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The Emotional Processing Theory of FND: Eight Years Later, Where Is the Proof?

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In 2019, a review published in the Journal of Neurology, Neurosurgery & Psychiatry proposed that abnormal emotional processing could help explain the neurological symptoms attributed to Functional Neurological Disorder (FND). The proposed mechanism involved heightened amygdala activity, increased autonomic arousal, altered communication between emotional and motor networks, and disturbances in the brain systems responsible for movement and bodily awareness.

The theory was that abnormalities in emotional processing might contribute to symptoms such as paralysis, tremors and seizures. Nearly eight years after the paper first appeared online in November 2018, however, its central causal mechanism remains unvalidated by the research examined here. Researchers have identified associations between emotional processing, brain activity and neurological symptoms, but associations do not establish what caused those symptoms.

There is also a remarkably obvious question that deserves far more attention: these patients are ill, often severely disabled, and may have spent years trying to understand what is happening to them. Why would anyone expect their emotional and physiological responses to resemble those of healthy people?

And there is an even more revealing question. If researchers performed similar experiments on people with multiple sclerosis (MS), epilepsy or other disabling neurological conditions, would they find comparable abnormalities? In the case of MS, published research demonstrates that several of the broad emotional-processing abnormalities described in FND research also occur in a disease with established neurological pathology.


The Original Theory Was Never an Established Mechanism

The paper, Emotional processing in functional neurological disorder: a review, biopsychosocial model and research agenda, was authored by Susannah Pick, Laura H Goldstein, David L Perez and Timothy R Nicholson. It reviewed experimental studies examining emotional processing in patients diagnosed with FND, using behavioural testing, physiological measurements and functional neuroimaging.

The authors proposed that heightened responses to emotionally significant stimuli, particularly involving the amygdala, might disrupt brain networks involved in voluntary movement, cognitive control and bodily awareness. They also suggested that these alterations could be associated with neurobiological adaptations arising from prolonged psychosocial adversity.

But the authors acknowledged that the underlying mechanisms of FND were not fully understood and that no well-accepted explanatory model existed. Their proposal was an attempt to explain the observations, not a demonstration that the proposed mechanism actually caused neurological symptoms.

That distinction matters because much of the evidence came from studying people who had already received an FND diagnosis. Identifying differences between those patients and comparison groups does not establish that the differences preceded their illness, caused their symptoms or are unique to the diagnostic category.


The Problems Were Already Documented in 2019

The original review acknowledged substantial methodological weaknesses, including:

  • Small samples: Many neuroimaging studies involved fewer than 20 participants, limiting statistical power and confidence in the results.
  • Inadequate comparison groups: Most studies compared FND patients with healthy controls rather than patients with other neurological or psychiatric conditions.
  • Psychiatric confounding: Depression, anxiety and other psychiatric conditions were not consistently accounted for.
  • Medication effects: Psychotropic medications were rarely adequately controlled for, despite their potential effects on cognition, emotional responses and brain activity.
  • Diagnostic heterogeneity: Different FND presentations were studied, but the review identified no direct experimental comparisons between FND subtypes using emotional-processing paradigms.
  • Reverse inference: Researchers sometimes interpreted activity in emotion-associated brain regions as evidence of emotional-processing disturbances without corresponding behavioural or physiological evidence.

The final issue is particularly important. The amygdala participates in multiple processes, including emotional salience, attention and learning. Increased activity in this region does not establish that emotional dysfunction caused paralysis, seizures or abnormal movements. Nor does altered connectivity between emotional and motor networks demonstrate which process initiated the symptoms.

The researchers recognised these limitations and recommended replication, larger samples and better clinical comparison groups. The question is whether subsequent evidence has established the causal mechanism they proposed.


These Patients Are Ill. Why Is an Emotional Response Surprising?

Consider someone experiencing unexplained neurological symptoms. They may be unable to walk, work, drive or care for themselves. They may have undergone repeated investigations, received conflicting medical opinions or spent years without a satisfactory explanation. They may be frightened about their future, worried about deterioration and uncertain whether something serious has been overlooked.

