Un approccio dimensionale al disturbo di personalità borderline

Background: Borderline Personality Disorder (BPD) is one of the most prevalent personality disorders affecting approximately 1-2% of the general population in the U.S., with an incidence up to 20% in psychiatric settings. Complex interactions between genetic, neurobiological and environmental factors are involved in the pathogenesis of BPD, resulting in core dimensional symptoms such as emotional dysregulation, impulse dyscontrol, aggression, cognitive dysfunctions and dissociative states. Comorbidity with other mental disorders is frequent in BPD, particularly for mood and anxiety disorders, psychotic spectrum disorders, other personality disorders and substance abuse/dependence. Suicidal ideation is frequently experienced by BPD subjects as well, and almost 10% of affected patients who have committed suicide by adulthood. As a consequence, BPD patients are high utilizers of health care resources and the correct clinical management of this disorder represents a challenge for psychiatrists. The aim of the present review is to provide a dimensional approach to BPD with specific emphasis to neuropsychological and biological findings in BPD and their relation to clinical aspects such as comorbidity patterns and treatment issues. Methods: Review of existing literature, through search of relevant papers in the major medical and psychological data bases. Results: Neurobiological studies have shown that symptoms and behaviors of BPD are partly associated with alterations in basic neurocognitive processes, involving glutamatergic, dopaminergic and serotoninergic systems. In addition, neuroimaging studies in BPD patients indicated differences in the volume and activity of specific brain regions related to emotion and impulse control, such as the prefrontal cortex, cingulate cortex, amygdala and hippocampus (Table I). As for other mental disorders, genetic vulnerability and environmental factors play a critical role for the development of these neuropsychobiological alterations and, ultimately, to the development of BPD. Nevertheless, a multiple concomitant involvement of different neurobiological circuits in BPD is supposed to produce specific cognitive dysfunctions and results in heterogeneous symptom dimensions that may be targeted with specific treatment interventions including different forms of psychotherapy and the combination of pharmacological agents. Conclusion: In the light of the complex neuropsychobiological aspects underlying the pathophysiology of BPD, a dimensional approach including the use of different spectrum models and a comprehensive investigation of the main comorbidity patterns and symptom dimensions, seems not only of academic interest but, particularly, of great clinical importance in order to orient clinicians to the most appropriate treatment choice (Table III).