tackle, their orthostatic intolerance issues. He shows that providing the right drugs, or ameliorating the movement restrictions present, or by resolving anatomical issues, has, in some patients improved their ability to exercise.
Finally, Dr. Rowe reported on several, formerly healthy, post-COVID-19 patients who have developed orthostatic intolerance.
BIG (Little) Drive – For a Big Topic
Thanks to the over 280 people who have contributed to Health Rising in the past few weeks 🙂
We say we’re covering ME/CFS/FM, but that is a lie. The truth is that covering those conditions also means covering postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), spinal stenosis, craniocervical instability, chronic lyme disease, post-COVID-19, migraine, mold sensitivity, environmental illness (and I’m sure I missed a few). An upcoming blog is going to dig into how concussions can contribute to these illnesses. It’s a huge field that seems to be getting bigger by the day. We’re trying our best to cover it all. If you appreciate a wide-screen approach to these illnesse, please support us.
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I have addressed OI with drugs, elastic bandages and oral rehydration solution, my BP is normal, my heart rate is under control 99% of the time, my BDNF is normal, I don’t eat dairy… Yet I have severe ME/CFS, severe dysautonomia and I am constantly deteriorating. None of that helped me have more energy, let alone exercise.
I have religiously been “exercising” my legs from the moment I became bedridden to avoid blood clots, and not only did it not improve my dysautonomia but it has gotten worse.
I used to have PT come for passive PT and I liked it but just having her in my room, touching me and talking to me, would crash me for days. I kept on deteriorating.
I can see they are slowly making progress in POTS, OI, and dysautonomia without ME/CFS, but I can’t help but feel they still don’t know a thing about how much exercise is detrimental for ME/CFS.
I’m sorry that nothing has really worked for you. While some things help some people the sad truth – which is not stated nearly enough – is that we just don’t have the therapies to help everyone. His remarks regarding exercise were couched – if you can improve your orthostatic intolerance – that will help you exercise. Since you obviously can’t do that – then it’s no surprise that you’re not able to exercise.
There are so still many questions unanswered unfortunately – too many people who don’t benefit from anything no matter how hard they’ve tried. You’ve obviously tried really hard. Hopefully more things will show up. I don’t know if you’ve tried Ivabradine but it’s getting a lot of interest.
Sorry I wasn’t clear, I did improve my orthostatic intolerance. With combination of medications, increased fluids and elastic bandages.
But my ability to exercise did not increase.
To accuse even some ME/CFS sufferers of over-reaction to CBT/GET is without evidence and dangerously disparaging.
When Peter Rowe – who has been treating ME/CFS patients since the mid-1990’s says something – it is not without evidence. How could that be without evidence? He has 25 years of evidence.
I would note as well that Peter Rowe, as much as anyone, has worked on refuting the damaging beliefs left behind by CBT/GET. He’s worked on large exercise and orthostatic intolerance studies which have done just that.
When Rowe states that removing muscle restrictions or fixing spinal stenosis- or adding Florinef to a patient who then started doing three minutes of exercise a day who then worked up to 30 minutes – he’s speaking from experience. I wouldn’t have thought ANY of that was possible but that’s his experience. I imagine that the Florinef patient wouldn’t have tried that without his suggestion.
You certainly have a point that it didn’t work for you but I don’t think what he said was disparaging. Some people are always going to go too far in any direction. That’s just human nature. I can’t remember who, but someone said 75% of us are doing too much and 25% are doing too little. That doesn’t leave much room for those who are doing it right (lol)
1. I am aware he’s one of the good ones, and did useful things for ME/CFS community, but that does not make him immune to mistakes, nor should it shield him from criticisms when he makes unfounded accusations that could be used against us.
2. Where is that evidence that some people over-reacted to CBT/GET? We have been accused of fear of exercise for too long without any evidence. It’s time to stop, no matter whose mouth it came out of.
3. Seeing one person improve here, another person there, is not evidence, it is a case report. And a clue in which direction to go look for the evidence.
