Current research indicates that personality disorders affect about 12% of the general population and constitute a significant mental health issue (Zanarini, 2005a). Recent studies have found that personality disorders (PDs) are more powerful predictors of quality of life than any one of the following: (1) socio-demographic variables; (2) Axis I disorders; and/or (3) somatic health (Zanarini, 2005a). It is also well known that patients with personality disorders make extensive use of mental health facilities and have more extensive histories of inpatient and outpatient treatment when compared to patients presenting only with Axis I disorders such as major depression (Zanarini, 2005a). All of the above highlight the importance of considering personality disorders in treatment planning and management of patients with dual diagnosis (Zanarini, 2005a).
Although it is generally recognized that personality disorders have a poorer response to treatment across all treatment modalities, there are a number of emerging findings that suggest more optimistic outcomes to treatment and management (Zanarini, 2005a). Most notably, emerging patterns indicate that personality disorders are not as stable as initially thought and studies indicate that they tend to go into remission at a quicker pace than expected (Zanarini, et al., 2007). It also appears that certain aspects of personality disorder are more amenable to treatment (Zanarini, et al., 2007). Further, there is now more evidence to suggest that borderline personality disorder (BPD) responds relatively well to treatment (Zanarini, et al., 2007).
Although borderline patients are very difficult to work with and pose many dilemmas for the treatment process, evidence suggests that they have a reasonably good prognosis when compared to other PDs and anxiety disorders (Zanarini, et al., 2005).
In this paper, I will review some of the current debates and trends in the diagnosis, course, and etiology of BPD. Current findings in these areas suggest new ways of thinking about BPD that have important consequences for guidelines to treatment. At the heart of the condition of patients with BPD, lies the experience of intense dysphoria or psychic pain that has been related to both adverse early experience and temperament (Zanarini, et al., 2007). It has been suggested that “…borderline patients have a temperament that leads them unconsciously to transform unbearable feelings of rage, sorrow,shame and/or terror into unremitting attempts to get others to pay attention to the enormity of the emotional pain that they feel” (Zanarini, et al., 2007). These intense emotional states likely are sensed as an internal source of harm and probably reflect disturbed early development. It is in the interaction with the early care giving environment that such dominant and painful affects become established (Clarkin, Lenzenweger, Yeomans, Levy & Kernberg, 2007). While it is right to direct effort toward containing self-harming behaviors, it is in the development of a treatment alliance (Paris, 2005) and a sustained attachment relationship (Bateman & Fonagy, 2000) that therapeutic progress is likely to occur.
Zanarini remarks that it is “reasonable to suggest that BPD, and other personality disorders, are slow moving disorders…relatively slow to resolve. This is a very different view than that they do not change over time and, thus, are chronic” (Zanarini, 2005a). The view of personality disorder as chronic, intractable disorder becomes a recipe for failure when attempting engagement (Zanarini, 2005a). It is perhaps more reasonable to view these disorders as those of relatedness and/or self that require a relationally based approach (Sherry, 2007). This may require a shift in focus away from a symptom-based approach (Sherry, 2007). The Psychodynamic Diagnostic Manual (PDM) places “personality patterns” first in diagnostic classification because “symptoms OR problems cannot be understood, assessed or treated in the absence of an understanding of the mental life of the person…” (PDM task force, 2006). This involves recognition “of the characteristic ways the individual organizes mental functioning and engages with the world” (PDM task force, 2006). These patterns will be established early in life as internal “working models” (Bowlby, 1971), and experientially, in terms of attachment patterns. Diagnosis and core features of BPD BPD patients reflect various combinations of problems with impulse control, affect dysregulation, and cognitive and interpersonal functioning (Sherry, 2007). The Diagnostic and Statistical Manual (DSM-IV-TR) defines BPD as a pervasive pattern of instability in self-image, relationships, affects and impulsivity beginning in early adulthood. (DSM-IV-TR, 2000). The criteria for diagnosis are grouped into basic trait dimensions and the patient must meet five of the nine criteria to warrant a BPD diagnosis (DSM-IV-TR, 2000). The variability of the diagnosis has led many to question the validity of the diagnosis as delineating a specific disorder (Oldham, 2004). Similarly, some have argued that BPD is simply the sum of multiple Axis I diagnoses (Tyrer, 1999). Notwithstanding a great deal of research on the disorder, it still remains difficult to definitively outline the core features of BPD (Zanarini, et al., 2007).
