The Falsification Problem: FND Resolved After CSF Leak Repair
FND Nope
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A 2026 case report described a patient diagnosed with FND whose symptoms completely resolved following surgical repair of a cerebrospinal fluid leak.
One of the things I look for in the FND literature is evidence that could falsify an established diagnosis. Without the possibility of falsification, it becomes difficult to determine when an FND diagnosis should be reconsidered or withdrawn in light of new evidence. That has implications not only for identifying potential misdiagnoses, but also for evaluating the scientific robustness of the diagnostic framework itself.
At first glance, this case seems like an obvious candidate. Yet, surprisingly, the opposite occurs. Rather than replacing the FND diagnosis, the newly identified condition is incorporated as a comorbidity or functional overlay, leaving the original diagnosis intact.
The authors explain in some detail why FND was diagnosed. The patient presented with what they considered a typical clinical presentation, a typical event captured on video EEG without an electrographic correlate (which they describe as highly consistent with FND), as well as a history of psychiatric comorbidities and recent psychological stressors.
In other words, this was not a superficial diagnosis. The authors present a careful rationale for why they believed FND was the correct initial conclusion.
Once the CSF leak was identified, surgically repaired, and the patient's symptoms completely resolved, they never conclude that the original FND diagnosis was incorrect. They never claim that the CSF leak fully explained the presentation. Instead, they retain the concept of a functional overlay.
However, they also state the following:
โฆthis case illustrates that history-taking and judicious workup of symptoms may identify functional-appearing symptoms obscuring or accompanying another etiology that is curable.
I find the wording particularly interesting. The authors do not describe the symptoms as functional, or even as FND. Instead, they describe them as functional-appearing. Not only was the accompanying pathology treated, but the symptoms that appeared functional resolved as well.
Rather than asking whether the patient had FND or a CSF leak, another possibility is that the CSF leak produced a functional-appearing phenotype. Under this interpretation, the presentation is not itself the disease, but a common neurological phenotype that can emerge from multiple underlying biological disturbances.
If this interpretation is correct, then some conditions currently described as comorbidities may instead provide important clues to the biological processes giving rise to the functional-appearing phenotype.
Which brings us back to the original question.
This creates a deeper falsification problem. Positive signs are treated as rule-in evidence for FND, yet when another condition later explains the presentation, those signs can be regarded as having been misattributed by the clinician, although rarely does this appear to result in the FND diagnosis being withdrawn. More often, the new condition can simply coexist with FND as a comorbidity or functional overlay. So what evidence actually falsifies the original diagnosis?
If complete resolution following treatment of another neurological disorder does not necessarily invalidate an FND diagnosis, what observation would?
The authors do a great job explaining their rationale for the FND diagnosis and why the incidental finding could not explain the motor symptoms. It is odd that they then say โfunctional appearing symptomsโ when they just concluded she did have FND and the structural finding is most often asymptomatic. Resolution of symptoms after surgery, is not sufficient evidence to conclude the CSF leak was causing the clear FND symptoms. It is well known that surgery can lead to large placebo effects. It is not unreasonable to hypothesize that being given a structural diagnosis as an explanation for previously unexplained symptoms (they said she was never told she had FND) and having the structural defect corrected likely contributed to updating the brainโs prediction model. Itโs also possible that the CSF leak could have caused some of her symptoms like headaches which indirectly contributed to the FND symptoms. FND symptoms are mediated by attention and so other health conditions can lead to excessive attention towards the body which contributes to the development and maintenance of FND. Take away the other symptoms by correcting the structural defect and you are likely to see improvement in FND symptoms. It is reasonable to think both of those explanations were at play here. The danger here is thinking this means we should overly investigate and surgically correct all incidental findings. That will lead to more harm. It is also possible that her FND symptoms could return in the future under certain circumstances.
Regarding the question you propose at the end: FND would be invalidated if she didnโt have FND symptomsโฆbut she had all the textbook FND symptoms which cannot be explained by a CSF leak. If this were Parkinsonโs disease or migraines, would you ask the same question?
The scientific construct of FND is falsifiable: FND models make testable claims regarding altered agency, attention, prediction, motor control, interoception, threat/arousal regulation, and abnormal integration of sensory-motor predictions. These claims can be tested with behavioral experiments, neurophysiology, imaging, treatment-response studies, and predictive-processing/active-inference models.
The FND diagnosis can be falsified or weakened by evidence such as:
In this case, none of that applies but if it did it would invalidate the FND diagnosis. This case is a good example of comorbidity and the importance of treating comorbidities (although it is questionable here if the CSF leak truly needed to be repaired) but it doesnโt tell us anything about the validity of FND.
Thanks for the thoughtful comment.
