The international day of action “Long Covid Awareness Day” aims to draw attention and awareness to the disease Long Covid and those affected. It is often said that little is known about the causes of Long Covid and the post-viral sequela Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). There are also few laboratory markers, examination methods or medication. But that is only partly true. You may not know the exact trigger mechanisms that set everything in motion. However, we now know quite a bit about the cell-biological background of the symptoms.
Many of these symptoms and mechanisms are known from other health conditions for which medications exist. The Austrian neurologist Michael Stingl has compiled them on his website and, in an interview with MIT Technology Review, advocates listening carefully to long-Covid and ME/CFS patients, using known tests and pragmatically trying to alleviate the symptoms with existing medication.
The interview with neurologist Michael Stingl was first published on August 10, 2022. On the occasion of “Long Covid Awareness Day” on March 15, we are republishing the interview.
Mr. Stingl, what did you learn from ME/CFS that you now use in diagnosis and therapy for Long Covid – and vice versa?
Because ME/CFS is so similar, it was obvious from the start to apply what you know about ME/CFS to Long Covid and vice versa. For me, a subgroup of Long Covid corresponds to ME/CFS. It mostly affects young people between the ages of 15 and 45, often with a mild course, who then experience what is known as post-exertional malaise, or PEM for short. So they often experience a massive deterioration in their condition while doing very mundane activities, and that’s fairly typical of post-viral fatigue. PEM is a core feature of postviral fatigue. So I don’t mean Covid patients who have had pneumonia and need rehabilitation or other organ damage.
What treatment options are there?
Unfortunately we don’t have any therapies that treat ME/CFS and Long Covid causally because we don’t know the exact reasons yet. But there are many symptomatic therapies and medications that have another effect in addition to the actual indication, namely mostly [zur Behandlung, Anm. d. Red.] inflammatory processes. You try this, adapted to the patient, in a trial-and-error process.
Evidence of Long Covid
Many sufferers report that doctors often just look at the standard tests and when they don’t find anything they say, ‘There’s nothing there.’ What are you doing differently?
We know from experimental studies that this is indeed something. And there are definitely tests that you can look at. The most important thing: To clarify whether ME/CFS or Long Covid is present, I look at the circulatory function with a simple test – the so-called Schellong test or NASA Lean Test: People lie on their back for ten minutes and have their blood pressure and pulse measured and then they get up, lean against the wall and we take blood pressure and pulse every minute for ten minutes. However, this is often not done in clinical practice because it takes too long.
What does this test show?
A syndrome called POTS, which means Postural Orthostatic Tachycardia Syndrome. POTS causes an excessive increase in heart rate, accompanied by symptoms such as dizziness, a feeling of pre-collapse, nausea and sweating. This affects a lot of people with ME/CFS and also a lot of people with Long Covid. It is now increasingly stated in guidelines that this must be done. There you often have a very good lever of symptomatic therapy.
What else can be evidence of ME/CFS and Long Covid?
Many patients with postviral syndrome are very susceptible to infections. If you say, for example, that I have an infection for two weeks seven times a year, that is significantly more than you would expect. That needs to be well clarified immunologically, there may be something behind it.
The third very important possibility is the so-called mast cell activation syndrome. Mast cells are immune cells that produce histamine and other inflammatory mediators. These cells are often overactive in ME/CFS and Long Covid and this can lead to a variety of issues such as impaired digestion, circulatory problems, joint pain, groggy feeling and itching. The problem is, there are no really reliable laboratory markers for it.
You can’t measure the excess of messenger substances well?
The increases can often only be detected fleetingly. The measurement is therefore often complex. It is then primarily a matter of listening to what symptoms the patients describe and knowing that this is quite common after viral diseases. You can pragmatically give harmless, cheap antihistamines for three to four weeks. If it doesn’t help, leave it out.
Antihistamines are well-established anti-allergic drugs because they block specific receptors that inhibit the action of histamine.
You don’t lose much there. Those three things alone would be a giant step for ME/CFS. Then there are a few more options.
“Many don’t have the autonomic nervous system on their radar”
What are you looking for?
It is always important to examine indications of a malfunction of the so-called autonomic nervous system, [das Körperfunktionen wie die Herzfrequenz und die Atmung steuert, Anm. d. Red.]. Many people don’t have that on their radar, also because the autonomic nervous system is unfortunately often not very accessible to the measuring methods.
How do you find this so-called dysautonomia and how does it manifest itself?
We had an example with postural orthostatic tachycardia syndrome, this common dysfunction of circulatory regulation. Then too little oxygen gets into the tissue and you will feel that as limited performance. Clinically, the typical functions of the autonomic nervous system are also queried, such as dry mouth and eyes, altered sweating, constipation, disorders of sexual function, problems with emptying the bladder and disorders of temperature regulation. If several of these are conspicuous, dysautonomia is quite likely. Some of it, like sweating, can also be measured.
As a doctor, what do you need to better treat patients with ME/CFS and Long Covid?
The big problem with ME/CFS is that we don’t know the one underlying mechanism. We have to diagnose based on symptoms and there are probably different causes that cause a very similar clinical picture. I am involved in a project at the University of Vienna in which questionnaires are used to try to distinguish between clinical subtypes and to see what the possible causes are.
The therapies depend on that?
Yes. There are many hypotheses. That it could be an autoimmune reaction is one of them. Such antibodies are found in 30 to 70 percent of those affected. Whether they really have the basic pathophysiological relevance is not yet clear. But if you have auto-antibodies, for example, you could use BC007 [von Berlin Cures, Anm. d. Red.] help. If you don’t have autoantibodies, it doesn’t make sense.
If the studies show that BC007 works, then the pharmaceutical industry will take an interest. Then I’m reasonably optimistic that new medicines will be found in the next few years. This has also been seen in multiple sclerosis. 30 years ago you had nothing and now there are numerous drugs that can often stop this serious neuroimmunological disease.
Until then, are you treating with existing medications that you give off-label?
I don’t promise anyone salvation, I can’t. Normally, nothing makes the symptoms go away. But the point is simply that you can at least produce an improvement in performance. In the guideline of the Austrian Society for General Medicine there is now an addition to the Chronic Fatigue Syndrome, which basically contains what I am trying to do pragmatically. We cannot wait for evidence to be generated and meanwhile do nothing!