Borderline personality disorder


Psychlopedia, Psychology wiki written by scholars

Psychlopedia -- Key concepts -- Psychological disorders and difficulties -- Borderline personality disorder
Jump to the comments Section

Overview

People with borderline personality disorder are inclined to be very sensitive to interpersonal problems and act aggressively as a consequence. That is, they might idealize someone, and then demonize the same person minutes later, a form of splitting (see also compartmentalization model of self structure). Thus, borderline personality disorder involves heightened sensitivity to rejection.

This sensitivity can translate into many other problems. These problems include an inability to control outbursts, the need to seek attention, frequent and intense fluctuation in mood, a chronic feeling of emptiness or even dissociation, and impulsive behavior, sometimes sexual in nature, often coinciding with substance abuse, suicide, and self harm.

Borderline personality disorder could, at least sometimes, originate from a variety of events or challenges, such as inconsistent and unpredictable parents and sexual abuse during childhood. Furthermore, this disorder seems to be associated with biological factors, such as dysfunction of the endogenous opioid system--the system that produce beta endorphins.

The term borderline is controversial. Indeed, in the ICD-10 manual, an analogous disorder is called emotionally unstable personality disorder.

Psychosocial correlates and antecedents

Developmental trauma

In both males and females with borderline personality disorder, traumas during childhood are especially prevalent (Timmerman & Emmelkamp, 2001). Child sexual abuse, for example, is associated with borderline personality disorder (Ludolph, Westen, Misle, Jackson, Wixom, & Wiss, 1990). Indeed, in one study, 74% of people with borderline personality disorder reported they were the victims of sexual abuse, whereas 6% of people in a healthy control group reported they were the victims of sexual abuse (Bandelow, Krause, Wedekind, Broocks, Hajak, & Ruther, 2005).

Nevertheless, child sexual abuse is not the sole cause of borderline personality disorder. Indeed, 80% of individuals who were the victims of sexual abuse exhibit no personality disorders (Goodman & Yehuda, 2002). Furthermore, child sexual abuse, as well as child physical abuse, are no more associated with borderline personality disorder than with other personality disorders (Bierer, Yehuda, Schmeidler, Mitropoulou, New, Silverman, & Siever, 2003).

Attachment to parents or other figures

Child sexual abuse might also be associated with attachment style during childhood--that is, the extent to which children expect they will receive adequate support whenever problems transpire (see attachment theory). Insecure attachment styles might sometimes translate into borderline personality disorder, as demonstrated by Fossati, Feeney, Carretta, and Grazioli (2005). Specifically, the support that some children receive is unpredictable and inconsistent. Sometimes these children feel supported; other times, this support is withdrawn. Accordingly, they develop an anxious, rather than avoidant, attachment style. That is, they vigorously seek the support of their parents, or other key figures in their life, but also dread rejection.

Because of this dread, these individuals are very sensitive to subtle indications of rejection. Even a frown can evoke profound anxiety. If they feel they might be rejected, these individuals might attempt to protect themselves by denigrating this person. That is, they conceptualize this person as a rival instead of an attachment figure, behaving aggressively and impulsively. This aggressive and impulsive behavior manifests as borderline personality disorder.

This model was substantiated by Fossati, Feeney, Carretta, and Grazioli (2005). In this study, 466 admitted outpatients completed the Structured Clinical Interview for DSM-IV Axis II Personality Disorders (V. 2.0) to diagnose borderline personality disorder. These individuals were also administered the attachment Style Questionnaire, the Barratt Impulsiveness Scale, and the Aggression Questionnaire. Structural equation modeling confirmed the hypothesis that attachment style was associated with impulsiveness and aggression, both of which were associated with borderline personality disorder (RMSEA = .023).

As Ayduk, Zayas, Downey, Cole, Shoda, and Mischel (2008) showed, the extent to which sensitivity to rejection is associated with borderline personality disorder partly depends on the capacity of individuals to control emotions, impulses, and behaviors. That is, sensitivity to rejection, as well as neuroticism (see five factor model of personality), was especially associated with borderline personality disorder when the ability of individuals to control their emotions and impulses was deficient.

