Although the term borderline has been in clinical use since the late 1930s, it only became an official Axis II diagnosis in 1980 with the publication of DSM-III. Currently, DSM-IV-TR emphasizes that patients with borderline personality disorder (BPD) show a "instability of interpersonal relationships, self-image, and affects, and marked impulsivity beginning by early adulthood and present in a variety of contexts," and any five out of nine listed criteria must be present for the diagnosis to be made.
Classification and Diagnosis
Gunderson (2001) portrayed DSM-defined BPD as a diagnostic category layered between neurotic and psychotic disorders, and he differentiated BPD from Otto Kernberg, M.D.'s, theoretical concept of intrapsychic structure referred to as borderline personality organization, an umbrella concept that encompasses a number of Cluster A and Cluster B personality disorders that are characterized by the presence of primitive defenses and identity diffusion, yet with the maintenance of reality testing (Kernberg, 1975). It is now clear that DSM-IV-defined BPD is a heterogeneous construct that includes patients on the mood disorder spectrum and the impulsivity spectrum (Siever and Davis, 1991), in contrast to the original speculation that these patients might be near neighbors of patients with schizophrenia or other psychoses. Patients with schizotypal personality disorders are, instead, the genetic cousins of those patients with schizophrenia.
Considerable controversy exists regarding the use of a categorical diagnostic system for the personality disorders because dimensional models of personality are widely utilized in personality studies and can accommodate style, traits and pathology (e.g., the five-factor model of neuroticism, extraversion, openness, agreeableness and conscientiousness [Costa and McCrea, 1992]). A reasonably robust literature supports the validity of a quantitative model (sometimes referred to as a "hypertension" model), implying that pathological functioning, disability and distress accompany the extreme exaggeration of an otherwise adaptive trait (Oldham and Morris, 1995). However, it has been difficult to achieve consensus on a single dimensional model, and the dimensional approach is not easily applicable to medical systems of classifying pathology.
Etiology and Neurobiology
A general convention that has been relatively universally accepted in personality studies is that personality itself involves two components: temperament (largely the genetic/constitutional component) and character (largely the component resulting from the molding and shaping influences of life events and development). There are a number of theories of the etiology of BPD (Oldham, 2002; Zanarini and Frankenburg, 1997), which need not be mutually exclusive. Due to the extensive heterogeneity within the DSM-IV-TR definition of BPD, there are inevitably multiple combinations of temperamental and environmental factors that lead to its development.
A general stress/vulnerability conceptual framework is useful in considering varying combinations of predisposing genetic risk factors and stressful life experiences (Paris, 1999). Among the factors contributing to the etiology of BPD that have been suggested are:
- Affective dysregulation (Akiskal, 1981; Akiskal et al., 1985; Klein and Liebowitz, 1982)
- Deficit in impulse control (Hollander, 1993; Links and Heslegrave, 2000; Siever, 1996; Zanarini, 1993)
- Excessive aggression, either as primary temperament or secondary to severe and sustained childhood abuse (Kernberg, 1975; Zanarini and Frankenburg, 1997)
- Impaired development of autonomy, perhaps related to parental separation-resistant pathology, resulting in intolerance in the patient with BPD to being alone (Gunderson, 1996; Masterson, 1972; Masterson and Rinsley, 1975)
- Lack of a stable sense of self or identity, perhaps secondary to inconsistency, neglect or abuse in early parenting (Adler, 1985; Adler and Buie, 1979)
Increasing numbers of studies are exploring the neurobiology of BPD, but findings to date are relatively nonspecific. It has been recognized that a complex process of gene-environment interaction is involved in the determination of personality types and disorders (Cloninger, in press; Siever et al., 2002; Torgersen, 2000). Endophenotypes are being studied, such as impulsive aggression in BPD, that are thought to reflect underlying genetic vulnerabilities (Siever et al., 2002). Reductions in central nervous system serotonin levels have been correlated with impulsive aggression in patients with BPD (Hansenne et al., 2002; New and Siever, 2002; Skodol et al., 2002b). Affective instability characterizes other patients with BPD, perhaps related to cholinergic irregularities (New and Siever, 2002; Pally, 2002).
In addition, patients with BPD who have experienced sustained childhood abuse may demonstrate hyperresponsiveness of the hypothalamic-pituitary-adrenal system (Rinne et al., 2002). Neuroimaging studies have suggested abnormalities in the prefrontal cortex in patients with BPD (Juengling et al., 2003; New and Siever, 2002), as well as reduced volume in the hippocampus and the amygdala (Schmahl et al., 2003). Further work is needed before the relevance and specificity of these findings for patients with BPD can be elucidated.
