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Functional neurological disorder (FND) represents a paradigmatic neuropsychiatric disorder; patients present neurological physical symptoms but associated psychosocial stressors play a role as predisposing and precipitating factors.1 Recent neuroscience research has shed light on how the physical symptoms arise in terms of aberrant brain mechanisms2 but little is known in terms of why certain individual develop the disorder. Childhood abuse and life adversities have been linked to FND but cannot be viewed solely/exclusively as causal,3 as this association is partially non-specific. A multifactorial causal model has to be considered and a gene–environment interaction is plausible, as it could theoretically integrate life stressors as precipitating factors in a subset of susceptible individuals. There is to date no evidence for genetic risks of FND with only one study reporting familial cases suggesting disease modelling in families rather than genetic transmission.4 Twin studies in other functional symptoms (chronic fatigue, irritable bowel syndrome, etc)5 have found potential, even if weak, genetic influences but no studies looked specifically at neurological functional symptoms. In order to explore potential gene–environment interaction, epigenetics offers promising new routes. In particular, epigenetics in stress research and related psychopathologies has generated novel findings that remain to be replicated in large-scale datasets.6 Methylation of …
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