Self regulation

Individuals with borderline personality disorder seem to exhibit a deficiency in their capacity to regulate emotions and behavior. One facet of regulation, called regulatory mode, for example, seems to be associated with borderline personality disorder. Specifically, some individuals demonstrate an assessment mode. These individuals are not especially persistent, active, ambitious, energetic, eager or inclined to begin one initiative as soon as they have completed their last endeavor. Instead, they feel the need to evaluate their plans, other individuals, as well as themselves carefully and thoroughly. Interestingly, this assessment mode is positively associated with borderline personality disorder, even though this disorder tends to coincide with impulsivity.

Specifically, perhaps reflecting an anxious attachment style, individuals with borderline personality disorder exhibit a profound fear they might be rejected or abandoned by friends and colleagues. Consequently, they feel the need to evaluate their behavior cautiously, almost obsessively, to prevent unsuitable decisions. This obsessive assessment of options and evaluations of themselves precludes the enactment of plans. That is, they seldom experience the necessary confidence to execute their goals.

This premise was proposed and validated by Bornovalova, Fishman, Strong, Kruglanski, and Lejuez (2007). These researchers discovered that measures of borderline personality disorder correlate highly with an assessment mode.

Self discrepancies

According to self discrepancy theory, when individuals feel they have not fulfilled their duties--that is, the qualities they feel obliged to satisfy--they anticipate punishment, eliciting agitation. In contrast, when individuals feel they have not fulfilled their aspirations--that is, the qualities they hope to achieve in the future--they anticipate a sense of loss, evoking dejection.

As Parker, Boldero and Bell (2006) demonstrated, both of these discrepancies are correlated with features of borderline personality disorder. Nevertheless, the effect of these discrepancies was partly dependent upon self complexity, representing the extent to which individuals feel their traits vary across the different aspects of their lives.

Specifically, if individuals felt they had not fulfilled their duties, they were more likely to exhibit symptoms of borderline personality disorder, regardless of self complexity. The corresponding agitation, presumably, increases the sensitivity of individuals to cues of rejection.

In contrast, if individuals felt they had not fulfilled their aspirations, they were more likely to exhibit symptoms of borderline personality disorder, but only if self complexity was low. When self complexity is high, individuals feel that a few shortfalls are unlikely to undermine their entire life, increasing resilience.

Discrepancies between explicit and implicit self esteem

Another form of discrepancy is also associated with borderline personality disorder: the discrepancy between explicit and implicit self esteem. That is, individuals often maintain they feel confident and worthy, called a high explicit self esteem. Nevertheless, other subtle measures indicate they may doubt themselves and actually feel unworthy. Individuals who do not like their initials or name, for example, feel a subtle, almost unconscious, sense of doubt that compromises their resilience and wellbeing, called a low implicit self esteem.

Vater, Schroder-Abe, Schutz, Lammers, Claas, and Roepke (2010) showed that a discrepancy between implicit and explicit self esteem is associated with borderline personality disorder. That is, an elevated explicit self esteem, but low implicit self esteem--as well as a low explicit self esteem but elevated implicit self esteem--were positively related to this disorder, but not to depression.

In particular, Vater, Schroder-Abe, Schutz, Lammers, Claas, and Roepke (2010) showed that such discrepancies between explicit and implicit self esteem are associated with specific symptoms. First, these discrepancies were positively related to autoaggression, such as suicidal thoughts and other forms of self harm, as well as impaired self perception. Such behaviors or tendencies are assumed to be primed by a sense of internal tension, doubt, uncertainty, or contradiction, corresponding to the discrepancies between implicit and explicit self esteem.

Biological correlates and antecedents:Genetics and neuroanatomy

Genetic causes

Genetic characteristics strongly affect the likelihood that individuals will demonstrate borderline personality disorder. As Torgersen, Lygren, Oien, Skre, Onstad, Edvardsen et al. (2000) showed in a study that compared identical and fraternal twins, 69% of the variance in borderline personality disorder can be ascribed to genetics. That is, identical twins are particularly more likely than fraternal twins to both exhibit this disorder.

Neuroanatomy

Schmahl and Bremner (2006) reviewed the research that has subjected patients with borderline personality disorder to brain imaging. In response to pictures or scripts that represent abandonment, trauma, or other problems, abnormal activity has been shown in regions that relate to emotional processing and regulation, such as the hippocampus, amygdala, anterior cingulate cortex, and dorsolateral prefrontal cortex. Furthermore, the volume of these regions, and baseline levels of metabolism in these regions, is also diminished.