4. “if you can find a way to improve your orthostatic intolerance, your ability to exercise will increase,” is a generalized statement that makes it sound like it applies to everyone and is always true. Yet it clearly isn’t so.
@Neunistiva:
Would you have by chance bad morning nausea taking hours to clear and it being at worst close to what I call “sleep poisoning”?
Of course everyone makes mistakes. There’s a natural emphasis on showing success stories. Not everyone works out as well as the patients Dr. Rowe mentioned. I know of some people who he’s treated who have not. I think that often gets lost.
We would all love to be one of those people. Hopefully we all will be at some point. For now, I think they present possibilities and for many of us options.
Rowe, himself, noted that we don’t have stats on how many or how much patients improve – and so we are relying on case reports. I just didn’t get that in there.
It may be that I stated this “if you can find a way to improve your orthostatic intolerance, your ability to exercise will increase” too bluntly. I was working from notes – not from the actual presentation. I’ve amended it to say “your ability to exercise MAY increase”. I think that’s more accurate. I apologize to Dr. Rowe if I overstated anything he said.
Ah, I thought those were his exact words. I understand how difficult it is to retell someone else’s talk, especially for us, don’t worry about it.
I’m fine with him highlighting success stories, and everything else,
I just still have huge issue with: “Still, is it possible that a backlash against CBT/GET has gone a bit too far at times? Rowe stated that in some cases, an over-reaction to CBT/GET has left some people believing that exercise of any sort is bad for you,”
It anything backlash hasn’t gone far enough. Countless people have been permanently harmed, and there is no evidence that there are people with ME/CFS who baselessly believe any exercise is bad for them. Especially not to the point where it would be worse for their health not to exercise.
I finally got the video. My apologies to Lauren Stiles for getting her question wrong – she simply asked, noting the differences between how POTS and ME/CFS patients and doctors approach exercise – for Dr. Rowe’s recommendations. I also apologize to Dr. Rowe’s talk for mischaracterizing part of the Q&A section. In particular he did not say “over-reaction” – he said “the reaction” to harmful CBT/GET regimen – which is a very different thing indeed.
Thanks Cort, for the note of correction. That makes it much more reasonable than what seemed to be implied before.
But one note…….POTS people with or without ME/CFS have issues with PEM and fatigue. Some POTS people faint the second they try to sit up. They have to be in a reclined wheelchair and cannot be upright. Some are totally bed bound and can’t raise up at all. So, I wouldn’t say that either is worse or better than the other. It just depends which aspect of it you are talking about. And there are many people less likely to be able to exercise, despite determination and trying. Those of us that can get more functional and are able to have some quality of life, feel we got the greatest gift available and a blessing. (There are some nice “purple bandaids”?, we just have to find them.)
POTS people also have severe fatigue. If your heart is going near 160 beats a minute every time you stand up and you get dizzy, naseau and near faint…..you can see how that and the adrenal surge and anxiety that causes can be exhausting. But having both ME/CFS and POTS, is really no ride in a Park, I can vouch for that.
Yes, indeed Issie. One the speakers at the conference noted how often exercise therapy fails in POTS. The symptoms of the two diseases are almost identical – which come to think of it – if reduced blood flows to the brain play a fundamental role in both.
Try a power plate vibrating platform.
Have you ever looked into cervical instability or cervical compression? There is definitely correlation between these and dysautonomia, I am one of those rare patients. This is something treatable with surgery and is worth looking into. Disc compression into the spinal cord or areas around it can cause dysautonomia
Makes so much sense I have EDS – CCI- Stenosis and when I got reactivated mono I got so very ill!
