Borderline Personality Disorder (BPD) is an Axis II disorder which falls under the ‘dramatic’ Cluster B personality disorders in the DSM-IV-TR (APA, 2000). It is an extremely complex and serious disorder characterised by a high prevalence of suicide attempts and NSSI (Chapman, Derbidge, Cooney, Hong, & Linehan, 2009). Symptoms of BPD are broad and include a wide range of behaviours, however, individuals with BPD characteristically experience turbulent interpersonal relationships, marked impulsivity, impaired self-image, and recurrent unstable affect (APA, 2000).
Compared to other personality disorders, BPD is frequently described as less stable both in symptom presentation and course of the disorder (Benazzi, 2008). Like other personality disorders, an accurate diagnosis of BPD can only be made in adults, although there is debate in the literature regarding the possibility of identifying the disorder in adolescents (Bernstein, Cohen, Skodol, Bezirganian, & Brook, 1996) or even children (e.g., Robson 1983). Recently, the research has been interested in the ways in which early detection of BPD may improve assessment and treatment outcomes for those individuals with the disorder (Chanen et al., 2007; Rathus & Miller, 2002). This is certainly something which future research may wish to explore, however, DSM-IV-TR (APA, 2000) states that “adolescents and young adults with identity problems (especially when accompanied by substance use) may transiently display behaviours that misleadingly give the impression of Borderline Personality Disorder” (p. 708). Hence, one needs to apply caution when generalising findings from adult populations with BPD to adolescents.
The current DSM-IV-TR (APA, 2000, p.710) classification for BPD includes 9 criteria, 5 of which must be met in order to accurately make a diagnosis. The 9
criteria listed are:
1. Frantic efforts to avoid real or imagined abandonment. Note: Do not
include suicidal or self-mutilating behaviour covered in (5).
2. A pattern of unstable and intense interpersonal relationships
characterized by alternating between extremes of idealization and
devaluation. This is called “splitting.”
3. Identity disturbance: markedly and persistently unstable self-image or
sense of self.
4. Impulsivity in at least two areas that are potentially self-damaging (e.g.,
spending, sex, substance abuse, reckless driving, binge eating). Note: Do
not include suicidal or self-mutilating behaviour covered in (5).
5. Recurrent suicidal behaviour, gestures, or threats, or self-mutilating
behaviour.
6. Affective instability due to a marked reactivity of mood (e.g., intense
episodic dysphoria, irritability, or anxiety usually lasting a few hours and
only rarely more than a few days).
7. Chronic feelings of emptiness.
8. Inappropriate, intense anger or difficulty controlling anger (e.g., frequent
displays of temper, constant anger, recurrent physical fights).
9. Transient, stress-related paranoid ideation or severe dissociative
symptoms.
There is a great deal of variation in the prevalence rates given for BPD, but estimations remain at 1 to 2% for the general population (Lenzenweger, Lane,
Loranger, & Kessler, 2007; Paris, 1999; Torgersen, Kringlen, & Cramer, 2001), 11% of all psychiatric outpatients (Heard & Linehan, 1993) and up to 25% of all psychiatric inpatients (Baker, Silk, Westen, Nigg, & Lohr, 1992; Widiger & Weissman, 1991). Recent studies by Jackson and Burgess (2000) suggested that approximately 6.5% of the adult Australian population have one or more personality disorders. BPD is by far the most commonly diagnosed personality disorder (Gunderson, 1984; Widiger & Weissman, 1991) and the most researched (Zimmerman & Mattia, 1999). BPD is a disorder that is more commonly diagnosed in young women (Becker, 1997; Swartz, Blazer, George, & Winfield, 1990).
There has been growing interest in so-called juvenile BPD, such that there has even been a special edition of Development and Psychopathology devoted to the topic (Lenzenweger & Cicchetti, 2005). The problem with this assumption is that, by definition, personality disorders are supposed to be enduring, lifelong conditions (APA, 2000) and this cannot be established in a very young person. However, it is perhaps an accurate assumption that symptoms manifest most strongly during early adulthood given hormonal shifts and developmental challenges associated with this age group (Paris, 2005; Zanarini, Frankenburg, Khera, & Bleichmar, 2001).