Nevertheless, as Bandelow, Schmahl, Falkai, and Wedekind (2010) highlighted, drug use does complicate these conclusions. Patients are often treated with antidepressants, antipsychotics, hypnotics, antihistamines, and mood stabilizers. Nevertheless, because the utility of these drugs is often limited, coupled with the impulsive behavior of patients, adherence to these regimes is often impaired. Furthermore, and perhaps for similar reasons, illicit substance abuse is also prevalent in this population.

Biological correlates and antecedents: Neurotransmitters

The serotonin system

The serotonin system has also been implicated in borderline personality disorder. In patients with borderline personality disorder, the metabolite of serotonin, 5-HIAA, is diminished in cerebrospinal fluid (for a review, see New, Goodman, Triebwasser, & Siever, 2008). Other manifestations of impairments in the serotonin system have also been uncovered, potentially impairing attention and control of behavior. That is, this system influences the extent to which individuals are meticulous, conscientious, and traditional (Fisher, Rich, Island, and Marchalik, 2010).

The dopaminergic system

Dysfunction in regions that are mediated by dopamine might also explain some manifestations of borderline personality disorder. Dopamine increases the sensitivity of individuals to possible rewards. Dysfunction could explain deficiencies, prevalent in people with borderline personality disorder, in the regulation of impulses. Furthermore, antipsychotic agents, which obstruct some dopamine receptors and thus curb this sensitivity to reward, do indeed contain a few symptoms of borderline personality disorder (Friedel, 2004).

The endogenous opioid system

Dysfunction of the endogenous opioid system also seems to be integral to borderline personality disorder. The endogenous opioid system comprise three classes of neurotransmitters: beta-endorphins, enkephalins, and dynorphins (for a review, see Bandelow, Schmahl, Falkai, & Wedekind, 2010). These opioids also activate three categories of receptors, called mu, delta, and kappa opioid receptors. Beta-endorphins are synthesized in the pituitary gland, the hypothalamus, and the nucleus tractus solitaries. This neurotransmitter is released during acute stress, such as intense exercise or war injuries, often to curb pain and elicit euphoria (Roth-Deri, Green-Sadan, & Yadid, 2008).

The endogenous opioid system is closely connected to the reward system--the circuits that underpin feelings of pleasure. This reward system, sometimes called the mesolimbic reward system, emanates from the ventral tegmental area, releases dopamine, and projects to the nucleus accumbens. These systems underpin both primary rewards--that is, stimuli that are vital to survival, such as food, water, and sex--as well as secondary rewards that could foster these primary rewards, such as money, touch, respect, and attention. To illustrate, activity in the nucleus accumbens is associated with monetary gains (Knutson, Adams, Fong, & Hommer, 2001), observation of beautiful faces (Aharon, Etcoff, Ariely, Chabris, O'Connor, & Breiter, 2001), and so forth. Stimulation of the nucleus accumbens has been shown to curb anhedonia in depressed patients (Schlaepfer, Cohen, Frick, Kosel, Brodesser, Axmacher, et al., 2008).

Many studies confirm the connections between the endogenous opioid system and this reward system. Neurons that are activated by beta-endorphins terminate at the ventral tegmental area and nucleus accumbens. Opioids also curb GABA release, ultimately increasing the production of dopamine (De Vries & Shippenberg, 2002). Furthermore, administration of dopamine into the nucleus accumbens also elevates levels of beta-endorphins (Roth-Deri, Green-Sadan, & Yadid, 2008).

In short, both dopamine and opioids seem to be associated with pleasure and reward. Conceivably, as Barbano and Cador (2007) propose, dopamine might elicit the preparatory responses to reward behavior. That is, dopamine might prime the responses that need to be implemented to secure the reward. In contrast, opioids might underpin the subjective experience of pleasure.

According to Bandelow, Schmahl, Falkai, and Wedekind (2010), dysfunction in the endogenous opioid system might underpin borderline personality disorder. Endorphin receptors, for example, might not be sensitive enough. Levels of endogenous opioids, such as beta-endorphins, might be diminished. Activation of kappa-receptors, wassociated with depersonalization and other negative states, might be excessive. However, research into these possibilities is limited. Although the evidence is scarce, this account could explain several interesting findings. Patients with borderline personality disorder do not seek dopamine agonists but do covet opioids, for example.

