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FND Hope's Founder, a Misdiagnosis, and Sneddon's Syndrome

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There is a question in medicine so basic that it should barely need saying: if we are not sufficiently sure what is causing a patient's symptoms, how certain should we be about treating the supposed cause? This is not an argument that doctors must achieve absolute diagnostic certainty before doing anything. Medicine routinely operates under uncertainty. It is an argument that uncertainty should make us more careful, particularly when the treatment itself depends upon a specific theory of what is going wrong.

I recently came across a remarkable 2015 article called Turning Patients into Numbers. Its author was Bridget Mildon, the founder of FND Hope. Mildon described being given a psychosomatic or conversion disorder diagnosis while doctors struggled to explain her symptoms. She wrote about what happened afterwards in language that could comfortably appear on this website today: once that label entered her medical record, she believed subsequent investigation and care were compromised. She eventually found another doctor who looked beyond the psychosomatic explanation, and she reported that her symptoms dramatically subsided after treatment for what she described as an autoimmune-related neurovascular condition.

That condition was Sneddon's syndrome. In the comments beneath the article, Mildon said it took about five years and countless doctors to reach that diagnosis. More importantly, she explicitly referred to the earlier diagnosis as a misdiagnosis. This is not me retroactively declaring her FND diagnosis wrong. This is the founder of FND Hope describing her own earlier diagnosis that way.


And there is an irony here that is impossible to miss: this is almost literally the namesake of FND Nope. FND was the answer until, eventually, it wasn't. The founder of FND Hope herself has described an experience in which a functional diagnosis became embedded in her medical care, another disease was eventually identified, and the earlier diagnosis was subsequently described by her as a misdiagnosis. If ever there were a story explaining why this site is called FND Nope, this is it.

Sneddon's syndrome is not a trivial alternative diagnosis. It is a rare, chronic disorder affecting small and medium-sized arteries, classically associated with a mottled skin pattern called livedo racemosa and recurrent cerebrovascular events, including transient ischaemic attacks and strokes. Neurological manifestations can accumulate as vascular injury occurs, and patients may develop headaches, cognitive problems, seizures and other neurological deficits. In other words, Mildon's eventual diagnosis involved an actual vascular process capable of injuring the brain. That makes the consequences of interpreting neurological symptoms through a psychosomatic or functional framework particularly difficult to brush aside: while clinicians were trying to explain why her symptoms might be functional, the eventual diagnosis was a disease in which recognising and managing vascular risk matters.

Her wording about what remained of the functional explanation is fascinating. Mildon wrote that her then-current doctor could account for all of her symptoms, but added that she “may have had some form of functional overlay.” Notice the language: may have. She did not identify which symptoms constituted that overlay, did not describe evidence independently establishing it, and did not say that another clinician had demonstrated a second functional disorder. The possibility was simply left on the table.

FND Hope's own website makes the history even harder to ignore. Its current biography of Mildon describes her as having been wrongly labelled psychosomatic before receiving another diagnosis and treatment. An FND Hope page telling Mildon's own story goes further. It says that her story once ended with her saying she had FND, before recording her 2012 diagnosis of Sneddon's syndrome. The updated ending describes her as someone who was “at one point in my life diagnosed with a Functional Neurological Disorder” and who is now diagnosed with Sneddon's syndrome. FND Hope still prominently identifies Mildon as its founder.

This is where the story starts colliding rather spectacularly with the common phenotype hypothesis I have been developing on FND Nope. If a patient has neurological symptoms interpreted as functional, and an underlying neurological disease is subsequently discovered that can account for those symptoms, why must the remaining explanation be disease plus functional overlay? Why could the supposedly functional presentation not have been part of the phenotype produced by the disease itself? Calling it an overlay does not answer that question. It merely preserves the functional interpretation.

That does not prove my hypothesis. It does, however, expose the problem rather beautifully. Comorbidity and common phenotype are competing interpretations of the same observation. If neurological diseases can produce presentations that clinicians interpret as functional, seeing the functional phenotype does not necessarily tell us what produced it. The phenotype may be real. The signs may be real. The suffering is certainly real. The disputed bit is the mechanism.


Then treatment enters the picture

This would mostly be an academic argument if an FND diagnosis were simply a descriptive label. It isn't. The diagnosis can determine treatment, and FND treatment is not necessarily mechanism-neutral. The influential consensus recommendations for physiotherapy in functional motor disorder explicitly describe treatment based upon a particular model. They recommend addressing illness beliefs and self-directed attention, demonstrating that normal movement can occur, retraining movement using diverted attention, challenging maladaptive behaviours and encouraging an expectation of improvement. The paper describes FMD as involving learnt habitual movement patterns and recommends explaining that the problem concerns nervous-system functioning rather than irreversible neurological damage.

Read that again in the context of diagnostic error. This is not simply, “We don't know why your leg is weak, so let's safely preserve mobility while we continue looking.” The treatment is built around an explanation of why the leg is weak. Indeed, those consensus recommendations say that patients should normally have received an unambiguous FMD diagnosis before this treatment and should understand that the problem has the potential for reversibility.

