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Title: | Stress and functional neurological disorders: mechanistic insights. | Austin Authors: | Keynejad, Roxanne C;Frodl, Thomas;Kanaan, Richard A A ;Pariante, Carmine;Reuber, Markus;Nicholson, Timothy R | Affiliation: | The Florey Institute of Neuroscience and Mental Health, Melbourne, Victoria, Australia Section of Women's Mental Health, Health Service and Population Research Department, Institute of Psychiatry Psychology & Neuroscience, King's College London, London, UK Section of Cognitive Neuropsychiatry, Institute of Psychiatry Psychology & Neuroscience, King's College London, UK Department of Psychiatry, Austin Health, The University of Melbourne, Heidelberg, Victoria, Australia Department and Hospital of Psychiatry and Psychotherapy, Otto von Guericke University Magdeburg, Magdeburg, Germany Stress Psychiatry and Immunology Lab, Institute of Psychiatry Psychology & Neuroscience, King's College London, London, UK Academic Neurology Unit, University of Sheffield, Royal Hallamshire Hospital, Sheffield, UK Section of Cognitive Neuropsychiatry, Institute of Psychiatry Psychology & Neuroscience, King's College London, London, UK |
Issue Date: | 2019 | Date: | 2018-11-08 | Publication information: | Journal of neurology, neurosurgery, and psychiatry 2019; 90(7): 813-821 | Abstract: | At the interface between mind and body, psychiatry and neurology, functional neurological disorder (FND) remains poorly understood. Formerly dominant stress-related aetiological models have been increasingly challenged, in part due to cases without any history of past or recent trauma. In this perspective article, we review current evidence for such models, and how research into the role of traumatic stress in other disorders and the neurobiology of the stress response can inform our mechanistic understanding of FND. First, we discuss the association between stress and the onset or exacerbation of a variety of physical and mental health problems. Second, we review the role of hypothalamic-pituitary-adrenal axis dysfunction in the neurobiology of ill-health, alongside evidence for similar mechanisms in FND. Third, we advocate a stress-diathesis model, in which biological susceptibility interacts with early life adversity, where FND can be precipitated by traumatic events later in life and maintained by psychological responses. We hypothesise that greater biological susceptibility to FND is associated with less severe remote and recent stress, and that FND precipitated by more severe stress is associated with lower biological vulnerability. This would explain clinical experience of variable exposure to historical and recent traumatic stress among people with FND and requires empirical investigation. A testable, evidence-based stress-diathesis model can inform nuanced understanding of how biological and psychological factors interact at the individual level, with potential to inform personalised treatment pathways. Much-needed research to establish the aetiology of FND will enhance clinical care and communication, facilitate effective treatment and inform prevention strategies. | URI: | https://ahro.austin.org.au/austinjspui/handle/1/19829 | DOI: | 10.1136/jnnp-2018-318297 | ORCID: | 0000-0003-4434-3526 0000-0003-0992-1917 |
Journal: | Journal of neurology, neurosurgery, and psychiatry | PubMed URL: | 30409887 | Type: | Journal Article | Subjects: | conversion disorder functional neurological disorder neuropsychiatry stress trauma, psychol seque |
Appears in Collections: | Journal articles |
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