Associations between the endogenous opioid system and symptoms of borderline personality disorder

Indeed, Bandelow, Schmahl, Falkai, and Wedekind (2010) show that many of the symptoms that characterize borderline personality disorder may represent an attempt to activate opioid receptors or boost endorphins to normal levels. To illustrate, dysfunction in the endogenous opioid system might underpin difficulties in forming solid relationships. Beta-endorphins, for example, are integral to the formation of social bonds (Panksepp, Herman, Conner, Bishop, & Scott, 1978). Indeed, separation anxiety might reflect withdrawal or limitations in endogenous endorphins; opioids have been shown to curb various manifestations of withdrawal anxiety (e.g., Carden & Hofer, 1990).

Dysfunction in the endogenous opioid system might also compromise the capacity of individuals to coordinate the ventral tegmental area and various cortical regions, ultimately increasing the likelihood of splitting in which patients shift from ebullient to hostile feelings about other people. Specifically, when individuals feel love, activation of the ventral tegmental area increases, arguably underpinning the positive evaluations of partners. In contrast, this love curbs activation of the cortical activities associated with critical or harsh judgments (Zeki, 2007). If these two sets of regions are not coordinated properly, individuals are more likely to feel either unmitigated love or hate, sometimes called splitting.

Dysfunction in the endogenous opioid system could also, potentially, explain the frequent, impulsive, and risky sexual interactions that characterize patients with borderline personality disorder. Such activity tends to stimulate the mesolimbic dopamine system, increasing the release of dopamine, oxytocin, and endorphins. Hence, sexual activity might represent an attempt to activate the opioid system or related circuits. Similarly, the need to seek attention, manifested as tantrums, might also represent an attempt to activate this system.

Furthermore, dysfunction of the endogenous opioid system could also explain the profile of mood states that characterize borderline personality disorder, including symptoms of depression interspersed with transient feelings of euphoria. The symptoms of depression, especially feelings of emptiness, might be related to limited sensitivity of opioid receptors. Similarly, overactivity of the kappa receptors is also associated with this adhedonia. In response, opioid levels might sometimes rise dramatically, experienced as euphoria.

Many of the symptoms of borderline personality disorder can also be ascribed to an inability in these individuals to delay gratification: substance abuse, impaired capacity to study, and so forth. This inability to delay gratification might represent an immediate need to increase opioid levels, through activities that are immediately rewarding. Indeed, the substances that are often consumed by individuals with borderline personality disorder, such as heroin, cocaine, amphetamines, alcohol, nicotine and cannabis, all increase the transmission of dopamine in the nucleus accumbens (Nestler, 2005).

Acute oral administration of naltrexone--an opioid antagonist--has been shown to curb self injury. Self injury in people, especially females, with borderline personality disorder is common. In most people, self injury, such as cutting the body, elicits pain. In people with borderline personality disorder, however, this self injury can be addictive and evokes euphoria, presumably because of an escalation in beta endorphins, perhaps reflecting dysfunction in the opioid system. The naltrexone might preclude this escalation in beta endorphins and has been shown to curb self injury at least in the context of other disorders such as mental retardation (e.g., Symons, Thompson, & Rodriguez, 2004).

Similarly, as Bandelow, Schmahl, Falkai, and Wedekind (2010) maintain, eating disorders, reported in over 50% of patients with borderline personality disorder (Zanarini, Reichman, Frankenburg, Reich, & Fitzmaurice, 2009), can also be ascribed to dysfunction of the opioid system. Binge eating could represent an attempt to stimulate the reward or endogenous opioid system. Anorexia nervosa and food restriction, paradoxically, might represent a form of deprivation or pain that also stimulates the endogenous opioid system. Consistent with this premise, fasting in humans has been shown to increase beta endorphins (Komaki, Tamai, Sumioki, Mori, Kobayashi, Mori, Mori, & Nakagawa, 1990). In addition, many studies indicate that dysfunction in the endogenous opioid system coincides with eating disorders (for a review, see Bandelow, Schmahl, Falkai, & Wedekind, 2010).