Under those circumstances, heightened emotional arousal, vigilance, changes in heart-rate variability or altered responses to threatening stimuli would hardly be astonishing. These can occur in the context of serious illness, pain, uncertainty and prolonged stress. They do not automatically indicate that an emotional-processing abnormality caused the underlying neurological condition.

Yet much of the research reviewed in 2019 compared people diagnosed with FND against healthy volunteers. That comparison creates a fundamental interpretive problem. If one group is living with disabling neurological symptoms and the other is generally healthy, any differences in emotional or physiological responses could reflect numerous factors associated with illness rather than a distinctive mechanism responsible for FND.

Before interpreting heightened emotional responses as evidence of a neurological disorder's cause, researchers need to establish whether those responses are unusual for people experiencing comparable illness, disability and uncertainty.

The question is not whether the measurements are real. The question is what they mean. A measurable physiological difference can be genuine while the proposed causal explanation remains completely unproven.

There are several possibilities that need to be distinguished. Emotional-processing abnormalities could precede and contribute to neurological symptoms. They could develop as consequences of illness. An underlying neurological or systemic process could produce both the symptoms and the emotional-processing changes. Or several mechanisms could operate together. Simply observing an association cannot determine which explanation is correct.


What Happens When Researchers Study Multiple Sclerosis?

This is where the emotional-processing argument becomes particularly interesting. MS is an inflammatory, demyelinating disease of the central nervous system with established neurological pathology. Patients may experience weakness, sensory disturbances, tremor, fatigue, cognitive changes and other disabling symptoms. Emotional-processing abnormalities have also been documented in MS.

A 2021 study published in Scientific Reports, Emotional experience is increased and emotion recognition decreased in multiple sclerosis, compared 25 women with MS against 27 healthy controls matched for age, sex and education. Researchers assessed facial emotion recognition and emotional experience using the International Affective Picture System (IAPS).

They found that the MS group had greater difficulty recognising emotional expressions and showed altered, generally increased subjective emotional responses to affective images. Importantly, these emotional measurements were not significantly correlated with anxiety, depression or alexithymia in that sample. The findings therefore could not simply be reduced to participants reporting greater psychological distress.

Why is this so relevant? Because the 2019 FND review also discussed experiments using IAPS images, alongside studies examining facial emotion recognition. In both research areas, investigators identified differences in emotional processing when comparing patients with healthy individuals.

The studies were not identical, and the findings cannot be treated as a direct replication of the FND results in MS. Nevertheless, they demonstrate that abnormalities in the same broad emotional-processing domains can be found in a neurological disease whose underlying pathology is independently established.

In MS, nobody needs to invoke an emotional-processing disturbance to establish the existence of demyelinating disease. The emotional findings must instead be interpreted in the context of the neurological condition, its effects on brain function, the patient's circumstances and other possible contributing factors.

Why should comparable categories of findings in FND automatically receive a different causal interpretation?

The answer cannot simply be that the participants have been diagnosed with FND. That would use the diagnostic label to justify the proposed mechanism and then use the proposed mechanism to explain the diagnostic label. It would not independently establish causation.


The Same Measurements Can Have Different Explanations

MS is not the only relevant comparison. Altered autonomic regulation, emotional processing and brain-network activity have been described in other neurological and medical conditions, including epilepsy, Parkinson's disease and chronic pain. These findings are not necessarily identical across diseases, and their underlying causes can differ substantially.

That is precisely why diagnostic specificity matters. Reduced heart-rate variability, for example, can occur through several physiological pathways. Altered amygdala activity may be associated with emotional processing, neurological pathology, medication effects or other factors. Neither finding independently identifies FND or establishes that psychological processes caused neurological symptoms.

The MS comparison also prevents an overly simplistic counterargument. It would be equally unjustified to insist that all emotional-processing changes in FND are merely understandable reactions to illness. In MS, some emotional-processing differences may arise directly from neurological dysfunction rather than psychological distress. An underlying medical process could potentially affect both neurological symptoms and emotional regulation in other patient populations as well.