Maybe it whacked your connective tissues. I think this is going to be a big issue….I think something was just found in EDS regarding this…
I have had seven viral episodes (or severe immune responses to viruses),the first in 2002 and within 6months was diagnosed with sub acute thyroiditis. Was prescribed prednisone after which I had shortness of breath and prescribed symbicort. Within one month I had second episode in 2004 . I had further episodes, 2007-2012-2013-2013-2014 and with each episode I became weaker. Corticosteroids I think played a part. ANCA test positive for Vasculitis and also noted my Hb – Rcc- Hct rise notably from 2003 thyroid blood test and 2004 episode, and kept rising. Blood pressure did get lower as CFS worsened. EBV serology IgM was negative 2014 in 2018 IgM was positive, follow up PCR EBV DNA in 2019 DETECTED, below 500 copies/ml. Have just been diagnosed Chronic Active EBV by Infectious Diseases Specialist. Could there be more than EBV? Viruses, immune response, inflammation blood vessels,thick blood,Sticky Red blood cells,Narrowing of blood vessels and capillary,poor micro circulation and oxidative stress problems.
@dejurgen No, no nausea in the morning.
Only time I would get nausea was several years back when I was not on any medication and I would stand up right after waking up (time of day didn’t matter). I didn’t understand what was going on but I would get nauseated from tachycardia.
However, I haven’t felt any nausea for years.
I’m like you, Cort, I too had a gradual onset into ME/CFS. My ME/CFS is still progressing gradually, as I am aging. That has been the course for over 45 years now. I’m one who has had partial remissions now and then, does that hold true for you?
I’ve actually never had partial remissions…it’s been a pretty steady state for me except for some declines in the last two years.
Sorry Cort! You and I being same age, doesn’t help that we continue to have another year on us. Now, let us find you some ? bandaids!
Hang in there! Keep up the good work, you are much appreciated!
Great article I suffer from M.E fibromyalgia and pots ,the dizziness occurs on standing up , owing body a diffrent direction or heavy coughing, my last episode I fell unconscious and slammed my head of a chair , were my wife found me.
The intresting article on dairy is aslo an eye opener, I have in the last year become intolerant to lactose, gluten, egg protein , and refined sugars , any of these substances pass my mouth I m in a world of pain.
I also suffer from vitiligo and as my immune response ramped up I have lost all pigmentation to my body .
So defiantly an immune response goin nuts.
In regards to excercise , and I class myself as moderate to high sufferer , I find that a low graded excercise program works for me , the key is finishing the balance and slowly increasing this over months , I swam 2 lengths of a pool at first by 1 year in I was up to 30 , this allowed my body to gradually fell both physically better but mentally as well.
I combined this with mental health therapy for a year weekly
This was not CBT but it allowed me to address my illness my sense of loss (I was an extreme fit active guy) and my family , this allows the depression to be managed which also improved my health .
7 years in and still not working but have got some life back and better we’re I am To we’re I was .
Great stuff C.
Cort,
did Dr. Rowe discuss what his diagnosis ‘flowchart’ looks like?
did he feel serial tilt table tests over time are effective in showing response to treatment ?
does Dr. Rowe base tilt table test on whether test can be afforded by patients, or is it something he feels/believes/knows should be done on every patient?
what were his parameters on tilt table test?
…….especially if some have low cerebral blood flow, but do not show up on tilt table test?
did Dr. Rowe mention any new and minimally invasive test that can show decreased blood flow definatively —-that could be ordered by treating physicians?
is there a wearable sensor that combines real time heart rate readings and blood pressure readings and body position/activity?
@sunie, Mayo clinic did a test on me when I got my HyperPOTS DX. They try to sort out anything connected to POTS as there may be a way to tweak some dysfunctions if they are known. The test puts blood pressure cuffs on your ankles and thighs and seems there were some electrical connections too. (Long time ago.) It measures your blood pressure in those areas and the size of the limbs with lying and standing. Somehow, it then calculates if there is blood pooling in your legs. They can tell by the changes I guess. They determined I had low blood flow and blood pooling.
For HyperPOTS they did a catecholamines test on me. Both lying and standing. It has to be handled correctly and immediately put on ice for it to be accurate, they told me. But my lying was slightly over 200 and standing almost 900. If it goes above 600, that puts you into the HyperPOTS category. Then they check you for adrenal tumors. This is high norepinephrine levels that they check. All POTS people have more with standing. But not all have that much more. Some go even higher than I did. It feels like (one of my old POTS “friends” described perfectly) being locked in a room with a hungry lion and having no way out. For me, no adrenal tumor.