In BPD, there is evidence suggesting that the pattern of disorganized attachment, the most disturbed form of early attachment, lies at the heart of the condition (Silk, Wolf, Ben-Ami & Poortinga, 2005). Individuals grow up with the sense of incapacity to contain powerful affects due, in part, to their caregivers’ inability to assist in this process (Silk, Wolf, Ben-Ami & Poortinga, 2005). The result may be the experience that others react against communications and expressions (Silk, Wolf, Ben-Ami & Poortinga, 2005). Liotti (2002) argues that disorganization of early attachment “seems to reflect an inter-subjective reality rather than being a property of the child’s mind.” While caregivers often recognize the attachment-seeking behaviors of BPD, these tend to be viewed as behaviors to be defended against rather than expressions of legitimate needs requiring a care-giving response (Liotta, 2002). This may give rise to repetitive mismatches in social interactions and to failure in the development of parasympathetically mediated physiological systems of social reward (Zanarini, et al., 2007). Interpersonal systems of mismatch create a self-perpetuating cycle, perhaps corresponding to a dominant negative affectivity, particularly in interpersonal contexts (Zanarini, et al., 2007).
The tendency of patients with BPD to self-harm evokes significant responses in caregivers, who tend to become less sympathetic as the behavior becomes repetitive and established (Korner, Gerull, Meares & Stevenson, 2007). The recent finding on the Tridimensional Personality Questionnaire that patients with BPD have unusually high levels of harm avoidance challenges the view that these patients simply cause themselves harm and pain (Korner, Grull, Meares & Stevenson, 2007). The implication is that even when the overt behavior is clearly harmful, the effort of the person is directed at avoiding harm (Korner, Gerull, Meares & Stevenson, 2007). This may be explained by an internal sense of a greater harm or pain, from which such behaviors give some respite (Korner, Gerull, Meares & Stevenson, 2007).
The emotional pain referred to above may be underpinned by a dissociation between amygdaloid-medial frontal activity and hippocamusal-lateral frontal activity as demonstrated in pain studies conducted by Vogt (2005) and Grachev, Fredrickson & Apkarian (2002), and in responses to presentation of fearful facial emotional expression (Williams, et al., 2001).
The failure of the individual to have established pathways that sub-serve “effortful control” is associated with greater symptomology in BPD and with affective experiences of the world that are raw and unmodulated (Clarkin, et al., 2007). Thus, the failure to develop such pathways implies a difficulty with impulse control due to the fact that BPD patients have a powerful, immediate response to protect themselves against emotional pain which then manifests itself to the therapist and others as poor impulse control(Clarkin, et al., 2007). In practice, the individual has to make more of an “effort” to contain impulsive behavior (Clarkin, et al., 2007). Modification of such neural patterns would presumably only occur over relatively long periods (Clarkin, et al., 2007).
The dysphoric experience of the patient with BPD is one of the core features of the condition, according to current diagnostic systems (DSM-IV-TR, 2000). For these patients this level of intense dysphoria and emptiness may be the personal reality of their “affective core” (Cloninger & Syrakic, 2000).
This kind of experience colors other aspects of daily life, and it may be associated with heightened interpersonal interactions that lead to a repetitive cycle in which unpleasant interpersonal interactions lead to damage of self-esteem and consequent dysphoria (Cloninger & Syrakic, 2000). While such characteristics are often assessed to be aspects of “temperament,” one needs to remind oneself that emotions and affects are dynamic states, which develop in a context of relatedness (Cloninger & Svrakic, 2000).
Unless therapy succeeds in addressing this basic “atmosphere” in consciousness, the person will continue to suffer even if other features of the condition are modified (Zanarini, 2005b).
In this context, it may also be the case that measures of depression are more indicative of a “trait-like” characteristic of negative affectivity (Zanarini, 2005b). Depression in BPD has been found to be somewhat resistant to change with therapeutic approaches such as dialectical behavior therapy (DBT) and mentalization-based therapy, that otherwise show promise in the treatment of BPD (Zanarini, 2005b). The more dramatic self-harming symptoms may recede but “abandonment concerns, sense of emptiness, relationship problems and vulnerability to depression are likely to remain in at least half (Zanarini, 2005b). Affective symptoms also are known to be the symptoms that improve least in relation to the natural course of the disorder (Zanarini, 2005b). While researchers have been appropriately circumspect about outcomes in relation to affective change, it is important to note that some of these studies show improvements in levels of affective distress (Zanarini, 2005b).
This trait-like characteristic of emotional hyperreactivity and dominant negative affectivity in BPD manifests in the finding of significant discrepancies between self-report and observer ratings of depression in BPD (Zanarini, 2005b). Self-report measures are more likely to capture this aspect of the disorder (Zanarini, 2005b). There is no consensus on how to measure this developmentally/traumatically mediated form of depression, although, there have been, and are, continuing attempts to capture and operationalize this dimension of BPD, such as “dysphoric affect scale” and the “depressive experiences questionnaire” (Zanarini, 2005b). Whether one considers the presence of core dysphoria to be related to environment, temperament or, as is more likely, both, it is necessary to view BPD as a disorder with a substantial disturbance in the social substrate that allows the development of a sense of self (Zanarini, 2005b).
