Development and Psychopathology

Research Article

A neurocognitive model of borderline personality disorder: Effects of childhood sexual abuse and relationship to adult social attachment disturbance

Michael J. Minzenberga1 c1, John H. Poolea2a3 and Sophia Vinogradova2a3

a1 University of California, Sacramento

a2 University of California, San Francisco

a3 San Francisco Veterans Affairs Medical Center

Abstract

Borderline personality disorder (BPD) is a paradigmatic disorder of adult attachment, with high rates of antecedent childhood maltreatment. The neurocognitive correlates of both attachment disturbance and maltreatment are both presently unknown in BPD. This study evaluated whether dimensional adult attachment disturbance in BPD is related to specific neurocognitive deficits, and whether childhood maltreatment is related to these dysfunctions. An outpatient BPD group (n = 43) performed nearly 1 SD below a control group (n = 26) on short-term recall, executive, and intelligence functions. These deficits were not affected by emotionally charged stimuli. In the BPD group, impaired recall was related to attachment–anxiety, whereas executive dysfunction was related to attachment–avoidance. Abuse history was correlated significantly with executive dysfunction and at a trend level with impaired recall. Neurocognitive deficits and abuse history exhibited both independent and interactive effects on adult attachment disturbance. These results suggest that (a) BPD patients' reactivity in attachment relationships is related to temporal–limbic dysfunction, irrespective of the emotional content of stimuli, (b) BPD patients' avoidance within attachment relationships may be a relational strategy to compensate for the emotional consequences of frontal-executive dysregulation, and (c) childhood abuse may contribute to these neurocognitive deficits but may also exert effects on adult attachment disturbance that is both independent and interacting with neurocognitive dysfunction.

Correspondence

c1 Address correspondence and reprint requests to: Michael Minzenberg, Imaging Research Center, UC-Davis School of Medicine, 4701 X Street, Sacramento, CA 95817; E-mail: michael.minzenberg@udcmc.ucdavis.edu.

Footnotes

We acknowledge the assistance of Uyen Huynh, NiVonne Thompson, and Nami Kim with the study procedures. A portion of this work was presented at the 59th annual meeting of the Society for Biological Psychiatry in 2004.