Emotional reactivity to aversive primes impedes motor preparatory activity in functional neurological disorders

Patients with functional neurological disorders (FNDs) show impaired control of voluntary actions in the absence of organic neurological damage. The inconsistency between objective neurological clinical signs and actual performance of the same movements in slightly different contexts points to an abnormal self-focused attentional role towards movement execution. Yet, it remains unexplained what triggers a higher level of self-focused attention in FNDs and how this interferes with voluntary movements. Given the known threat sensitivity manifested by patients with FNDs, I hypothesized that under negative affective conditions self-focused attention might be heightened in FNDs in an automatic way so as to impede the execution of a voluntary action. Specifically, I used fMRI to investigate effective brain connectivity in "self-referential" and "limbic" circuits to delineate the causal functional architecture accounting for the FND specific activity when preparing a movement under aversive conditions with different levels of emotion awareness. Seventeen FND participants and seventeen healthy volunteers performed a motor task (key press and release) after having been exposed to an aversive or neutral picture prime using a sandwich mask paradigm. Behaviorally, the FND group had showed a slower reaction time across all task conditions and a high rate of missing key-press responses following associated to aversive primes. Dynamic Causal Modeling (DCM) analyses showed that the FND group emotional information did not engage a limbic network as observed in the healthy control group, but rather a different self-referential associated network. In this functional architecture, the aversive masked condition exerted a direct inhibitory effect on forward connections between the left IFG and left precentral motor cortex. These findings show how affective processing can impact on voluntary motor control in FND, helping to reduce the explanatory gap between emotionality and readiness to act as a potential process of functional motor symptom production.