The development of the conceptualisation of BPD
BPD remains a much debated diagnosis in the research literature. Much of the controversy surrounds issues such as the variability and number of symptoms in comparison with other DSM-IV-TR (APA, 2000) diagnoses (Asnaani, Chelminski, Young, & Zimmerman, 2007), issues with comorbidity and difficulty with diagnosis (Lieb et al. 2004), the appropriateness or meaningfulness of the name of the disorder
(Classen, Pain, Field, & Woods, 2006; Davis, Blashfield, & McElroy, 1993), and if BPD as a psychiatric condition even exists (e.g., Charland, 2007).
BPD was not formally included in the DSM until 1980 (DSM-III; APA, 1980), although research evidence has suggested that early conceptualisations of the disorder date back to Greek Scholars. For example, descriptions of conditions characterised by marked impulsivity and mood lability are noted in the works of Aretaeus, Hippocrates and Homer (Millon & Davis, 1996). Such observations are absent in Medieval documentation, however, they resurfaced in the 17th century with Bonet’s reference to folie maniac-melancholique which described a syndrome
characterised by impulsivity and emotional lability (Millon, 1992). Millon (1992) described reports from 1854 from Baillarger and Falret detailing their findings from 30 years of work with depressed and suicidal patients. These authors described a large group of patients whose symptoms waned from depression to intermittent episodes of anger, irritability, and elation to periods of normality. In 1890, Falret’s son and later Janet (1901) expanded on this description to include observations of patients who were emotionally volatile, impulsive, and prone to contradictions in their behaviour (Millon, 1992). The 19th century nosologist Kraepelin was one of the first theorists to refer more specifically to conditions affecting personality, and his observations of impulsivity, unstable relationships, anger, affective instability and self-destructiveness more closely reflect current conceptualisations of BPD (Millon, 1992).
More contemporary references to the term ‘Borderline’ can be attributed to Stern (1938) who described a group of patients whose behaviour could be classified as being on the ‘borderline’ between psychosis and neurosis. Terms such as
‘borderland insanity’ or ‘borderline insanity’ also were used by physicians around this time to describe a group of patients whose mental state appeared to fluctuate between ‘reason’ and ‘despair’ (Millon & Davis, 1996). During this time, emphasis was placed on the presence or absence of psychosis and patients with ‘borderline’ features or behaviours were vaguely conceptualised within the spectrum of Schizophrenia. A characterisation of the ‘borderline’ entity distinct from Schizophrenia was expanded upon by Zilboorg (1941) and Hoch and Polatin (1949) but was not included in the first published version of the DSM (APA, 1952). During the 1950s and 1960s interest in borderline phenomena re-emerged, as researchers conceptualised the disorder within more of a psychoanalytic framework, thinking of symptoms in terms of an affective disorder spectrum. Easser and Lesser (1965) formulated a ‘hysteroid’ borderline type which was something akin to histrionic personality, but recognised as more severe (Millon, 1992).
Grinker, Werble, and Drye (1968) published a landmark study in the area of BPD research in which they outlined groups of patients whose symptoms and behaviours were grouped on the basis of a factor analysis. The first group was referred to as the ‘psychotic border’ group whose behaviour was erratic, angry and depressed, and who demonstrated a clinically inappropriate level of negative behaviour towards others. The second group, referred to as the ‘core borderline syndrome’ was characterised by pervasive negative affect, demonstrated by ‘acting out’. This group also was described as depressed, angry and lacking in indications of a stable sense of identity. The third group, referred to as the ‘affectless’ group, described a group of patients who were anhedonic, withdrawn, lacking in a sense of identity and unable to form appropriate attachments to others. The fourth group,
referred to as the “border with the neuroses” group, demonstrated childlike “clinging” behaviour, depression, anxiety and neurotic behaviour (p. 89). To summarise their findings, the authors stated that Borderline individuals were characterised by the following: (1) anger; (2) defective relationships; (3) absence of consistent identity; and (4) depression and loneliness due to interpersonal difficulties.
