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 recovery 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.
Zachary Grin is a menace and has no treating patients with his lack of education on the subject matter.
FND Nope commented:
“Once an FND diagnosis is made, it more often than not marks the end of the road for further investigations.”
I’d argue that the curbing of those further investigations has formed part of a political/health economics selling point for FND e.g. -https://petition.parliament.uk/archived/petitions/200007#main-content, as it has been for medically unexplained symptoms (MUS), with FND being viewed by doctors and healthcare managers as a potential means of cutting costs within their healthcare setting/s via the possible reduction of investigations, appointments and length of inpatient stay.
I imagine that many people might assume that changing the FND diagnosis from rule-out to rule-in would be a beneficial move for patients, but surely that depends on how good the rule-in investigation/assessment is? If rule-out did actually mean excluding everything else by employing all the up-to-the minute investigations and assessments available, and rule-in involves testing for ‘signs’ developed in times gone past that historically were used to support/confirm diagnoses of exclusion (of pathological diseases known about then), then isn’t there a danger that rule-in could present a risk for patients that rule-out didn’t? Ruling out completely via thorough assessment and investigation will be considerably more expensive, so rule-in is bound to go down well with those who seek to reduce expenditure.
I think we could all do with a clear answer to this question:
Is FND still regarded as a subset of medically unexplained symptoms (‘MUS’ aka ‘functional symptoms’), yes or no? Because the petition I linked to earlier -https://petition.parliament.uk/archived/petitions/200007#main-content from 2017, which appears to have been associated with the FND HOPE UK charity (-https://x.com/FNDHopeUK/status/907635956878073859), included FND in MUS, whereas the FND Action charity posted this -https://x.com/FNDAction/status/1394184863012511752 in 2021, some 3+years later. I understand that the charities share several medical experts/advisors and have done so for some time so, unless the position on this has changed with time, this difference in opinion would seem somewhat bizarre.
If FND is no longer viewed as a subset of MUS then surely any FND brain network evidence is irrelevant to other conditions that have been classed as MUS/’functional symptoms’? The paper in question here seems to see FND as a subset of functional symptoms still, but more serious because the symptoms fail to resolve. But many conditions previously deemed to be MUS/’functional’ do not resolve either – I’m sure that lots of ME sufferers can vouch for that. One of the paper’s co-authors is on the medical advisory board of FND Action. Could this mean that ME is no longer considered a ‘functional disorder’?
(Forgive me if I’m losing the plot – the FND field is extremely confusing!)
Ah, silly me, I get it now, I think…the penny may have finally dropped? It kind of adds up, at least to an extent, if non-resolving ME is now being viewed as a subset of FND? So what’s the positive rule-in sign for that? Will these patients get fMRI scans as a matter of course? And if those scans are negative for brain dysfunction, will that change things for them? Will they remain as deserving FND patients anyway (like the Havana Syndrome/AHI study participants appeared to) or will they have to rejoin the ranks of those considered pesky, time-wasting, stress-inducing boring old MUS patients?
Questions, questions.
Can someone explain to me what brain software actually is? I’ve never understood it. Is it actually a thing recognised outside of the FND crowd?
Basically, your CNS (that is, your brain, spinal cord, and signals carried via the PNS, the nerves) is described as hardware, while the processing of those signals that flow from that hardware is described as the software.
In this analogy, the CNS and PNS are considered structurally intact, while the processing of those signals (the software) is considered flaky or glitchy. They are believed to not be processing those signals properly and correctly.
I wrote about it over here: https://fndnope.org/posts?postId=58
(bit of an ugly discussion in the comments in that page around an anonymous neurologist that completely missed the point)
When a neurologist first told me that he thought that my symptoms were ‘functional’, I imagined that he meant a disorder of biochemistry or physiology and thought ‘ok, that sounds reasonable’. I suspect that ‘functional’ problems may turn out to be that in the end, but the term ‘functional’ appears to have been quite widely used by neurologists to signify that the problem is due a ‘software’ problem that is all in the patient’s head and likely linked to/resulting from mental health/behavioural/trauma issues.
I think IBS is a good example here (the functional equivalent in gastroenterology). In certain subtypes of IBS, particularly IBS-D, it is likely that up to 80% of cases are actually due to small intestinal bacterial overgrowth (SIBO). In what world would we call bacterial causes “functional”?
Neurotoxicity can do the same thing. Just as apraxia and ataxia can mimic the core features of FND, I would personally be very reluctant to diagnose functional disorders on either front without proper investigations.
Heart defects can cause neurological symptoms, including seizures, but this never seems to get a mention. Deoxygenated blood going through abnormal connections bypass the lungs, causing transient hypoxia and affecting body chemistry, including serotonin. The hypoxia can affect the spinal cord and so mobility. Heart defects are also regularly missed on tests and who gets their heart tested when presenting with neurological symptoms. Examples are narrowing of the aorta and bi atrial draining of the superior vena cava. A friend of a friend’s daughter was misdiagnosed with epilepsy and it was her heart causing the seizures and she died.
Transient ischemic attack symptoms can be misdiagnosed as FND. Brain scans can be normal but there is wide reporting of lasting symptoms, despite the orthodoxy saying TIAs completely resolve. Research going back 10 years suggests TIAs can cause lasting damage.
It is not known what white matter intensities mean, if the medical establishment doesn’t know about the stuff it can see, it doesn’t inspire confidence dismissing things that can’t (yet) be seen on scans.
And then there’s the example of this paper on ‘functional’ cardiac symptoms -https://www.sciencedirect.com/science/article/pii/S1470211824033694?via%3Dihub where the authors synonymized so-called non-cardiac chest pain with cardiac syndrome X, even though the latter is also known as microvascular angina (-https://www.bhf.org.uk/informationsupport/heart-matters-magazine/medical/all-about-microvascular-angina) and is a type of INOCA (Ischemia with No Obstructive Coronary Arteries), a pathological cardiac condition which I understand had been known about for several/many years at that point. It seems that the synonymization was picked up on by two consultant cardiologists and a trainee who sent this letter to the journal editor -https://www.sciencedirect.com/science/article/pii/S1470211824033591?via%3Dihub. It’s a very restrained letter, (and IMO overly gracious), but nevertheless I think the point is made.
Following on from my last comment:
I’d so like it to have been the trainee (rather than either of the consultant cardiologists) who noticed and flagged up the problematic synonymization in that faulty functional cardiac symptoms paper I linked to above and who showed up the 2 consultant liaison psychiatrists and 2 specialist registrars, one in psychiatry and one in cardiology, who put their names to it. [Incidentally, it seems that one of those consultant liaison psychiatrists is acting as chair for a session on the “Post-COVID condition” (I guess that’s Long-COVID to the rest of the world?) at the upcoming international RCPsych congress in June -https://www.rcpsych.ac.uk/events/congress/programme that David flagged up before -https://virology.ws/2026/05/04/trial-by-error-news-bits-frail-biopsychosocial-poobahs-at-psych-confab-long-covid-advocates-channel-act-up/ .]
Who’d have thought… FND supporters are really great at gaslighting.