The borderline diagnosis II: Biology, genetics, and clinical course

In Part I of this three-part article, consideration of the core features of BPD psychopathology, of comorbidity with Axis I disorders, and of underlying personality trait structure suggested that the borderline diagnosis might be productively studied from the perspective of dimensions of trait expression, in addition to that of the category itself In Part II, we review the biology, genetics, and clinical course of borderline personality disorder (BPD), continuing to attend to the utility of a focus on fundamental dimensions of psychopathology. Biological approaches to the study of personality can identify individual differences with both genetic and environmental influences. The aspects of personality disorder that are likely to have biologic correlates are those involving regulation of affects, impulse/action patterns, cognitive organization and anxiety/inhibition. For BPD, key psychobiological domains include impulsive aggression, associated with reduced serotonergic activity in the brain, and affective instability, associated with increased responsivity of cholinergic systems. There may be a strong genetic component for the development of BPD, but it seems clear, at least, that there are strong genetic influences on traits that underlie it, such as neuroticism, impulsivity, anxiousness, affective lability and insecure attachment. The course of BPD suggests a heterogenous disorder. Predictors of poor prognosis include history of childhood sexual abuse, early age at first psychiatric contact, chronicity of symptoms, affective instability, aggression, substance abuse, and increased comorbidity. For research purposes, at least, biological, genetic, and prognostic studies all continue to suggest the need to supplement categorical diagnoses of BPD with assessments of key underlying personality trait dimensions and with historical and clinical observations apart from those needed to make the borderline diagnosis itself Biol Psychiatry 2002;51:951-963 (C) 2002 Society of Biological Psychiatry.