The evidence therefore requires researchers to distinguish between cause, consequence, shared pathology and unrelated associations. Without that distinction, finding an emotional-processing abnormality tells us considerably less than a causal theory requires.


The Comparison That Should Have Been Made

The original authors acknowledged that comparisons primarily involving healthy controls limited conclusions about FND specificity. They recommended including clinical comparison groups. But the issue deserves a more demanding experimental approach than simply adding patients with anxiety or depression.

Why not compare FND patients with people who have MS, epilepsy or other neurological illnesses, matched as closely as possible for disability, symptom burden, illness duration, medication exposure and psychological distress? Better still, include patients experiencing similarly unexplained neurological symptoms who are undergoing investigation and whose eventual diagnoses are not yet known.

Such research could address questions that healthy-control comparisons cannot:

  • Are emotional-processing abnormalities greater in FND than in similarly disabled patients with established neurological diseases?
  • Do patients experiencing comparable diagnostic uncertainty exhibit similar autonomic and emotional responses?
  • Are any observed differences still present after accounting for medication, pain, fatigue, depression, anxiety and disease severity?
  • Can the proposed emotional-processing measurements distinguish FND from other neurological conditions with clinically useful accuracy?
  • Do the abnormalities precede neurological symptoms, or do they emerge after symptoms and disability develop?
  • Does the proposed emotional-processing mechanism predict outcomes better than competing explanations?

Even a convincing difference between FND and MS would not, by itself, establish causation. It could demonstrate diagnostic association or specificity, but showing that a particular mechanism generates symptoms would require additional prospective and experimental evidence.

Without appropriate comparisons, however, researchers risk treating biological responses associated with being ill as though they reveal why the illness exists.


Subsequent Research Has Challenged the Underlying Assumptions

A 2023 paper, A New Science of Emotion: Implications for Functional Neurological Disorder, questioned conventional assumptions about identifying emotions through distinctive physiological patterns, facial expressions and activation of particular brain regions. These questions are relevant because the 2019 model depends partly on interpreting activity in emotion-associated neural circuits.

The later authors did not conclusively disprove the Pick model. They offered a different conceptual approach to emotion and FND. Nevertheless, the paper illustrates that the theoretical interpretation of emotional-processing measurements remains contested. Identifying activity in a brain region associated with emotion is not the same as demonstrating that a particular emotional process caused a neurological symptom.

A 2024 systematic review of anger regulation in FND examined 54 studies involving 2,502 patients. Only five studies were rated as good quality, with the remaining 49 rated fair or poor. Although some differences in anger-related processing were reported, the review did not establish that those abnormalities caused FND symptoms.

A 2025 review examining psychological heterogeneity in FND identified six potentially overlapping psychological patterns rather than a uniform psychopathological profile. Such heterogeneity complicates attempts to describe a single emotional-processing disturbance as a common explanatory mechanism across patients with very different neurological presentations.

These publications do not establish that emotional processing is irrelevant to every patient diagnosed with FND. They do, however, leave substantial questions about measurement, consistency, specificity and causation unresolved.


What Happens When Researchers Examine Changes Over Time?

One way to investigate causal explanations is to determine whether a proposed abnormality precedes the symptoms it is supposed to generate. Longitudinal studies can help establish temporal relationships, although temporal prediction alone still does not prove causation.

A 2026 longitudinal neuroimaging study in Brain Communications followed 32 patients diagnosed with FND over approximately seven months, with 28 completing follow-up imaging. Researchers investigated relationships between functional connectivity and changes in symptoms. Several reported associations weakened after accounting for affective symptoms or trauma.

That study concerned changes during an already established illness. It did not demonstrate that emotional-processing abnormalities originally generated the patients' neurological symptoms or directly establish the superiority of the Pick model over competing causal explanations.

