Phenomenological Psychology

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How Do Biological and Psychological Factors Interact in the Development and Maintenance of Personality Disorders?

June 15th, 2009 by David Kronemyer · No Comments

According to DSM-IV personality traits are “enduring patterns of perceiving, relating to and thinking about the environment and oneself that are exhibited in a wide range of social and personal contexts.” They become personality disorders (“PD”) when they become “inflexible and maladaptive and cause significant functional impairment or subjective distress.” The essential feature of a PD is “an enduring pattern of inner experience and behavior that deviates markedly from the expectations of the individual’s culture.” DSM-IV identifies 10 separate PDs grouped into three clusters. Those in Cluster A can be characterized as “odd or eccentric,” which includes paranoid, schizoid and schizotypal. Cluster B encompasses “dramatic, emotional or erratic” and includes antisocial, borderline, histrionic and narcissistic. Cluster C comprises “anxious or fearful” and includes avoidant, dependent and obsessive-compulsive.

The common thread of PDs is that they deviate from society’s contemporary expectations. This situates them firmly in the psychological – social axis identified above thus deemphasizing the role of biological factors. In other words we can accept the presence of psychological-social factors in any PD diagnosis as a “given” using the DSM-IV criteria. The more subtle question is what biological factors contribute and to what extent. By far and away the most heavily researched PD is borderline personality disorder (“BPD”), which has been characterized as the paradigmatic disorder of adult attachment (Paris, 2005). Even so its biology only now is becoming better understood.

Heritability. Although family studies of BPD tend to show genetic influences there only have been a few twin studies. The most recent is Distel et al. (2008), which analyzed data on 5,496 twins between the ages of 18 – 86 years from 3,644 families – a large sample size by any measure. Examining differences between monozygotic and dizygotic twins they concluded genetic influences explain 42% of the variation in BPD features, while unique environmental influences explain the remaining 58%.

Neurochemistry. BPD long has been linked to dysfunction in the serotonin (5-HT) system. In a recent study Xingqun et al. (2008) isolated the genes responsible for altered brain serotogenic functioning and associated them with impairments in the dopamine system, glutamate system and the HPA axis.

Brain defects or injury. Neuroimaging studies suggest BPD implicates prefrontal cortex and amygdala dysfunction. In the 1800s Phineas Gage famously sustained injury to his left prefrontal cortex. He subsequently underwent a dramatic change in personality, which might be characterizable retrospectively as BPD. More recently studies using CT and MRI show both the orbital frontal cortex and the amygdala are important in regulating aggression (Resnick et al., 2005). The most recent is Minzenberg et al. (2008), which concluded BPD patients exhibit temporal-limbic dysfunction (a biological cause) irrespective of the emotional content of stimuli (a psychological cause). They speculated BPD symptoms such as avoidance in attachment relationships might be a relational strategy (social outcome) to compensate for the emotional consequences (psychological outcome) of frontal-executive dysregulation (biological cause).

Infections, prenatal damage, nutrition, toxins. Obstetric factors, including pregnancy complications, birth complications and minor physical anomalies may play a role in the development of BPD (Raine et al., 2006).

References

Distel, M., Trull, T., Derom, C., Thiery, E., Grimmer, M., Martin, N., Willemsen, G. & Doomsma, D. (2008). “Heritability of borderline personality disorder features is similar across three countries.” Psychological Medicine, 38, 1219 – 1229.

Minzenberg, M., Poole, J. & Vinogradov, S. (2008). “A neurocognitive model of borderline personality disorder.” Development and Psychopathology, 20, 341 – 368.

Paris, J. (2005). “Borderline personality disorder.” Canadian Medical Ass’n J., 172(12), 1579 – 1583.

Raine, A., Baker, L. & Liu, J. (2006). “Biological Risk Factors for Antisocial and Criminal Behavior.” In Raine, A. (ed.) Crime and Schizophrenia: Causes and Cures, pp. 83 – 107. Hauppauge, NY: Nova Science Publishers.

Resnick, S., Goodman, M., New, A. & Siever, L. (2005). “The Biology of Borderline Personality Disorder: Recent Findings and Future Approaches to the Study of Impulsive Aggression and Affective Instability.” In Reich, J. (ed.) Personality disorders: current research and treatments, pp. 43 – 72. New York, NY: Routledge.

Xingquin, N., Chan, D., Chan, K., McMain, S. & Kennedy, J. (2008). “Serotonin genes and gene-gene interactions in borderline personality disorder in a matched case-control study.” Progress in Neuro-Psychopharmacology and Biological Psychiatry, 33(1), 128 – 133.