A systematic review of the neurobiological underpinnings of borderline personality disorder (BPD) in childhood and adolescence
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- Catherine Winsper
- Division of Mental Health and Wellbeing, Warwick Medical School, University of Warwick, Coventry, CV4 7AL, United Kingdom of Great Britain and Northern Ireland
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- Steven Marwaha
- Division of Mental Health and Wellbeing, Warwick Medical School, University of Warwick, Coventry, United Kingdom of Great Britain and Northern Ireland
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- Suzet Tanya Lereya
- Evidence Based Practice Unit (EBPU), University College London and the Anna Freud Centre, London, United Kingdom of Great Britain and Northern Ireland
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- Andrew Thompson
- Division of Mental Health and Wellbeing, Warwick Medical School, University of Warwick, Coventry, United Kingdom of Great Britain and Northern Ireland
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- Julie Eyden
- Department of Psychology, University of Warwick, Coventry, United Kingdom of Great Britain and Northern Ireland
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- Swaran P. Singh
- Division of Mental Health and Wellbeing, Warwick Medical School, University of Warwick, Coventry, United Kingdom of Great Britain and Northern Ireland
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説明
<jats:title>Abstract</jats:title> <jats:p>Contemporary theories for the aetiology of borderline personality disorder (BPD) take a lifespan approach asserting that inborn biological predisposition is potentiated across development by environmental risk factors. In this review, we present and critically evaluate evidence on the neurobiology of BPD in childhood and adolescence, compare this evidence to the adult literature, and contextualise within a neurodevelopmental framework. A systematic review was conducted to identify studies examining the neurobiological (i.e. genetic, structural neuroimaging, neurophysiological, and neuropsychological) correlates of BPD symptoms in children and adolescents aged 19 years or under. We identified, quality assessed, and narratively summarised 34 studies published between 1980 and June 2016. Similar to findings in adult populations, twin studies indicated moderate to high levels of heritability of BPD, and there was some evidence for gene-environment interactions. Also consistent with adult reports is that some adolescents with BPD demonstrated structural (grey and white matter) alterations in frontolimbic regions and neuropsychological abnormalities (i.e. reduced executive function and disturbances in social cognition). These findings suggest that neurobiological abnormalities observed in adult BPD may not solely be the consequence of chronic morbidity or prolonged medication use. They also provide tentative support for neurodevelopmental theories of BPD by demonstrating that neurobiological markers may be observed from childhood onwards and interact with environmental factors to increase risk of BPD in young populations. Prospective studies with a range of repeated measures are now required to elucidate the temporal unfurling of neurobiological features and further delineate the complex pathways to BPD.</jats:p>
収録刊行物
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- Reviews in the Neurosciences
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Reviews in the Neurosciences 27 (8), 827-847, 2016-08-12
Walter de Gruyter GmbH