Furthermore, Bandelow, Schmahl, Falkai, and Wedekind (2010) argue that aggression could also represent an unconscious attempt to stimulate the endogenous opioid system. That is, aggression is associated with fight for survival, a context that is known to stimulate the production of beta-endorphins.

Interventions

Rodrigues (2004) recommended a treatment called logotherapy to patients with borderline personality disorder. This treatment is intended to instill a sense of meaning in life, perhaps curbing the sensitivity of individuals to cues of rejection (see also meaning in life). Logotherapy entails a series of activities, all intended to foster meaning. One example is logoanalysis, comprising a systematic sequence of mental and written exercises, intended to set a direction in life and formulate achievable goals to pursue this meaning.

Most of the traditional psychotherapies, such as CBT, have been applied to borderline personality disorder. Another example is dialectical behavior therapy (see Lynch, Trost, Salsman, & Linehan, 2007). This form of therapy entails emotional regulation and mindfulness.

Some drugs are effective as well. Antipsychotic agents, for example, have been shown to alleviate some of the symptoms of borderline personality disorder (Friedel, 2004).

References

Aharon, I., Etcoff, N., Ariely, D., Chabris, C. F., O'Connor, E., & Breiter, H. C. (2001). Beautiful faces have variable reward value: fMRI and behavioral evidence. Neuron, 32, 537-551.

Ayduk, O., Zayas, V., Downey, G., Cole, A. B., Shoda, Y., & Mischel, W. (2008). Rejection sensitivity and executive control: Joint predictors of borderline personality features. Journal of Research in Personality, 42, 151-168.

Bandelow, B., Krause, J., Wedekind, D., Broocks, A., Hajak, G., & Ruther, E. (2005). Early traumatic life events, parental attitudes, family history, and birth risk factors in patients with borderline personality disorder and healthy controls. Psychiatry Research, 134, 169-179.

Bandelow, B., Schmahl, C., Falkai, P., & Wedekind, D. (2010). Borderline personality disorder: A dysregulation of the endogenous opioid system? Psychological Review, 117, 623-636.

Barbano, M. F., & Cador, M. (2007). Opioids for hedonic experience and dopamine to get ready for it. Psychopharmacology (Berlin), 191, 497-506.

Bierer, L. M., Yehuda, R., Schmeidler, J., Mitropoulou, V., New, A. S., Silverman, J. M., & Siever, L. J. (2003). Abuse and neglect in childhood: Relationship to personality disorder diagnoses. CNS Spectrums, 8, 737-754.

Bornovalova, M. A., Fishman, S., Strong, D. R., Kruglanski, A. W., & Lejuez, C. W. (2007). Borderline personality disorder in the context of self-regulation: Understanding symptoms and hallmark features as deficits in locomotion and assessment. Personality and Individual Differences, 44, 22-31.

De Vries, T. J., & Shippenberg, T. S. (2002). Neural systems underlying opiate addiction. Journal of Neuroscience, 22, 3321-3325.

Fisher, H. E., Rich, J., Island, H. D., & Marchalik, D. (2010). The second to fourth digit ratio: A measure of two hormonally-based temperament dimensions. Personality and Individual Differences, 49, 773-777.

Fossati, A., Feeney, J. A., Carretta, I., & Grazioli, F. (2005). Modeling the relationships between adult attachment patterns and borderline personality disorder: the role of impulsivity and aggressiveness. Journal of Social and Clinical Psychology, 24, 520-537.

Friedel, R. O. (2004). Dopamine dysfunction in borderline personality disorder: A hypothesis. Neuropsychopharmacology, 29, 1029-1039.

Goodman, M., & Yehuda, R. (2002). The relationship between psychological trauma and borderline personality disorder. Psychiatric Annals, 32, 337-346.

Komaki, G., Tamai, H., Sumioki, H., Mori, T., Kobayashi, N., Mori, K., Mori, S., & Nakagawa, T. (1990). Plasma beta-endorphin during fasting in man. Hormone Research, 33, 239-243.

Knutson, B., Adams, C. M., Fong, G. W., & Hommer, D. (2001). Anticipation of increasing monetary reward selectively recruits nucleus accumbens. Journal of Neuroscience, 21, RC159.

