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.)
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”.)
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.
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.
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.
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.
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.
- 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.
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
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