Functional neurological disorder (FND) is a common and highly disabling disorder, but its aetiology remains enigmatic. Conceptually, there has been reduced emphasis on the role of psychosocial stressors in recent years, with a corresponding increase in neurobiological explanations. However, a wealth of evidence supports the role of psychosocial adversities (eg, stressful life events, interpersonal difficulties) as important risk factors for FND. Therefore, there is a need to integrate psychosocial (environmental) and neurobiological factors (eg, sensorimotor and cognitive functions) in contemporary models of FND. Altered emotional processing may represent a key link between psychosocial risk factors and core features of FND. Here, we summarise and critically appraise experimental studies of emotional processing in FND using behavioural, psychophysiological and/or neuroimaging measures in conjunction with affective processing tasks. We propose that enhanced preconscious (implicit) processing of emotionally salient stimuli, associated with elevated limbic reactivity (eg, amygdala), may contribute to the initiation of basic affective/defensive responses via hypothalamic and brainstem pathways (eg, periaqueductal grey). In parallel, affect-related brain areas may simultaneously exert a disruptive influence on neurocircuits involved in voluntary motor control, awareness and emotional regulation (eg, sensorimotor, salience, central executive networks). Limbic-paralimbic disturbances in patients with FND may represent one of several neurobiological adaptations linked to early, severe and/or prolonged psychosocial adversity. This perspective integrates neurobiological and psychosocial factors in FND and proposes a research agenda, highlighting the need for replication of existing findings, multimodal sampling across emotional response domains and further examination of emotional influences on sensorimotor and cognitive functions in FND populations.
- conversion disorder
- functional neurological disorder
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DLP and TRN contributed equally.
Contributors TRN and SP formulated the idea and initial plan for the review and DLP contributed to refinement of the structure. SP conducted the literature searches and wrote the first and subsequent drafts. DLP, LHG and TRN contributed to revisions/editing of the manuscript. DLP designed and prepared figure 1, with contributions from SP. SP prepared online supplementary table 1 and figure 2, with contributions on revisions from DLP, LHG and TRN.
Funding DLP was funded by the Sidney R. Baer Jr. Foundation and the National Institute of Mental Health (NIMH) grant K23MH111983-02. SP and TRN were funded by the National Institute of Health Research (NIHR). This manuscript also represents independent research part-funded (LHG) by the NIHR Maudsley Biomedical Research Centre at the South London and Maudsley NHS Foundation Trust and King's College London.
Disclaimer The views expressed are those of the authors and not necessarily those of the NHS, NIHR, Department of Health (UK) or the NIMH (US).
Competing interests DLP has received honorarium from the Movement Disorders Society, American Academy of Neurology and Continuing Medical Education courses at Harvard Medical School.
Patient consent Not required.
Provenance and peer review Not commissioned; externally peer reviewed.
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