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“FND Fundamentalists”: New Study Exposes Deep Divisions Over Functional Neurological Diagnoses

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How much confidence should we place in a diagnosis when the clinicians making it cannot agree on what the symptoms mean? That is one of the uncomfortable questions emerging from a new international study published in Rheumatology International on 16 October 2026. Titled “False dichotomies” and “FND fundamentalists”, the research examines how clinicians and patients understand Functional Neurological Disorder (FND) when it is diagnosed alongside systemic autoimmune rheumatic diseases, including lupus, Sjögren's disease and vasculitis.

The researchers analysed survey responses from 1,853 patients, 400 clinicians and 463 members of the general population, alongside interviews with 19 patients and 27 clinicians. What emerged was not a reassuring picture of universal clinical agreement. Instead, the study documented conflicting diagnostic approaches, uncertainty about the causes of neurological symptoms, concerns about inappropriate functional attribution and accounts of patients experiencing serious consequences when their symptoms were dismissed or misinterpreted.

Perhaps the most interesting finding is that some clinicians appear to be reasoning along lines remarkably similar to those proposed in this website's Common Phenotypes Hypothesis: that recognisable neurological presentations may arise from different underlying mechanisms, and that identifying a symptom pattern does not necessarily establish its cause.


When the diagnosis depends on which doctor you see

The study identified substantial disagreement between clinicians about the interpretation of neurological symptoms in autoimmune disease. Some strongly favoured functional explanations, while others emphasised inflammation, immune-system activity and interactions between biological systems. A third group considered the available knowledge insufficient to justify strong conclusions. These disagreements were not confined to patients challenging their diagnoses. They existed among neurologists, psychiatrists, rheumatologists and other medical professionals.

The researchers described clinicians who believed some colleagues were too quick to attribute symptoms to FND, hypervigilance or psychological causes. One psychiatrist used the memorable description “FND fundamentalists”. Other clinicians were concerned about the opposite problem: potentially unnecessary medical treatment when symptoms might respond better to non-pharmacological approaches. The study therefore documents competing concerns about diagnostic error, rather than establishing that either clinical position is universally correct.

Particularly concerning were reports that some neurologists formed impressions before conducting a proper examination. Several reportedly believed that most lupus patients would have FND, with one clinician describing reaching that conclusion as patients walked into the clinic. That raises a fairly obvious question: if the diagnosis is effectively anticipated before the clinical assessment, how much opportunity remains for contradictory evidence to change the clinician's mind?

Another neurologist described repeatedly encountering patients with complex systemic diseases who had previously received FND diagnoses and subsequently identifying other explanations for their symptoms. These are clinician-reported experiences, not independently verified case outcomes, but they illustrate the diagnostic disagreement the study sought to investigate.


What patients and clinicians actually reported

Only 30% of patients who answered the relevant question agreed that their FND co-diagnosis was correct, compared with 86% agreement for depression. Meanwhile, 30% of clinicians responding to a question about lupus estimated that FND was incorrectly diagnosed in approximately half or more of cases. These figures should not be confused with independently established misdiagnosis rates: the study measured perceptions and reported experiences, not diagnostic accuracy through clinical reassessment.

The researchers also documented accounts of diagnostic overshadowing, where an existing functional diagnosis appeared to influence how subsequent symptoms were interpreted. One patient with lupus reported that neurological symptoms had been labelled conversion disorder before multiple strokes were eventually confirmed, leaving permanent disability. Other participants described delayed investigations, difficulties accessing treatment and clinicians interpreting symptoms through existing diagnostic labels rather than reassessing their possible causes.

These accounts matter because systemic autoimmune diseases can produce neurological manifestations that fluctuate, overlap with other conditions and may not be readily explained by routine investigations. The authors specifically discuss small-fibre neuropathy and cardiovascular autonomic dysfunction as biological possibilities that deserve consideration when symptoms are otherwise attributed to hypervigilance or anxiety.


The connection to the Common Phenotypes Hypothesis

For readers unfamiliar with the concept, the Common Phenotypes Hypothesis proposes that certain recognisable neurological presentations may represent shared clinical phenotypes arising from diverse underlying biological processes, rather than necessarily identifying a single primary disorder with one defining pathophysiology. The distinction is between recognising a pattern and establishing what produces it.

