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A developmental psychopathology model of borderline personality disorder. From Putnam KM, Silk KR: Emotion dysregulation and the development of borderline personality disorder. Dev Psychopathol 17:899-925, 2005 Note. OFC, orbitofrontal cortex; ACC, anterior cingulate cortex; DLPFC, dorsolateral prefrontal cortex
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This review summarizes recent neurobiological research into youth with borderline personality disorder (BPD) to better delineate the biological factors involved in the development of this disorder. Psychobiological studies when BPD first becomes manifest are of particular interest, because there are fewer confounding factors (e.g., duration of illn...
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... field may benefit from recent studies of the impact of childhood adversity on the developing brain, especially by investigating the associated possible disturbances of the brain network architecture (42) and the biological stress response systems (19,82). The etiopathogenic model of BPD as outlined by Putnam and Silk (83) (Figure 1) illustrates the potential interactions among biological, psycho- logical, and social factors in the genesis of BPD and identifies various areas and indicators for further investigation. To enhance our understanding of these areas and their interactions, an inter- disciplinary approach that includes a wide range of clinical research as well as basic neuroscience research is mandatory. ...
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Borderline Personality Disorder (BPD) is clinically characterized by emotional instability, interpersonal disturbances and dysfunctional behavior such as non-suicidal self-injury (NSSI). During NSSI, patients with BPD typically report analgesic or hypoalgesic phenomena, and pain perception and pain processing in BPD have been repeatedly investigate...
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... Results indicate that the alterations in the triad involving putamen, amygdala, and OFC represent the specificity of this disorder (42)(43)(44). This circuit has been largely associated with affective instability and anger control as a consequence of dysfunctional emotion regulation (see Figure 3) (3,10,11,29,30,80,81). ...
Previous morphometric studies of Borderline Personality Disorder (BPD) reported inconsistent alterations in cortical and subcortical areas. However, these studies have investigated the brain at the voxel level using mass univariate methods or region of interest approaches, which are subject to several artifacts and do not enable detection of more complex patterns of structural alterations that may separate BPD from other clinical populations and healthy controls (HC). Multiple Kernel Learning (MKL) is a whole-brain multivariate supervised machine learning method able to classify individuals and predict an objective diagnosis based on structural features. As such, this method can help identifying objective biomarkers related to BPD pathophysiology and predict new cases. To this aim, we applied MKL to structural images of patients with BPD and matched HCs. Moreover, to ensure that results are specific for BPD and not for general psychological disorders, we also applied MKL to BPD against a group of patients with bipolar disorder, for their similarities in affective instability. Results showed that a circuit, including basal ganglia, amygdala, and portions of the temporal lobes and of the orbitofrontal cortex, correctly classified BPD against HC (80%). Notably, this circuit positively correlates with the affective sector of the Zanarini questionnaire, thus indicating an involvement of this circuit with affective disturbances. Moreover, by contrasting BPD with BD, the spurious regions were excluded, and a specific circuit for BPD was outlined. These results support that BPD is characterized by anomalies in a cortico-subcortical circuit related to affective instability and that this circuit discriminates BPD from controls and from other clinical populations.
... Studies of the neurobiological bases and markers of BPD and NPD in adolescence are conducted in several directions [13]. Structural MRI methods have shown that in girls with BPD, compared with the norm, the volume of gray matter in the dorsolateral prefrontal cortex of both hemispheres and in the left orbitofrontal cortex is reduced [13,14]. ...
... Studies of the neurobiological bases and markers of BPD and NPD in adolescence are conducted in several directions [13]. Structural MRI methods have shown that in girls with BPD, compared with the norm, the volume of gray matter in the dorsolateral prefrontal cortex of both hemispheres and in the left orbitofrontal cortex is reduced [13,14]. In patients with NPD, the volume of gray matter in the fronto-paralimbic areas, including the rostral and middle cingulate gyrus, the anterior part of the left insula, and the dorsolateral and medial prefrontal cortex, is reduced [15]. ...
... Reference lists of included studies were inspected for relevant titles. We also examined the reference lists of related narrative reviews as a cross-check (Chanen et al., 2008a;Goodman et al., 2013;Brunner et al., 2015). ...
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.
... Brunner, Henze, Richter, and Kaess (23), in this issue, summarize the neurobiological research on borderline PD in youth. They argue for the importance of this line of research during adolescence, when potential confounding factors are less likely to be present. ...
... Research into normal personality development has challenged these assumptions by demonstrating that normal personality traits in childhood and adolescence, despite fluctuations within certain lower-order domains, are more stable than would commonly be expected, and also more stable than PD symptoms (87,(89)(90)(91)(92). Furthermore, contrary to common expectations, research reveals that normal personality undergoes normative changes throughout the entire lifespan (93). Hence, some degree of development and change in personality is to be expected throughout the life course, as a result of the complex interactions between heritable dispositions and the environment (94)(95)(96)(97)(98)(99). ...
In this article, the authors provide a narrative review of the mounting evidence base on personality disorder in childhood and adolescence. Topics covered include diagnostic validity, prevalence, developmental issues, comorbidity, risk and protective factors, and treatment. Novel indicated prevention and early intervention programs for borderline personality disorder in adolescence are given special priority. To conclude, directions for future research are provided.
