When FND's Own Diagnostic Guidelines Admit the Signs Are Not Exclusive
Functional Neurological Disorder (FND) is increasingly presented as a diagnosis established through positive clinical signs rather than the exclusion of other neurological conditions. Signs such as Hoover's sign, give-way weakness, distractibility and tremor entrainment are used to support this approach. But how confidently can these findings establish a functional disorder when the same or similar features can arise through other mechanisms?
A 2018 clinical review published in Clinical Medicine, titled Functional neurological disorders: acute presentations and management, provides an interesting opportunity to examine that question. Written by neurologists Hannah R Cock and Mark J Edwards, the paper describes the recognition and management of FND in emergency settings, particularly patients presenting with seizure-like episodes or stroke-like weakness.
The authors advocate diagnosing FND through characteristic clinical features rather than simply relying on normal investigations. However, the paper also contains explicit acknowledgements that several findings associated with functional presentations are not exclusive to FND. Those qualifications deserve attention because they complicate claims of diagnostic specificity.
When a positive sign is not exclusive
One of the clearest examples concerns give-way weakness, also called collapsing weakness. This occurs when a patient initially produces force against resistance but cannot sustain it. The finding is commonly associated with functional weakness and appears among the positive signs discussed by the authors.
Yet the paper makes an important admission:
Of note, people with acute pain often have a similar pattern of weakness.
That is not a minor qualification. Pain can interfere with force production during examination without requiring a functional neurological mechanism. The observation of collapsing weakness therefore cannot, by itself, establish why the weakness occurs.
The authors also describe Hoover's sign, in which hip extension appears weak during direct testing but improves during an automatic movement involving the opposite leg. They interpret this discrepancy as evidence that the nervous system retains the capacity to produce movement, even when voluntary movement is impaired.
But this interpretation raises a separate question. Demonstrating that movement can occur under one set of conditions does not automatically establish why it fails under another. The examination demonstrates a difference in performance between tasks. The explanation for that difference is a further diagnostic inference.
This distinction matters. The authors present preserved movement during automatic tasks as evidence supporting functional weakness. However, the paper does not establish that every possible neurological or physiological explanation for such a discrepancy has been excluded. A sign may have diagnostic value without being uniquely attributable to one disorder.
Seizure features are not foolproof either
The same problem appears in the discussion of dissociative seizures, now commonly described as functional seizures. The authors identify several features that can help distinguish these events from epileptic seizures, including prolonged duration, fluctuating movements, closed eyes, asynchronous movements and pelvic thrusting.
Crucially, the paper acknowledges that these characteristics are not completely reliable discriminators. Its own diagnostic table explicitly notes that asynchronous movements and pelvic thrusting can occur in frontal lobe focal seizures.
This is significant because frontal lobe epilepsy can produce unusual motor behaviours that may appear inconsistent with more familiar descriptions of epileptic seizures. Treating such movements as inherently functional would therefore be unjustified. The authors recognise that clusters of findings and clinical context are more informative than isolated observations.
The implications are straightforward: an event that looks unusual, fluctuates or involves movements commonly associated with dissociative seizures is not automatically nonepileptic. The diagnostic question is whether the complete clinical evidence supports that conclusion, including whether further investigation is necessary.
That distinction is particularly important in emergency medicine, where diagnostic decisions may be made under time pressure and where an incorrect classification can influence subsequent treatment.
From observed inconsistency to presumed mechanism
The paper repeatedly emphasises discrepancies between voluntary and automatic movement, changes during distraction and the temporary return of apparently normal function. These observations form the foundation of the positive-sign approach described by the authors.
However, there is a fundamental difference between identifying inconsistency and establishing its cause. Variability is an observation. Distractibility is an observation. Improvement during automatic movement is an observation. None of these findings, considered in isolation, directly identifies the underlying biological mechanism responsible for the presentation.
The authors argue that such findings indicate preserved basic neurological function and support a functional diagnosis. But the paper is a clinical review, not an experiment demonstrating that these signs arise exclusively from a single mechanism. Nor does it establish that alternative neurological processes cannot produce similar presentations.
Indeed, the authors acknowledge that diagnostic uncertainty sometimes requires specialist assessment or further investigations. That admission is important because it places limits on how confidently the signs can be interpreted.