Linehan, M. M. (1993). Skills Training Manual For Treatment of Borderline Personality Disorder. New York Guilford Press.

Linehan, M. M. (1995). Understanding Borderline Personality Disorder: The Dialectic Approach program manual. New York: Guilford Press.

Lynch, T. R., Trost, W. T., Salsman, N., & Linehan, M. M. (2007). Dialectical behavior therapy for borderline personality disorder. Annual Review of Clinical Psychology, 3, 181-205.

Ludolph, P. S., Westen, D., Misle, B., Jackson, A., Wixom, J., & Wiss, F. C. (1990). The borderline diagnosis in adolescents: Symptoms and developmental history. American Journal of Psychiatry, 147, 470-476.

New, A. S., Goodman, M., Triebwasser, J., & Siever, L. J. (2008). Recent advances in the biological study of personality disorders. Psychiatric Clinics of North America, 31, 441-461.

Parker, A. G., Boldero, J. M., & Bell, R. C. (2006). Borderline personality disorder features: The role of self-discrepancies and self-complexity. Psychology and Psychotherapy: Theory, Research and Practice, 79, 309-321.

Rodrigues, R. (2004). Borderline personality disturbances and logotherapeutic treatment approach. The International Forum for Logotherapy, 27, 21-27.

Roth-Deri, I., Green-Sadan, T., & Yadid, G. (2008). Beta-endorphin and drug-induced reward and reinforcement. Progress in Neurobiology, 86, 1-21.

Schlaepfer, T. E., Cohen, M. X., Frick, C., Kosel, M., Brodesser, D., Axmacher, N., et al. (2008). Deep brain stimulation to reward circuitry alleviates anhedonia in refractory major depression. Neuropsychopharmacology, 33, 368-377.

Schmahl, C., & Bremner, J. D. (2006). Neuroimaging in borderline personality disorder. Journal of Psychiatric Research, 40, 419-427.

Simmons, D. (1992). Gender issues and borderline personality disorder: Why do females dominate the diagnosis? Archives of Psychiatric Nursing, 6, 219-223.

Symons, F. J., Thompson, A., & Rodriguez, M. C. (2004). Self-injurious behavior and the efficacy of naltrexone treatment: A quantitative synthesis. Mental Retardation and Developmental Disabilities Research Reviews, 10, 193-200.

Timmerman, I. G., & Emmelkamp, P. M. (2001). The relationship between traumatic experiences, dissociation, and borderline personality pathology among male forensic patients and prisoners. Journal of Personality Disorders, 15, 136-149.

Torgersen, S., Lygren, S., Oien, P. A., Skre, I., Onstad, S., Edvardsen, J. et al. (2000). A twin study of personality disorders. Comprehensive Psychiatry, 41, 416-425.

Vaillant, G. (1992). The beginning of wisdom is never calling a patient Borderline. Journal of Psychotherapy Practice and Research, 1, 117-134.

Vater, A., Schroder-Abe, M., Schutz, A., Lammers, Claas, H., & Roepke, S. (2010). Discrepancies between explicit and implicit self-esteem are linked to symptom severity in borderline personality disorder. Journal of Behavior Therapy and Experimental Psychiatry, 41, 357-364. Zanarini, M. C., & Frankenburg, F.R. (1997). Pathways to the development of borderline personality disorder. Journal of Personality Disorders, 11, 93-104.

Zanarini, M. C., Frankenburg, F. R., Khera, G.S., & Bleichmar, J. (2001). Treatment histories of borderline inpatients. Comprehensive Psychiatry, 42, 144-150.

Zanarini, M. C., Reichman, C. A., Frankenburg, F. R., Reich, D. B., & Fitzmaurice, G. (2009). The course of eating disorders in patients with borderline personality disorder: A 10-year follow-up study. International Journal of Eating Disorders, 43, 226-232.





Created by Dr Simon Moss on 05/01/2011

Related objectives:
- Schizotypy - Narcissism - Alzheimer's disease - Jihadi radicalization - Workaholism - Borderline personality disorder - Williams syndrome -


Login require to comment




Free Personality Tests : Relationships - Personality - Beliefs - Wellbeing - Attitudes - Behaviour - Cognitive Abilities

All Rights Reserved © Psych-it.com.au