It was not until the 1970s that the ‘borderline syndrome’ (Kernberg, 1976) was more clearly defined as an affective disorder rather than as a variant or subtype of Schizophrenia. Kernberg (1976) used the term borderline to describe serious forms of character pathology, and this is generally accepted as the first modern conceptualisation of BPD. An extension of this concept is reflected in the work of Gunderson and Singer (1975) who provided a review which proposed six criteria for the diagnosis of BPD. Specific criteria for the diagnosis of BPD were outlined by Robins and Guze (1970), and then extended by Spitzer, Endicott, and Gibbon (1979) who further delineated a set of criteria that more closely resembles that of the current diagnostic criteria. Spitzer et al. comprised a list of 17 criteria which was reviewed by 4,000 psychiatrists. The discriminatory capacity of these criteria indicated that the list could accurately discriminate individuals with and without BPD individuals approximately 90% of the time. The second major conceptualisation of BPD is reflected in the work of Gunderson (1984) who used the term borderline to describe a specific personality disorder. Gunderson proposed that this disorder could be meaningfully distinguished from a number of other Axis II disorders in Cluster A (odd) and Cluster C (anxious).
In the 1960s and 1970s, research focused on the conceptualisation of borderline individuals as having a propensity to experience transient psychotic-like
symptoms. Researchers proposed that BPD was better explained as a schizophrenia spectrum disorder (Wender, 1977). When the disorder was first included in the third edition of the DSM, there were only 8 diagnostic criteria. Criterion 9, ‘transient, stress-related paranoid ideation or severe dissociative symptoms’, was not added until 1987 (DSM-III-R, APA, 1987).
The fourth conceptualisation appeared during the 1980s and this reflected a more thorough approach by combining aspects of clinical care with empirical research. This approach focused on the chronic dysphoria and affective instability of individuals with BPD. Within this conceptualisation, several researchers took the view that BPD was better explained as an affective spectrum disorder (e.g., Akiskal, 1981; Stone, 1980).
The fifth and sixth conceptualisations of BPD were developed during the 1990s. Several researchers proposed that BPD is best conceptualised as an impulse spectrum disorder, which is related to substance use, Antisocial Personality Disorder (ASPD), and possibly eating disorders (Links, Heslegrave, & van Reekum, 1999; Zanarini, 1993).
Another view that was first proposed by Herman and van der Kolk (1987) suggested that BPD can be conceptualised as a chronic form of PTSD. This led to the suggestion that BPD may be a trauma spectrum disorder, which is closely related to dissociative disorders. However, several researchers have disagreed with this conceptualisation, highlighting that there are nontraumatic pathways to BPD (Graybar & Boutilier, 2002; Paris & Zweig-Frank, 1992) and stating that it is unwise to view childhood adversity as the cause of BPD (Zanarini & Frankenburg, 2007).
accurately understood as a mood disorder, particularly within the context of Bipolar Disorder (BP, or sometimes confusingly referred to in the literature as BPD). Numerous papers have been dedicated to the topic of whether or not BP and BPD can be meaningfully differentiated, and whether or not these two disorders should be conceptualised within the same spectrum (e.g., Benazzi, 2008; Gunderson et al., 2006; Magill, 2004; Paris, Gunderson, & Weinberg, 2007; Wilson et al., 2007).
There are an alarming number of clinicians who either mistakenly view the emotional lability of BPD individuals as symptoms of BP (Paris, 2008; Zanarini & Frankenburg, 2007), or are choosing not to use BPD diagnoses for insurance reasons, or fear of stigma and poor outcome for their patients (Paris, 2008). The relationship between BPD and BP and potential issues with comorbidity will be discussed in more detail in Chapter 8.