The problem arises when a finding that should contribute to diagnostic reasoning is instead treated as a definitive explanation. Demonstrating that a patient can briefly generate normal strength does not explain why that capacity becomes unavailable during another task. The difference itself is not a mechanism.
The software analogy does not resolve the uncertainty
The authors recommend explaining FND to patients through the familiar analogy of a software problem rather than a hardware problem. The intended message is that the nervous system retains its basic capacity for normal function but that access to that function is disrupted.
As an explanatory metaphor, this may be easy to communicate. As evidence for an underlying mechanism, however, it contributes very little. The analogy does not identify the physiological process responsible for the disturbance, demonstrate that structural or other biological abnormalities are absent, or establish that different patients with similar presentations share the same underlying cause.
The authors themselves acknowledge that the precise reason FND occurs is not known. That uncertainty should not disappear merely because the diagnosis has been explained using a memorable analogy.
Calling a problem functional does not establish that it is independent of disease processes that have not yet been identified, investigated or adequately understood. An analogy is not a diagnostic test, and a diagnostic label is not a mechanistic explanation.
What this means for the Common Phenotypes Hypothesis
These limitations are directly relevant to the Common Phenotypes Hypothesis, which questions whether presentations classified as functional necessarily represent a distinct underlying disorder.
The hypothesis proposes that clinical presentations recognised as functional may arise through different neurological or physiological mechanisms, rather than necessarily sharing a single functional cause. It does not claim that all neurological symptoms are interchangeable, nor does it deny that clinicians can identify meaningful patterns during examination. It questions what those patterns establish about causation.
This is hardly a new question in medicine. Historical classifications such as dropsy and jaundice grouped recognisable clinical presentations before their diverse underlying causes became better understood. The observation was real; the assumption that it represented one disease process was not necessarily justified.
The parallel is conceptual, not proof that FND will follow the same historical trajectory. Nevertheless, the diagnostic qualifications acknowledged by Cock and Edwards illustrate why distinguishing a recognisable presentation from its underlying cause remains important.
If a sign associated with a functional presentation can also arise through pain or an established neurological disorder, the sign cannot be treated as an exclusive marker of functional causation. The relevant question becomes how reliably the entire diagnostic process distinguishes among competing explanations.
That is a question of diagnostic validity, not merely terminology.
The unanswered question
Cock and Edwards provide a practical account of how clinicians are encouraged to recognise and manage FND in acute settings. Their paper also makes clear that some supposedly characteristic findings overlap with other medical conditions, that individual seizure features are imperfect discriminators and that diagnostic uncertainty sometimes requires further investigation.
Those acknowledgements do not establish that every FND diagnosis is incorrect. They do, however, undermine any simplistic claim that observing a positive sign automatically proves a particular functional mechanism.
The central issue is not whether Hoover's sign, give-way weakness or distractibility can be clinically useful. It is whether the conclusions drawn from those findings extend beyond what they actually demonstrate.
A clinician may observe preserved movement, fluctuating weakness or an unusual seizure presentation. Those observations deserve investigation and interpretation. They do not become proof of an underlying cause merely because the presentation fits an established diagnostic category.
Recognising a pattern is not the same as explaining it. Until that distinction is respected, diagnostic confidence risks exceeding the evidence on which it rests.
References
- Cock HR, Edwards MJ. (2018). Functional neurological disorders: acute presentations and management. Clinical Medicine, 18(5), 414โ417. doi: 10.7861/clinmedicine.18-5-414.
- Avbersek A, Sisodiya S. (2010). Does the primary literature provide support for clinical signs used to distinguish psychogenic nonepileptic seizures from epileptic seizures? Journal of Neurology, Neurosurgery & Psychiatry, 81, 719โ725.
- Daum C, Gheorghita F, Spatola M, et al. (2015). Interobserver agreement and validity of bedside 'positive signs' for functional weakness, sensory and gait disorders in conversion disorder: a pilot study. Journal of Neurology, Neurosurgery & Psychiatry, 86, 425โ430.
- Stone J, Edwards M. (2012). Trick or treat? Showing patients with functional (psychogenic) motor symptoms their physical signs. Neurology, 79, 282โ284.
This post explores a hypothesis. It should not be read as an established fact or settled scientific conclusion.