I had told Dejurgen I wasn’t going to comment on this blog as it upset me. My having been around through early discovery with POTS and with lots of wrong ideas and treatments. I’ve seen and heard a lot. Same as with ME/CFS community, POTS has been badly handled at times. And apparently that is still ongoing according to what I read on this blog. I do hope he/Cort “didn’t get it all right”, as he said with his notes. Because it would make me sad to think these “old ways of thinking”, still exist. With science proving otherwise. There are so many “reasons” for one to have POTS and OI or any other number of Dysautonomias. Doing blanket statements of “exercise will fix this, you are all deconditioned “, flatly puts the blame on those not being ABLE to exercise and “causing” their own dysfunctions. We are deconditioned, but what came first?
Mayo Clinic had this as an idea, I’m not sure if they still do or not. But they started what they called a “boot camp” for children with Dysautonomia. They had parents put their children in this program for months to have them do graded exercise to “fix” their POTS. For some it was successful….to a degree. For others it was not. And was about like that PACE thing in the UK.
Then about that time, they said we all had too small hearts. There was a study of 19 POTS people and all had smaller hearts than controls. They also said that exercise would “fix” this. They called our illness “Grinch Syndrome”. (Well that didn’t set well, now did it.) Not all of us have too small hearts. In fact some larger, as it beats so much with tachycardia we should have athletic hearts. There was an uproar in the POTS community over that one.
I do agree, we need to move. And we especially need to move our legs as the pumping of our legs muscles will take some strain off our hearts having to do it all. But that can be done sitting, if need be. Something simple as bouncing legs on an exercise ball, helps. If one can walk, even better. We have to get our blood moving to help our heart and brains to have enough blood and oxygen. But don’t expect to be a marathon runner. Especially those of us with EDS and issues with collagen and holding us together. We stay tense and tight all the time, to hold ourselves into place. Else, we get vertebra out or shoulders out or knee dislocations. Or hips popping out of socket. We have to use good sense in what we do! There is NOT a one size fits all solution.
Which brings me to Florinef. I cringed when I saw that part. Not all of us can use that. I have issues with my kidneys. Some POTS people do. I have very low renin and aldosterone. I looked up what the doctor had written on me and his suggestions so I’d get it right. He said I have vasoconstriction issues and that is what causes my higher blood pressures with my POTS. I am NOT to use extra salt. And not to try to hold onto more salt at the kidney level due to having very low renin and aldosterone. (What Florinef does.) He said we have to approach me in a different way. He said normally with low renin and aldosterone they would use heavy amounts of diuretics. But with me with low blood volume and POTS, that was impossible to do. So we just have to address vasoconstriction with me. I had already found that to be the case as the Florinef and salt loading was most horrible for me. And Middodrine to vasoconstrict even worse, and was one of the worst experiments I ever did. (One of my POTS friends can vouch for that, as he and I trialed it together. He didn’t do so well either. But I got extremely cranky. Guessing less blood and oxygen to my head. Severe anxiety.)
So point is……a lot of the “traditional” POTS protocols, don’t work for everyone. Know your subset type. Know what your body is doing. Don’t trust that what is a “normal” treatment will be for you. Know what long term consequences of those treatments will be. And figure out, is the “symptom” you are having a compensation to something far worse. Should it be stopped, or is your body trying to “save” you? Know your WHYs!!!!!
Thank you both, Issie and Cort, appreciate you both taking time to answer Q’s.
Issie, you have cautioned me—thank you—you wrote enough that it is an eye opener for me
and also shows how hard it is for docs to help when there are limitation on tests they can run….. and harder for us too.
I hope 2021 is the year of redress for you.
My hopes are increased that Bhupesh Prusty and group are narrowing in on parameters for their test—
and Ron Davis are running meds through their system to see if any effective.