My point is not that this case proves the patient never had FND or that CSF leaks generally explain FND. It is about what evidence would actually count against an established FND diagnosis.
That is also why I don't think the comparison with Parkinson's disease is quite equivalent. Parkinson's has converging biological evidence and established biomarkers, making questions of falsification considerably less ambiguous. My question is specifically about what would falsify a clinical FND diagnosis.
The explanations you propose, such as placebo effects, predictive processing, attention, functional overlay, or future relapse, are all possible. However, from a strict Karl Popper perspective, they function as auxiliary hypotheses that preserve the original diagnosis rather than exposing it to the risk of falsification. If every seemingly contradictory observation can be accommodated by adding another explanation, then the diagnosis becomes increasingly difficult to falsify.
That is what I find interesting. If complete resolution following successful treatment of another neurological disorder is still insufficient to prompt reconsideration of the diagnosis, what observation would?
I am also intrigued by the authors' choice of the phrase "functional appearing symptoms" rather than simply "functional symptoms." That wording seems to leave open the possibility that the presentation resembled FND without necessarily reflecting its proposed mechanism, which is why I raise the common phenotype hypothesis as an alternative interpretation rather than a conclusion.
๏ปฟ@Copper Comet of Lagoon๏ปฟ Your comment inadvertently illustrates exactly the point of the post. Even though the patient had remained symptom free for up to three months after the CSF leak was repaired, you preserve the FND diagnosis through explanations like functional overlay, comorbidity, placebo, attention, predictive processing, or by questioning the significance of the repair itself, something the authors of the paper do not question.
One other point is that the paper itself does not treat the CSF leak as an incidental finding or question whether it required repair. Those are additional interpretations. The authors accepted it as a curable underlying pathology, repaired it, and reported complete symptom resolution, yet still retained the FND diagnosis.
I answered your question regarding what would falsify a clinical diagnosis of FND. The clinical diagnosis of FND can be falsified or weakened by evidence such as:
Again, none of those apply to this case which is why FND was kept as a comorbidity and is not considered a misdiagnosis. The authors propose maybe a CSF leak could cause these FND symptoms but then contradict themselves by clearly stating it could not cause the motor symptoms and that the motor symptoms are consistent with FND.
Parkinsonโs Disease and migraines are both clinical diagnoses and diagnosed the exact same way as FND - presence of characteristic features in the history and examination. Parkinsonโs is not diagnosed based on biomarkers. We can verify the diagnosis with an autopsy after death but we are talking about clinical diagnosis so it is the same as FND in this scenario.
We can certainly discuss emerging evidence from ฮฑ-synuclein seed amplification assays (SAAs) and other biomarkers, but this post is not about Parkinson's. It is an interesting side discussion though. I agree that Parkinson's remains a clinical diagnosis (Parkinson's diagnosis is also subject to clinician bias and diagnostic error). However, over time the diagnosis is typically either strengthened or weakened as the disease evolves.
Likewise, only time will tell whether the functional symptoms return in this case. At present, however, the patient has remained symptom free for the reported three month follow up after repair of the CSF leak.
Technically, what you're laying out is a syllogism or deductive argument:
The point I am exploring is whether premise 2 is necessarily true, or whether the CSF leak, or the underlying biological process associated with it, could instead have produced a functional appearing motor phenotype.
What do we make of an FND diagnosis that completely resolves following treatment of another neurological disorder? If a patient once met the diagnostic criteria for FND, does that diagnosis remain indefinitely, regardless of what happens afterwards? Or should complete resolution following treatment of another neurological disorder at least prompt reconsideration of the original diagnosis? If the patient remains symptom free for 1 year, 5 years, or 10 years after repair of the CSF leak, at what point would the longitudinal data become sufficient to reconsider the original diagnosis?
One thing I also find interesting is that most of your criteria are retrospective. They describe how to reassess an existing FND diagnosis after new information becomes available. From a strict Karl Popper perspective, however, falsifiability is about specifying what observations would count against a hypothesis, not simply how we reinterpret observations after the fact. That is why I find the falsifiability question so interesting.
Of course, if FND is ultimately better understood as a common neurological phenotype rather than a distinct disorder, then much of this discussion becomes largely irrelevant. The question would no longer be whether the patient "still had FND," but rather what underlying biological process produced the functional appearing phenotype in the first place.
๏ปฟ@Copper Comet of Lagoon๏ปฟ Just out of interest (I'm not sure what your background is, cons of anonymous comments), based on your comment, am I right in thinking that you consider the CSF leak to have been incidental and the surgery unnecessary? That doesn't appear to be the interpretation of the authors.
If so, and assuming you're a clinician, wouldn't that make you less likely to consider or investigate a CSF leak as a differential diagnosis in a similar patient? That's what concerns me.
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