BPD has remained a valid diagnosis in subsequent versions of the DSM (APA, 1994, 2000) and also is included in the International Classification of Disease (ICD-10) (World Health Organisation, WHO, 1993) system. Research has indicated that BPD has a unique clinical presentation that successfully can be differentiated from other disorders (Zanarini, Gunderson, Frankenburg, & Chauncey, 1990). It has been established that BPD likely has both a biological and environmental aetiology (Torgersen et al., 2001; Zanarini, Frankenburg, & Frances, 1997).
Criticisms of the use of BPD diagnosis
Despite the fact that BPD has been considered to be a sufficiently reliable and valid diagnosis by the International Personality Disorder Examination (IPDE; Loranger, Sartorius, Andreoli, & Berger, 1994), there have been examples where
researchers have questioned whether or not BPD actually exists, or they have emphasised that the term reflects a dated or unhelpful diagnosis (e.g., Herman, Perry, & van der Kolk, 1989). Charland (2007) pointed out that within the Chinese Classification of Mental Disorders (CCMD-III, in Charland, 2007) there is no mention of BPD or allusion to its existence. The reasons for this absence of a BPD diagnosis appear to be related to cultural concerns with medicalisation of behaviour and avoiding stigma. However, it is apparent that even though BPD does not ‘officially exist’ in China, there certainly are individuals in China with BPD (Zhong & Leung 2007 in Charland, 2007).
Over time, the term ‘borderline’ has been used as something of a miscellaneous category to define those patients that clinicians do not know how to diagnose (Kreisman & Straus, 2004), or to describe individuals who demonstrate challenging behaviour (Markham & Trower, 2003). Certainly, there is indication that BPD has been over diagnosed or inappropriately diagnosed (Winstead & Sanchez- Hucles, 2008). Kreisman and Straus (2004) provided the following description, which defines how many researchers and clinicians view this disorder:
“In many ways, the borderline syndrome has been to psychiatry what the virus is to general medicine: an inexact term for a vague but pernicious illness that is
frustrating to treat, difficult to define, and impossible for the doctor to explain
adequately to his [sic] patient” (p.5).
Researchers such as Classen and colleagues (2006) suggested that the problems associated with the diagnosis of BPD stem from the time it took for the first mention of the disorder in 1938 (Stern, 1938) to inclusion in the DSM-III in 1980. The validity of the BPD diagnosis has long been questioned (Paris, 1994) for
being vague and stigmatizing, particularly towards women (Courtois, 2004; Zanarini et al., 1997).
Furthermore, there has been the suggestion that a diagnosis of BPD does not fully acknowledge the influence of environmental factors which contribute to maladaptive behaviour such as childhood abuse and attachment problems. One author has suggested that a dual diagnosis of PTSD and BPD is insufficient and that the conceptualisation of BPD should be changed to better accommodate trauma, abuse and dysfunctional parental attachment experiences of these individuals (Classen et al., 2006). Rates of comorbid PTSD in this group are high, with 56% of individuals with BPD also experiencing comorbid PTSD and 68% of individuals with PTSD also receiving a diagnosis of BPD (Shea, Zlotnick, & Weisberg, 1999). However, despite these suggestions that the diagnosis of BPD should encapsulate more of these contributing factors, it needs to be maintained that the DSM-IV-TR (APA, 2000) is designed to be atheoretical in its classification of psychiatric disorders (Bender & Skodol, 2007).
For these reasons, some researchers have proposed to change the name of the disorder to reflect additional experience of trauma. Posttraumatic Personality Disorder and Complex Posttraumatic Stress Disorder (Classen et al., 2006) are two alternatives that have been proposed. Although these proposals clearly recognise some important aspects of BPD that may otherwise be missing, they do not account for the fact that not all individuals with BPD have experienced similar levels of trauma and/or attachment problems. There is research to suggest that despite popular belief, not all individuals diagnosed with BPD come from dysfunctional family backgrounds and, similarly, not all individuals have experienced trauma and abuse
(Gunderson & Sabo, 1993; Paris, 2008). The relationship between BPD functioning and PTSD will be explored further in Chapter 8.