Two parts to the solution, imo, will be establishing from cfs/me independents a form that is all inclusive for doctors to complete and send to the patient’s insurance providers, and/or gov. service providers. For two big reasons—-one, so nothing is missed that is needed (doctors are not lawyers, so lets make it easier for them)
AND—-two, to give insurance/pertinant companis/gov. consistent, well constructed info, so layout in itself provides a logical read. So that consistencies in symptom and test results become more meaningful for decision purposes.
(This CFS/ME FM POTS Dysautonomia form’s inclusive, in depth , and consistent layout may have strong benefits.
Constructed to usefully and accurately define an individual’s disabilities in these invariably ‘variable’ diseases, it should be useful for doctors dealing with patients havingbmany other serious diseases.
No diagnostic flowchart that I remember / nothing on serial tilt table tests/or affordability. If you check out the blog that is featured in that section of this blog it will provide some information on cerebral blood flow test. It’s not readily available as this was the first time this kind of technique was used. Dr. Rowe believes it’s used will spread, though.
I’m not an expert on wearables but I would be surprised if anything able to that was available commercially. I wonder if the Bateman Horne Center is or has incorporated those readings into its tool that measures upright activity. That would be cool.
There is a test for measuring blood flow to the brain, and although it is not widely available, it is spreading slowly to autonomic labs. It is called transcranial Doppler and it measures cerebral blood flow velocity. It is non-invasive and consists of a headset that the patient wears during testing.
Dysautonomia International gave out grants for more to be set up. Here are the recipients:
Tae Chung, Johns Hopkins – has an interest in exercise rehabilitation
https://vimeo.com/483090164
Melissa Cortez, University of Utah – has an interest in headache and migraine
https://vimeo.com/359102751
Nate Robbins, Dartmouth Hitchcock – neurologist
https://www.dartmouth-hitchcock.org/findaprovider/provider/2145/Nathaniel-M-Robbins
Satish Raj, University of Calgary – cardiologist with lots of POTS research under his belt, frequent speaker at DI conferences
https://vimeo.com/589514511
Some hospitals now have a transcranial Doppler device and are using it for other conditions, such as stroke. If you have a specialist with good connections at such a hospital, they may be able to organise combining the transcranial Doppler with a tilt table test.
Finally, there’s a wearable sensor coming out soon-ish that will track heart rate and blood flow to the brain. Cort has just written an article on it. It is registered as a wellness device, not a medical device, so is for personal monitoring rather than diagnostic use.
the more supplements I try the more I’m starting to think that iodine may be an underlying cause of all our sh*t, 5 out of the 14 I’m on now are or contain it, and since it’s closely linked to potassium, which of course you know deals with blood pressure, POTS could be 1 of the indirect consequences…
Cort-thanks for standing up for Dr. Rowe. If there are relative newbies reading this, they can be helped with this “heads up”. I was not getting any help until I found Dr. Klimas’s video advice and learned to take my own BP and HR measurements. I then presented 10 days of data to a cardiologist who diagnosed POTS. However, she told me medication does not work for POTS. My D.O. then found a 25 page paper of Dr. Peter Rowe concerning possible courses of medication with specific dosage advice and started medication for me. I got 3 minutes of standing time as a result and ability to stay upright walking for a block.
Dr. Rowe is the best when it comes to POTS – he has been researching it and treating it (pediatrics) forever.
He also happens to be very kind, always making time to help patients, presenting at conferences.
I hope his recent paper translates to clinical medicine soon. It’s a stunning finding.
I posted earlier comment on how my CFS began and progressed with each viral episode and severe immune responses, seven in total and weaker after each one. Also became worse after prescribed steroids. As I said earlier I have been diagnosed Chronic Active EBV by PCR- DNA test, but I am not sure if it is the only active virus. I believe active viruses are the cause of ME/CFS but most serology testing is not reliable (sensitive enough). Before the PCR test I had EBV serology and when the IgM came back negative the doctors said you didn’t have EBV active, but when the IgM came back positive the pathology report said equivocal, must be false positive and the doctors said the test is unreliable. They seem to want it both ways! I think the only way to be sure is to have PCR-DNA test for all HHViruses and CMV. People may have different viruses active together giving different symptoms. Investigating the multitude of symptoms only confuses the issue. I am sure my CFS is the result of active virus or viruses with an immune response causing inflammation and affecting blood and blood flow (immune response, antibodies makes blood sticky) and having a major problem in micro circulation and removal of oxidative stress. I am from Australia and it took years to finally get a PCR- DNA- EBV test and diagnosis for which they say there is no treatment. If there is no treatment for the virus/viruses maybe medications for inflammation (not steroids) or vasodilation medications to help with circulation and micro circulation.
