The question of whether functional neurological disorder (FND) is genuine — or whether patients are simulating, exaggerating, or seeking attention — has burdened this field for decades. The review by Edwards, Yogarajah, and Stone addresses this question systematically and comprehensively, drawing on clinical observations, neuroimaging, electrophysiology, and psychophysics.
FND symptoms show consistent internal patterns that differ from the patterns one would expect in deliberate simulation. Motor symptoms of FND follow neurobiological logic — they are influenced by attention, distraction, and suggestion in predictable ways that a simulator could not sustain over time. The Hoover sign, tremor entrainment, and other positive clinical signs exploit precisely these attentional mechanisms, which are not under conscious control.
Studies that systematically observed patients with FND during blind investigation (e.g. EEG video monitoring during seizures) show that their behaviour is not consistent with deliberate performance. The duration of episodes, the motor patterns, and the post-ictal state in functional seizures differ characteristically from epileptic seizures — but also from what actors or simulators produce when asked to reproduce such an episode.
If FND were simulation, we would expect it to disappear as soon as the external motive for simulation disappeared. This is not what we observe. FND persists — often for years — even after the elimination of potential secondary gains. Long-term follow-up studies show that many patients remain symptomatic even years after diagnosis, regardless of whether disability claims have been resolved.
fMRI studies show altered activation of the prefrontal cortex, amygdala, and supplementary motor area in patients with FND — consistent with a model of disrupted motor preparation and abnormal inhibition. EEG studies show abnormal pre-movement potentials. Psychophysical studies demonstrate altered proprioceptive processing and changed body ownership. These are measurable biological changes, not personality traits.
The authors introduce the active inference framework as a compelling explanatory model for FND. In this model, the brain continuously generates predictions about sensory input and motor outcomes. In FND, these predictions become "stuck" — the brain generates a strong prediction of weakness, tremor, or altered sensation, and this prediction overrides incoming sensory evidence. The result is a real subjective experience of the symptom, without a structural lesion to explain it. This model makes testable predictions and has begun to guide new therapeutic approaches.
The authors devote a section to the cognitive biases that lead clinicians to incorrectly identify FND as simulation. Key among these: the assumption that symptoms that respond to psychological intervention must have had a psychological (intentional) cause; and the tendency to attribute unexplained symptoms to patient motivation rather than neurobiological mechanism. These biases are not harmless — they lead to withheld treatment, damaged trust, and worsened outcomes.
FND does not exist in isolation. It frequently co-occurs with anxiety disorders, depression, PTSD, and other neurological conditions (including epilepsy). This co-occurrence does not indicate that FND is a "symptom" of these conditions — rather, it reflects shared neurobiological vulnerabilities and overlapping pathophysiological mechanisms. Treatment of comorbidities is part of comprehensive management of FND, but does not substitute it.
The review concludes with practical recommendations for clinical practice. Key among them: the diagnosis of FND should be made positively, on the basis of clinical signs, and communicated clearly to the patient. The explanation should be honest and accessible — neither dismissive ("it's all in your head") nor overly technical. A multidisciplinary team — neurologist, psychologist, physiotherapist — produces better outcomes than any single-specialist approach.
The review primarily concerns adults, but the conclusions transfer to the paediatric population with important modifications. Children are less likely to maintain deliberate simulation over long periods; their symptoms are more closely tied to current psychosocial stressors; and their nervous systems are more plastic — which, on the one hand, makes them more susceptible to FND, and on the other, makes them more responsive to treatment. Early diagnosis and a team approach are particularly important in children.