Other researchers have suggested that BPD should be renamed Emotion Regulation Disorder or Emotion Dysregulation Disorder (e.g., Pfohl, 1999). It has recognised for some time that the term ‘Borderline Personality Disorder’ is vague and means little to laypeople who are trying to understand this complex disorder (Paris, 2008). It has been suggested that difficulties in the regulation, expression and management of emotions is at the core of BPD (Pfohl, 1999), hence a change of name would better account for and explain the diagnosis (Pfohl, 1999). Despite these concerns, the name of the disorder will remain unchanged in DSM-V, on the grounds that (a) changing the name will not reduce stigma, and (b) the names of other disorders such as Anorexia Nervosa (AN) and Schizophrenia also are inaccurate ways of describing psychopathology, yet remain unchanged (Skodol, 2011). The role of emotion regulation in BPD will be discussed further here and in Chapter 4.
Theories regarding BPD
There is perhaps no single theory with which to adequately explain the aetiology of BPD. Like many other psychological phenomena, the debate about whether the development of BPD is more accurately attributed to environmental or biological influences is ongoing (Paris, 2008). Early conceptualisations of BPD stem from psychoanalytic theory. Traditionally, this theory stresses that BPD symptoms result when the mother has failed to provide appropriate nurturance, tending to respond to her child in an unpredictable way (Stern, 1938). As a result of this poor nurturing, the child responds with aggression and may have difficulty synthesising
conflicting positive and negative emotions, which results in ‘splitting’ (Kernberg, 1976). In addition, some researchers have suggested that failures in early mothering lead to a failure to develop stable object constancy (Adler & Buie, 1979). It is also within psychoanalytic theory that Masterson (1972) first suggested that fear of abandonment is a central feature in BPD.
Traditional psychoanalytic treatment focuses on the resolution of unconscious conflicts that the individual with BPD experiences, sometimes through the use of transference in a therapeutic relationship (Stern, 1938). In more modern times, psychoanalytic approaches have become less popular after widespread criticism that this approach ignores the important influences of biology, social learning and cognition (Westen, 1991).
Environmental theories of BPD share some similar concepts of psychoanalytic theory in that the role of early life experiences, particularly the influence of trauma, is viewed as critical. In particular, five environmental factors are believed to be of aetiological importance: (1) early separation and loss, (2) disturbed parental involvement, (3) experiences of verbal and emotional abuse, (4) experiences of physical and sexual abuse, and (5) experiences of physical and emotional neglect (Zanarini & Frankenburg, 2007). These factors derive from years of clinical observations that many patients with BPD reported a history of abuse.
Some researchers have claimed that the experience of early trauma is a causal factor in the development of BPD (e.g., Bleiberg, 1994; Brown & Anderson, 1991; Bryer, Nelson, Miller, & Krol, 1987; Herman et al., 1989; Ogata et al., 1990; Silk, Lee, Hill, & Lohr, 1995). However, other researchers have argued that this view represents an oversimplification and that meta analyses indicate that the relationship
between these factors is weak (e.g., Fossati, Madeddu, & Maffei, 1999; Paris, 2003). It appears that although trauma may be a risk factor for BPD, it is not the primary cause, as research has indicated that there are several non traumatic pathways to the development of BPD (e.g., Graybar & Boutilier, 2002, Paris & Zweig-Frank, 1992). Approximately one third of individuals with BPD report an absence of childhood trauma (Paris, 2007), and another third report isolated incidents with little clinical significance (Paris & Zweig-Frank, 1996). It certainly is the case that not all individuals who experience childhood abuse and trauma develop BPD, just as it is not true to state that all individuals with BPD report a history of abuse.
Similar to these environmental theories are the attachment theories of BPD. Some researchers have suggested that there is a direct causal link in disturbed parental attachment between nascent BPD children and their parents. A range of studies have investigated the role of parental bonding or attachment (e.g., Barone, 2003; Hooley & Hoffman, 1999; Nickell, Waudby, & Trull, 2002; Patrick, Hobson,