Dennis, I have what they call Chronic Lyme and also a type fungus in my blood and organs that came from mosquitoes bite (they think). I have been using an antiviral herb for over a year. I do think it has helped. I heard about it from a doctor who husband had Chronic Lyme. I was told it would take 18 months to get rid of it. I don’t know if I’m rid of it, but I do feel a lot better. It is called Lomatium. (Do your research as it can cause a most horrible rash if your liver isn’t detoxing well enough.) I also use Red Root to help keep my Lymph draining properly.
I think virus and pathogens can be a big issue with us.
I can’t use steroids either. They make me feel horrible! I have autoimmune issues and lots of inflammation.
I too have too thick blood. Have you looked into APS or some of the other clotting disorders that can cause too thick blood? I use enzymes to thin my blood. (And they think it also eliminates or at least keeps at bay this fungus.)
There for sure can be so many pieces to our puzzles. This is a very individual journey to find answers.
Sorry you have had worsening relapse. It is sooooo very tiring and frustrating!
Hi Issie,
I was wondering what the latin name is, of the Red Root herb you were referring to that keeps the lymph moving and draining. Red Root is a common name that is used for several plants, so rather confusing.
Ceanothus americanus, I found the tincture to work better than the capsules for me. But both seemed to help, lymph drainage.
Ehlers-Danlos News Update! Research group thinks they might have identified the gene variant responsible for Hypermobile EDS!
https://medicine.musc.edu/departments/regenerative-medicine/research/norris-lab?fbclid=IwAR0hM-eQPR4i1CvF_cLgRYkzkMkeHd-PeTBAQpSRKwfAfZNyqrKdDkUYFFI
Since EDS and ME/CFS are rather like cousins, and often ‘travel together,’ thought I’d post this breaking news.
Here’s a link to watch the lecture:
https://vimeo.com/486073469
I have been wondering lately whether some people diagnosed with CFS might have OCHOS (orthostatic cerebral hypoperfusion syndrome).
It can be tested for with transcranial Doppler (TCD) ultrasound added on to a tilt table test, which is available here and there at autonomic testing centres.
If you have OCHOS with hypertension, symptoms can often improve with a vasodilator such as a calcium-channel blocker (CCB).
If you can’t get the testing, just trying a CCB could be a way to test via treatment.
Initial paper on OCHOS: https://pubmed.ncbi.nlm.nih.gov/26909037/
Later paper including possible treatment: https://www.amjmed.com/article/S0002-9343(18)30951-3/pdf
POTS is caused by vaccines and antibiotics. They also both cause food intolerance.
Hi. While some studies suggest that one vaccine can trigger POTS (other studies don’t) many people who have not had that vaccine nevertheless have POTS.
Cerebral hypoperfusion is also a problem in Parkinson’s disease. It can be found with or without orthostatic hypotension, so some cases have gone undetected until recently.
There are so many diseases in which transcranial Doppler ultrasound could be of benefit to patients and doctors.
Who knows where we will find it once we start testing more patients.
Cort, I did a search in PubMed to see whether anyone has done any testing on fibromyalgia patients in conjunction with transcranial Doppler ultrasound yet. A couple popped up, but unbelievably they didn’t include any positional change. What a missed opportunity. They were recent too.
Also, wouldn’t it be good if the Bateman Horne Center had a transcranial Doppler ultrasound set-up? If I win the lottery, I’ll offer to buy them one.
I hope you win! 🙂