An additional 2026 study, Momentary predictors of dissociation in functional neurological disorder, repeatedly assessed 17 patients with FND and 17 healthy controls over one week. The researchers examined negative emotional states, subjective arousal, heart rate and dissociative symptoms.

Negative affect and subjective arousal were associated with dissociative symptoms measured at the same time. However, the time-lagged analyses did not identify significant associations. Furthermore, the group differences in dissociative symptoms did not remain significant after controlling for depression, and heart rate lost significance when considered alongside subjective emotional measures in combined models.

These results do not establish that emotional changes caused subsequent dissociative symptoms. Nor do they conclusively exclude such a relationship: the study was small, and its measurement intervals may not capture every relevant process. Nevertheless, the distinction between simultaneous association and demonstrated temporal causation remains important.

Notably, Susannah Pick, the lead author of the original emotional-processing review, was also a co-author of this 2026 investigation. The research therefore reflects continued investigation of related mechanisms, not confirmation that the original causal explanation has been established.


What Has Actually Been Proven?

The research supports the conclusion that some groups diagnosed with FND exhibit measurable differences in emotional processing, autonomic physiology and brain activity under certain experimental conditions. That is a much narrower finding than demonstrating that abnormal emotional processing causes their neurological symptoms.

The following claims remain unestablished by the evidence examined here:

  • That the proposed emotional-processing abnormalities consistently precede the onset of FND symptoms.
  • That heightened amygdala activity causes functional paralysis, tremors or seizures.
  • That altered emotional–motor network connectivity is a demonstrated cause rather than a correlate or consequence of symptoms.
  • That the proposed findings are sufficiently specific to FND when compared with appropriately matched neurological patients.
  • That the emotional-processing model predicts symptom development better than alternative neurological or physiological explanations.
  • That the proposed causal mechanism has been independently validated across the different presentations grouped under FND.

There is also a separate issue concerning diagnostic classification. Researchers studying people already diagnosed with FND can describe the characteristics of that selected population, but those observations do not independently demonstrate that every participant shares the same underlying disease process. Nor can group-level findings establish the cause of an individual patient's symptoms.

That matters clinically. A person presenting with neurological symptoms needs an assessment that remains responsive to new evidence, evolving symptoms and plausible alternative diagnoses. An explanatory theory should not become a substitute for investigating an individual patient's condition.


Eight Years Later, Where Is the Proof?

The 2019 emotional-processing model attempted to explain how emotional and neurological processes might interact to generate FND symptoms. Its authors acknowledged substantial weaknesses in the supporting research and identified the need for better-controlled studies.

Subsequent research has continued to identify associations, but the causal mechanism remains unestablished in the studies examined here. More importantly, research in MS demonstrates that differences in emotional recognition and emotional experience are not exclusive to patients diagnosed with FND. The overlap does not prove that the precise mechanisms are identical, but it makes claims of diagnostic specificity impossible to take for granted.

The most obvious question remains unanswered: when a person is living with disabling neurological symptoms, uncertainty and the possibility of serious illness, what emotional and physiological responses should researchers reasonably expect? And how do those responses differ from those of someone living with MS or another established neurological disease?

If patients with MS can exhibit altered emotional processing while having independently established neurological pathology, finding emotional-processing abnormalities in patients diagnosed with FND cannot, by itself, establish that those abnormalities caused their neurological symptoms.

The burden of proof is not satisfied by showing that patients respond differently from healthy volunteers. It requires demonstrating that the proposed abnormalities are relevant, sufficiently specific and causally connected to the symptoms being explained.

Nearly eight years after the original paper appeared online, the research examined here has not established that causal connection. That does not mean every possible emotional contribution has been excluded. It means the proposed mechanism has not earned the status of a demonstrated explanation.

Patients do not owe an unproven theory their diagnostic future. If researchers claim emotional dysfunction generates neurological symptoms, they need to demonstrate it, distinguish it from the consequences of illness, and show why comparable findings in established neurological diseases do not undermine their interpretation. Until then, the theory remains a theory. It is not proof of what is wrong with a patient.


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