The same recommendations include things that become particularly interesting if the diagnosis is wrong: encouraging early weight bearing, focusing on automatic movement rather than impairment, avoiding adaptive equipment and mobility aids where possible, and challenging beliefs and behaviours considered unhelpful. None of those things proves that FND physiotherapy is dangerous when correctly prescribed. That is not my argument. My question is much simpler and much nastier: what happens when you apply those assumptions to somebody whose nervous system actually is progressively being damaged?

We have already encountered a case on this site where that question is anything but theoretical. In ALS or FND? The Troubling Case of Tanea “Rebel” Brooks, I documented Rebel's extraordinary medical journey. By November 2025, FND had been diagnosed as an explanation for her neurological symptoms and she was publicly discussing her rehabilitation journey. During early 2026 her neurological function deteriorated dramatically, including difficulty walking, talking, swallowing and using her hands, and she underwent inpatient speech, occupational and physical rehabilitation. On 1 May 2026, Mayo Clinic diagnosed ALS, reported as explaining her progressive neurological symptoms.

We need to be precise here because the point is strong enough without embellishment. We do not have evidence that FND rehabilitation accelerated Rebel's ALS. I am not claiming that physiotherapy caused motor neurons to die faster, and the available public record cannot establish that. What it does establish is the far more uncomfortable situation of a patient undergoing rehabilitation while a progressive motor neuron disease was apparently producing neurological decline, after those neurological symptoms had previously been labelled FND.

And ALS rehabilitation does not start from the same assumptions. The ALS Association's guidance on mobility and exercise supports appropriate physical and occupational therapy, stretching and carefully selected exercise, but specifically warns that not all exercise is helpful and that attempting additional resistance with a sufficiently weakened muscle may be harmful. Its exercise guidance emphasises avoiding muscle soreness, excessive fatigue and overexertion.

Compare the underlying assumptions. Specialist FND physiotherapy may tell the patient that movement is available, that the problem is potentially reversible, that attention and learnt movement patterns matter, and that normal movement needs to be accessed and retrained. ALS rehabilitation has to accommodate genuine progressive motor neuron loss, weakening muscles, fatigue, falls and an evolving need for assistance and equipment. These are not interchangeable explanations of the same disability. If you choose the wrong one, the error is not merely semantic.

That is why I think the usual debate about FND misdiagnosis rates misses something much more important. A diagnostic error matters not merely because somebody eventually receives a different name for their illness. It matters because diagnoses cause things to happen. They change what clinicians investigate, what they stop investigating, what they tell patients about their bodies, what rehabilitation they prescribe, how deterioration is interpreted and what equipment or assistance is considered appropriate.

Mildon herself understood at least part of this problem more than a decade ago. In Turning Patients into Numbers, she asked us to imagine medicine allowing for medical uncertainty. She argued that unexplained symptoms should be allowed to remain pieces of an unfinished medical puzzle rather than becoming grounds for dismissal. Most strikingly, she described the psychosomatic label as compromising subsequent investigation and care. This came from the woman who founded what became one of the world's best-known FND advocacy organisations.

There is an uncomfortable symmetry between her story and Rebel's. Mildon's symptoms were given a conversion or psychosomatic interpretation before Sneddon's syndrome was diagnosed. Rebel's neurological symptoms were labelled FND before ALS was diagnosed. These are very different diseases, very different histories and they should not be conflated. But both force exactly the same patient-safety question: what happens when treatment is based upon a mechanism that turns out not to be the mechanism producing the patient's deterioration?

And this is where I become extremely uncomfortable with appeals to comorbidity or functional overlay as though those words make the problem disappear. Maybe a patient genuinely can have both. Of course that is possible. But merely saying “FND can coexist with neurological disease” does fuck all to establish that it actually did in a particular patient. If the alternative disease can explain the presentation, the burden should be on us to demonstrate why a second functional mechanism is necessary, not simply preserve it because the patient once displayed signs or symptoms interpreted as functional.

More importantly, uncertainty should have consequences. If we genuinely do not know whether a patient's weakness represents a reversible functional disturbance, progressive motor neuron loss, inflammatory disease, vascular disease or something we have not yet identified, then treatment should reflect that uncertainty. Rehabilitation aimed at preserving function and safety is one thing. Rehabilitation that tells the patient what mechanism is producing the disability is something else entirely.

The sensible question before any mechanism-specific treatment should therefore be brutally simple: what happens to this patient if we are wrong? If the answer is that the treatment remains useful, investigation continues, deterioration triggers reassessment and nothing important is lost, fine. If the answer is that we may push a genuinely weak patient harder, discourage aids they actually need, reinterpret deterioration as maladaptive behaviour, or delay investigation of progressive neurological disease, then diagnostic uncertainty is no longer an abstract philosophical problem. It is a safety problem.

We do not need perfect knowledge before treating people. That would make medicine impossible. But there is a vast difference between treating carefully while uncertain and pretending uncertainty has been resolved because we have given it a diagnostic code. Mildon's story should make that obvious. Rebel's story should make it impossible to ignore.

If we don't know what something is, we should be very fucking careful about treating it as though we do.

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