The Neurobiological Basis of Adolescent-onset Borderline Personality Disorder.

Borderline personality disorder (BPD) is a disabling disorder characterized by poor affect regulation and impulse control. This often results in impaired interpersonal relationships and maladaptive behavior patterns, including aggression towards others and deliberate self-harm. The disorder remains notoriously difficult to treat effectively, with many patients responding poorly or partially even to the most widely accepted treatment strategies (Paris, 2005). Evidence suggests that early detection of BPD can attenuate the severity of symptoms (Chanen et al., 2008a); however, little is known about early predictors of this disorder. By assessing adolescents using diagnostic instruments similar to those used in adults, researchers are exploring the adolescent presentation of BPD in an effort to describe its incidence, phenomenology and prognostic import for the development of Axis I/II disorders in adulthood (Chanen et al., 2008b; Crawford et al., 2008). Prevalence estimates of adolescent-onset BPD in the community range from 0.9 to 3.0% (Lewinsohn, Rohde, Seeley, & Klein, 1997; Bernstein et al., 1993), while the prevalence in clinical populations is considerably higher – 11% in outpatient populations (Chanen et al, 2004) and 32–49% in adolescent inpatient units (Burket & Myers, 1995; Grilo et al., 1996). Clarifying the underlying biology of BPD, including etiological mechanisms, genetic factors and pathological processes, is essential for a full understanding of the disorder and for the development of more effective treatment and preventive strategies (Beauchaine, Hong, & Marsh, 2008). Over the past two decades, neurobiological studies in adult BPD have made important strides, but inquiry into adolescent-onset BPD is still in its infancy.