By David Tuller, DrPH
When I write about functional neurological disorder (FND) or functional neurological symptoms, I sometimes get feedback from Zachary Grin, a physical therapist in New York. As an FND specialist, he disagrees with pretty much everything I write about the topic.
At first, I tried to engage with Zachary in a good-natured manner. I had some sympathy for him because he’s a young gay guy—well, much younger than me, at any rate—and had publicly expressed having had some difficulty with his family over the issue. But that period was short-lived. I blocked him on X quite a while ago when he accused me of “lying” about the PACE trial.
Specifically, he accused me of lying when I pointed out that the authors had lowered their outcome thresholds so dramatically that trial participants could be simultaneously “recovered” at baseline on two key self-reported measures—fatigue and physical function. Instead, he parroted the PACE authors’ response to this criticism—that no one was “recovered” at baseline because there were four separate recovery variables, and participants had to meet the designated thresholds for all four of them.
This was a bogus response that avoided the facts. I have never claimed that anyone was “recovered” fully at baseline by the PACE definition of the term. What I have pointed out—accurately—is that some people met the “recovery” thresholds at baseline for two of the four “recovery” metrics. Even after I explained Zachary’s error, he continued to insist that he was right and I was “lying.” That was the last straw for me. He was only the second person I have ever blocked on the platform—and I haven’t blocked anyone since.
In general, life is too short to pay attention to Zachary. But sometimes he forces himself on my attention by commenting on a post—as he recently did.
The post was about a letter I wrote to the journal CNS Spectrums seeking a correction for the flat assertion that “functional symptoms are neurological symptoms which are generated by abnormal brain processing.” As I pointed out, this is their best guess, not a documented fact. Zachary objected and posted a comment under the blog, to which I responded.
I have posted both his comment and my rebuttal.
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Zachary’s comment
David, I hope you read this, accept you are wrong, and issue an apology to the journal and authors.
The sentence “Functional symptoms are neurological symptoms which are generated by abnormal brain processing” is NOT an unsupported causal claim. It is a basic mechanistic description. This isn’t about semantics…etiology and mechanism (pathophysiology) are very different things! You must know this.
There is a very obvious difference between saying symptoms are generated by abnormal brain processing and claiming to know the cause of FND. The first broadly describes the mechanism producing the symptoms which has plenty of evidence – “the how”. The second would explain why that mechanism developed in a particular person – “the why”. No one claims to fully understand “the why” & the authors certainly do not with that sentence.
To use an example the neurology field has somehow managed without correction letters: “seizures are produced by abnormal electrical discharges in the brain” does not require a disclaimer acknowledging that epilepsy’s etiology remains incompletely understood.
The journal does not need to issue a correction. You need to correct your misunderstanding. There is no way for you to twist this one.
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My response
Zachary, you’re so cute when you’re on your high horse. I don’t need instructions from you on the difference between “etiology” and “mechanism,” but thank you anyway. The home page of neurosymptoms.org has this to say: FND and functional neurological symptoms are “Caused by a PROBLEM with the FUNCTIONING of the nervous system,” and they involve “a ‘software’ issue of the brain, not the hardware.” That statement says it very clearly and directly: the symptoms are “caused” by malfunctioning software and the “hardware” is apparently irrelevant.
So if you have a problem with the use of the word “cause” in this context (I didn’t use “etiology” in the letter), I suggest you take it up with Professor Stone. The sentence in question in the new paper makes the same definitive claim about what is “generating”/producing/creating–ie “causing”–the symptoms. You also assert that there is plenty of evidence for this statement, so you think the categorical assertion is just fine. But that doesn’t make it true. It’s still an assumption or theory.
Because we are also told in the recent Perez paper [I blogged about that paper here] what has become obvious from all the research about structural changes in recent years–that this whole domain is “a “software” AND a “hardware” problem.” That means that the factors causing the symptoms could relate to the structural changes and not, as always asserted, the “software” problems. Moreover, the Perez paper says the research supports that FND is “in part” a brain network disorder–a much more modest claim than that it is 100% a “software”/brain activity problem, as the home page of neurosymptoms.org still asserts.
No one has claimed function isn’t involved. But obviously neither you nor Stone nor Perez nor the authors of the new paper know what exactly is producing what, despite your strong support of the theory that software/brain network activity is generating ALL of the symptoms. I’m sorry, but brain scan associations do not provide proof that one thing is generating or producing or causing another. That’s an assumption.
Have a good day!
Well, it added some light entertainment to my day, so thanks to both of you for that!
What Dr Tuller is highlighting here goes well beyond semantics.
FND is presented as a positive rule in, non exclusionary primary diagnosis. Its underlying mechanisms are presented as established fact rather than theory, even though they are closer to hypotheses.
However, once you delve into the actual literature, the neuroscience, and the mechanisms described in Bayesian models (which are also used in robotics – another software analogy here – though not used as one in this context), it becomes clear that much of what is presented as fact is actually speculation.
If we are being honest, this is technically more of a buy in diagnosis than a true rule in diagnosis.
Having a hypothesis is perfectly fine. It guides research. The problem arises when unknowns are treated as knowns. That is a fundamental issue.
Once an FND diagnosis is made, it more often than not marks the end of the road for further investigations. If honesty prevailed and FND were treated as an area of uncertainty rather than settled knowledge, the clinical picture and patient outcomes would likely be very different.
In short: use the FND label and apply FND treatment plans where appropriate, but always keep in mind that the diagnosis is likely provisional, stay agnostic.