Any intervention that is likely to change this situation will require a sustained engagement with the patient (Zanarini, 2005b).
Stability and course Recent research indicates that the DSM-IV-TR definition and conceptualization of personality disorder as a “pervasive pattern” that is stable over time is not supported by research evidence (Cohen, et al., 2005). The research consistently indicates that personality disorders, as defined by DSM-IV-TR, are remarkably unstable (Cohen, et al., 2005). With specific reference to BPD, this instability refers to three factors: (1) remission has been found to occur at a much faster rate than expected; (2) clinical features fluctuate rapidly over time; and (3) some aspects of BPD are more dependent on situational factors than previously thought (Cohen, et al., 2005).
Other studies indicate that BPD undergoes remission over a much shorter period than previously thought and reoccurrences are relatively rare (Zanarini, et al., 2005). This is despite the fact that BPD usually has a higher rate of co-morbidity with other disorders (Zanarini, et al., 2005).
Although BPD appears to ebb and flow in its presentation, it is much more stable than major depression for example (Zanarini, et al., 2005). While Major Depressive Disorder quickly resolves itself, recurrences are common, leading to a common pattern to remission and relapse (Zanarini, et al., 2005). BPD, on the other hand, takes a longer time to remit and rarely reoccurs (Zanarini, et al., 2005). Researchers found this non-relapsing course, not usually found in other personality disorders, continues as long as they continue to have mental health service involvement (Zanarini, et al., 2005).
Emerging findings also indicate that various components of BPD appear to have different courses but findings remain inconsistent and contradictory (Zanarini, et al., 2005). The affective component of BPD was found to be the most stable over time, while symptoms relating to impulse control resolved themselves quickly (Zanarini, et al., 2005). The course of the cognitive and interpersonal aspects of the disorder appeared to occur somewhere in between (Zanarini, et al., 2005).
Further, intense anger and affective instability were most stable over time whereas abandonment fears and self-injury were not (Zanarini, et al., 2005). There appears to be still even greater acknowledgment that BPD symptoms are acutely influenced by situational factors such as the nature of the relationship the patient is in, current living conditions, and so forth (Gunderson, et al., 2003). This has led most treatment approaches to emphasize the importance of stabilizing the patient’s current life stressors before attempting to deal with core pathology (Gunderson, et al., 2003).
In order to treat BPD it is important to have a clear understanding of its profile (Zanarini, et al., 2005). How one views the occurrence of co-morbidity will influence the way the clinician assesses the presentation and manages the treatment (Zanarini, et al., 2005). There are four possible models of co-morbidity that are not necessarily mutually exclusive: (1) PD traits create a vulnerability to Axis I conditions (vulnerability model); (2) personality features are exaggerated by an Axis I condition (scar model); (3) the PD and the Axis I diagnosis have a common origin (common vulnerability model); and (4) the PD influence on the course and presentation of an Axis I condition is etiologically independent (Pukrop & Krischner, 2005).
BPD often co-exists with a number of Axis I and Axis II diagnoses (Zanarini, et al., 2005). BPD patients were twice as likely to receive three or more co-existing Axis I disorders when compared to non-borderline patients and a life-long pattern of multiple diagnosis appears to be predictive of BPD (Zanarini, et al., 2005). They also found that BPD patients were four times more likely to receive four concurrent Axis I diagnoses, when compared to a control group (Zanarini, et al., 2005).
BPD most commonly co-occurs with mood disorders with a prevalence of 70% to 90% (Zanarini, et al., 2005). This is closely followed by anxiety disorders with a prevalence of about 80% relating mainly to PTSD (55%) (Zanarini, et al., 2005). Substance abuse (61%), eating disorders (53%) and other Axis II disorders are also prevalent (Zanarini, et al., 2005). It is widely accepted that severity of the personality disorder and co-morbidity worsen prognosis with regard to all treatment modalities, there are no consistent findings regarding co-morbid relationships (Pukrop & Krischner, 2005).
Finally, difficulties in isolating the relationship between BPD and co-morbid diagnoses may occur because different categories of mental illness and personality disorder have different pathogeneses and influences (Pukrop & Krischner, 2005). Some have argued that a complication in evaluating co-morbid diagnoses is the division between Axis I and Axis II disorders (Pukrop & Krischner, 2005). They argue that when one compares the course, etiology, and phenomenology of Axis I and Axis II disorders, there appears to be little reason to justify the division of the two (Zanarini, et al., 2005). In terms of BPD however, the weight of evidence suggests that there are core etiological features that point to BPD being a distinct disorder (Bateman & Fonagy, 2001).