Historically, medicine has repeatedly encountered situations in which a recognisable clinical presentation was initially treated as a diagnostic entity before its different causes became better understood. Dropsy, an older term for oedema, is a useful analogy: the swelling was real and recognisable, but it could arise from cardiac, renal, hepatic and other mechanisms. The Common Phenotypes Hypothesis asks whether at least some neurological presentations currently classified as FND deserve similar scrutiny.

The new study does not explicitly propose this hypothesis. Nevertheless, several clinicians expressed reasoning consistent with important parts of it. One neurologist challenged the assumption that symptoms which cannot be readily localised must therefore be functional, explaining that systemic inflammation and interactions between biological processes can produce widespread neurological dysfunction. Others questioned rigid divisions between functional and organic, or emphasised the need to keep investigating when symptoms could have more than one explanation.

That is an important point of conceptual convergence. These clinicians are not necessarily arguing that FND is an invalid diagnosis, nor are they claiming that every neurological presentation has an undiscovered autoimmune cause. They are challenging the reliability of simplistic causal distinctions in complex patients. The Common Phenotypes Hypothesis takes that reasoning further by questioning whether some apparently distinctive functional presentations and positive clinical signs might be shared across multiple underlying conditions.

That additional proposition remains to be tested. The study does not establish the specificity of Hoover's sign, tremor entrainment or other positive FND signs across independently confirmed diseases, and it cannot determine whether FND represents one disorder or a heterogeneous collection of mechanisms. It does, however, provide a relevant clinical context for investigating those questions.


The problem with diagnostic certainty

Modern FND diagnosis is commonly described as a positive, rule-in process based on clinical findings rather than simply excluding other diseases. Yet the researchers encountered patients who reported receiving functional diagnoses following negative investigations, sometimes without clear explanations of the supposed positive signs. Clinicians also disagreed about how consistently these signs were interpreted and applied.

The study's discussion raises a particularly important concern about recommendations in some FND literature discouraging clinicians from reconsidering a diagnosis once established. The authors instead support ongoing clinical review and diagnostic flexibility, especially in diseases characterised by overlapping and fluctuating neurological symptoms.

This is not a minor disagreement about terminology. When a diagnosis influences which investigations are performed, which specialists are consulted and which treatments are offered, diagnostic certainty has practical consequences. A functional label should not become a reason to disregard new symptoms, emerging clinical evidence or alternative explanations.

The paper also documents substantial psychological distress associated with poorly communicated diagnoses, including reports of suicidal thoughts and attempts. In one account, a functional misdiagnosis was reportedly mentioned in a suicide letter. These are serious participant reports, although the study cannot establish the precise causal contribution of the diagnosis or independently verify each event.


What this research establishes and what it doesn't

The study provides evidence of substantial disagreement among participating clinicians and patients about FND co-diagnoses in systemic autoimmune rheumatic diseases. It documents competing approaches to symptom attribution, reported diagnostic overshadowing, concerns about stigma and the potential consequences of treating uncertain explanations as settled conclusions.

Its limitations are also important. Participants were recruited through online networks, diagnoses were self-reported, and clinical records were not independently verified. The sample was not representative of all patients or clinicians, and the qualitative findings cannot establish how frequently particular diagnostic errors occur in routine practice.

Consequently, this research cannot be used to claim that most FND diagnoses are wrong, that positive clinical signs are inherently unreliable or that the Common Phenotypes Hypothesis has been confirmed. Those claims require different research designs, including independently verified diagnoses, appropriate comparison groups and direct testing of the diagnostic specificity of clinical signs.

What the paper does demonstrate is that uncertainty about neurological symptom attribution is not confined to patients, campaigners or critics of FND. It exists among clinicians themselves, including specialists who encounter these presentations in patients with complex systemic diseases.

For the Common Phenotypes Hypothesis, that is an important observation. The hypothesis is not established by this study, but neither is its underlying question some bizarre invention disconnected from clinical medicine. Some clinicians are already describing the same fundamental problem: similar neurological presentations may arise through different mechanisms, and recognising the presentation does not automatically settle the explanation.

The appropriate scientific response is not to declare the matter resolved in either direction. It is to investigate which clinical findings genuinely distinguish mechanisms, which presentations overlap across diseases, and how reliably those distinctions can be made in practice. A diagnosis should explain the evidence, not prevent further evidence from being considered.


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