Neurocognitive function in borderline personality disorder

Abstract

A battery of neuropsychological measures considered sensitive to dysfunction in prefrontal or temporal cortices was administered to patients with borderline personality disorder (BPD) and healthy controls. BPD patients exhibited striking deficits on measures of nonverbal executive function and nonverbal memory but were unimpaired on tests of alternation learning, response inhibition, divergent thinking, verbal fluency, and verbal working memory. A second study found that university students obtaining high scores on a self-report measure of BPD symptoms exhibited a similar pattern of neuropsychological impairment, although performance deficits were much less pronounced in the student sample. Taken together, these studies suggest that dysfunction of a right hemisphere frontotemporal regions may be associated with borderline personality.

Introduction

Borderline personality disorder (BPD) is a chronic, debilitating syndrome. Clinical features include intense and labile affect, irritability, inappropriate anger and paroxysmal rage, behavioral dyscontrol, transient paranoid ideation, unstable interpersonal relationships, and an unstable sense of self American Psychiatric Association., 1994, Gunderson, 1982, Gunderson, 1984, Gunderson and Kolb, 1978, Gunderson and Singer, 1975, Millon, 1981, Pollack, 1990, Stone, 1988. The clinical presentation of BPD suggests that the integrity of neural systems involved in affect regulation, impulse control, and social cognition may be compromised. Researchers have documented the onset of BPD following traumatic brain injury and speculated on the association between central nervous system dysfunction (e.g., prefrontal and temporolimbic dysfunction) and borderline personality Andrulonis et al., 1981, Andrulonis et al., 1982, Andrulonis and Vogel, 1984, Stone, 1988, Streeter et al., 1995, van Reekum, 1993, van Reekum et al., 1993. BPD patients also display a greater number of neurologic soft signs in comparison to control subjects Gardner et al., 1987, van Reekum et al., 1993. Investigators have speculated on the role orbitofrontal and temporal lobe dysfunction may play in the emergence of BPD Streeter et al., 1995, van Reekum, 1993. Prefrontal and temporolimbic dysfunction may underlie the behavioral dyscontrol, affective dysregulation, and social cognition deficits that characterize BPD (see van Reekum, 1993). Below we review studies that support this contention.

BPD patients exhibit performance deficits on neurocognitive tasks considered sensitive to prefrontal dysfunction Swirsky-Sacchetti et al., 1993, van Reekum et al., 1993. de la Fuente et al. (1997) reported that medication-free BPD inpatients demonstrated prefrontal hypometabolism in comparison to matched control subjects. In addition, PET revealed hypoactivity in the anterior cingulate and thalamic and caudate nuclei among BPD patients relative to control subjects. Goyer et al. (1994) also reported that patients with BPD exhibited prefrontal hypometabolism; however, BPD subjects also demonstrated increased prefrontal metabolism in other, more inferior, prefrontal regions. Lyoo et al. (1998) reported that BPD was associated with structural brain abnormalities (i.e., reduced volume in prefrontal regions). Soloff et al. (2000) employed PET to examine patterns of neuroactivation among patients with BPD and healthy control subjects following the administration of fenfluramine, a serotonin agonist. At baseline (following administration of placebo), healthy controls demonstrated increased activity (i.e., FDG uptake) in medial–prefrontal and orbitofrontal regions (both right and left hemispheres), left superior temporal gyrus, and right insular cortex relative to patients with BPD. After receiving fenfluramine, healthy controls demonstrated increased activity (relative to placebo response) in right medial–prefrontal and orbitofrontal regions, left superior and medial temporal gyri, and parietal and caudate regions relative to activation patterns observed among patients with BPD. Soloff et al. (2000) observed that patients with BPD were hyporesponsive to serotonin stimulation in prefrontal and temporal regions.

It is important to emphasize that the prefrontal region is not a unitary structure; rather, it is fractionable into functionally distinct systems. These subsystems may be differentially engaged in BPD. For example, the orbitofrontal system plays an integral role in affect regulation, impulse control, and social awareness. A substantial body of research suggests that orbitofrontal cortex modulates emotional arousal and sensitivity to reinforcement contingencies Baker et al., 1997, Northoff et al., 2000, O'Doherty et al., 2001, Rolls, 1995, Rolls, 1998. Diminished impulse control and social cognition deficits among BPD patients suggest that the functional integrity of the orbitofrontal system may be compromised. Clinicians have observed that BPD patients frequently misinterpret social cues and demonstrate poor social perspective-taking skills. Baron-Cohen et al. Baron-Cohen, 1995, Baron-Cohen and Ring, 1994, Baron-Cohen et al., 1994 contend that a cortical–subcortical circuit involving orbitofrontal cortex plays a significant role in social cognition. Patients with orbitofrontal lesions frequently exhibit behavioral disinhibition, affective dysregulation, social cognition deficits, and impulsive, antisocial behavior Blair and Cipolotti, 2000, Blumer and Benson, 1975, Cummings, 1993, Damasio, 1994, Meyers et al., 1992, Stone et al., 1998, Stuss et al., 1992. However, orbitofrontal lesion patients typically exhibit shallow emotions, while BPD is characterized by intense/labile affect. One possible explanation is that diminished impulse control and social cognition deficits among BPD patients may stem, at least in part, from orbitofrontal hypofunction, while the explosive emotionality exhibited by BPD patients may be associated with temporolimbic dysfunction (see van Reekum, 1993).

Neuropsychological testing has also revealed a pattern of neurocognitive impairment among BPD patients that implicates the temporal lobes Judd and Ruff, 1993, O'Leary et al., 1991, Swirsky-Sacchetti et al., 1993. O'Leary et al. (1991) found that medication-free BPD patients were impaired on tasks assessing complex memory function and visual discrimination. They observed that BPD subjects exhibited performance deficits on measures considered sensitive to dominant and nondominant temporal lobe dysfunction. Patients with temporal lobe epilepsy (TLE) demonstrate a similar pattern of impairment on tests assessing verbal and nonverbal memory. Patients presenting with a left temporal lobe seizure focus demonstrate verbal memory deficits Falk et al., 2002, Wegesin and Nelson, 2000, while patients presenting with a right seizure focus exhibit performance deficits on tests of visual and spatial learning and memory function Abrahams et al., 1999, Baxendale et al., 1998, Falk et al., 2002, Helmstaedter et al., 1991. It is interesting to note that diagnostic criteria for BPD resemble classical descriptions of the interictal behavioral syndrome (i.e., the temporal lobe personality) (see Bear et al., 1984). This raises the question of whether at least a subset of BPD patients have an undiagnosed seizure disorder (e.g., temporolimbic epilepsy). However, in the present paper, we did not explore the possibility that the emotional dysregulation and behavioral dyscontrol of at least some BPD patients may be associated with temporolimbic seizures and may represent interictal phenomena. Of course, performance deficits on tests considered sensitive to temporal lobe dysfunction (e.g., tests of verbal and nonverbal memory) among patients with BPD would certainly lend support to the TLE hypothesis.