Etiological and mediating factors It is thought that there are five contributing factors leading to the emergence of BPD, namely, affective, dysregulation, poor impulse control, excessive anger (temperamental or secondary to child abuse/neglect), separation-individuation problems, and lack of a stable sense of self (secondary or primary) (Cohen, et al., 2005). There is general agreement that all of these factors have important influences on the development of BPD (Cohen, et al., 2005). How these factors emerge or interact still remains largely unknown (Cohen, et al., 2005). Similarly, the extent to which such contributing factors are in fact etiological or simply exacerbate or amplify existing personality traits still remains unknown (Cohen, et al., 2005).
It is now generally accepted that our personalities are structured by complex interactions between temperamental (genetic, constitutional components) and characterological or traumabased factors (shaping by life events and development) (Livesley, 2003). Genetic studies on personality indicate that personality traits are more or less 50% heritable, leaving the remaining 50% to external factors (Livesley, 2003). With the emergence of behavioral genetics, the idea that genetic links to personality expression cannot change is incorrect (Livesley, 2003). Because genes require specific environmental conditions to be activated fluctuations in behavioral expression is inevitable (Livesley, 2003). Therefore, the expression of traits is amenable to change (Livesley, 2003). It still remains difficult to say which prominent factors in the development of personality disorder exist as causal or mediating factors (Livesley, 2003). It is possible for genetic influences, neurobiology, upbringing, culture, and so forth, to be conceptualized either way (Livesley, 2003). At present it seems reasonable to assume that these factors will depend on the individual case and complex ideographic combination of these factors (Zanarini, et al., 2007). Therefore, it appears that our understanding and evidence-base concerning etiological factors has proliferated in recent years (Zanarini, et al., 2007).
While studies have confirmed a link between BPD and genetic predisposition, and there is evidence to suggest that increased activity in the dopaminergic system is likely to be linked to a high-level of sensation-seeking behavior, and individuals with BPD report higher rates of trauma in their early history, one of the most highly discussed etiological influences is the impact of child and infant-rearing on personality (Bateman & Fonagy, 2004). While at present there is no clear agreement as to any particular aspect of child rearing, parenting, and so on being more etiologically significant (Bateman & Fonagy, 2004). (there should not be a paragraph break) there is some evidence that parental loss and separation play an etiological role (Bateman & Fonagy, 2004). Other studies found that early separations from parents (1 to 3 months) were more frequently observed in BPD patients (Bateman & Fonagy, 2004). These findings tend to support psychoanalytic theories emphasizing the impact of early separation and the loss of self (Bateman & Fonagy, 2004). Individuals from families that adhere around a rigid denial of problems or exhibit a high degree of discord appear to be most vulnerable (Bateman & Fonagy, 2004). It is often thought that parental over-involvement is important (Bateman & Fonagy, 2004).
However, this does not appear to be specific to BPD (Bateman & Fonagy, 2004). Overinvolvement seems to be only a general indicator of possible psychopathology and appears to be equally represented in BPD, neurotic, and normal groups (Bateman & Fonagy, 2004).
Interestingly, the fathers’ over-involvement of the disapproving attitudes of fathers have been found to be a specific factor in the development of BPD (Bateman & Fonagy, 2004).
Invalidation in primary relationships is viewed as a key etiological factor in DBT (Bateman & Fonagy, 2004). Certainly, BPD patients often appear to have suffered from a great deal of invalidation (Bateman & Fonagy, 2004). The problem here, however, is that invalidation is far too general a term when it comes to exploring etiological factors and many other forms of psychopathology show evidence of invalidation as being an influential factor (Bateman &Fonagy, 2004).
There is also mounting evidence that attachment styles from birth may have etiological significance (Bateman & Fonagy, 2004). BPD patients are more likely to display angry withdrawing patterns of attachment and compulsive care-seeking patterns (Bateman & Fonagy, 2004). Within this dynamic attachment figures are often felt to be unavailable (Bateman & Fonagy, 2004). Although no clear causal link between attachment style and BPD has been states “personality disorder is a biopsychological entity with a complex etiology involving multiple genetic and psychological factors.” Further, it is held that personality disorders develop when risk factors in the environment amplify existing personality traits (Livesley, 2003). In Livesley’s model, social and psychological factors are precipitating factors rather than causes (Livesley, 2003). This appears supported by research on resilience and evidence that most people exposed to a traumatic childhood will not develop PDs or other psychopathology (Livesley, Differing predisposing factors may account for why individuals seem to present with different types or dimensions of BPD (Zanarini, et al., 2005). This may also help further explain why some symptoms remit very quickly in BPD patients (Zanarini, et al., 2005). It is likely that complex and variable configurations of biological, social, and psychological factors may also influence treatment outcomes (Zanarini, et al., 2005). However, no one factor can be prioritized (Zanarini, et al., 2007). In their words: “each borderline patient has a unique pathway to the development of BPD that is a painful variation on an unfortunate but familiar theme” (Zanarini, et al., 2007).