Neurocognition and Borderline Personality Disorder: Status and Future Directions

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Eric A. Fertuck1,2, Mark F. Lenzenweger3, John F. Clarkin4, and Barbara Stanley1,2,5 1New York State Psychiatric Institute, 2Columbia University, College of Physicians and Surgeons, 3State University of New York at Binghamton, 4Weill Medical College of Cornell University, 5City University of New York, John Jay College

Research in borderline personality disorder (BPD) now indicates it is a syndrome that warrants individualized treatment and research attention. This review summarizes our prior review on current status of neurocognition in BPD. Additionally, we extend the prior review with a summary of social neurocognition and neuroimaging research in BPD. A mechanistic understanding, with a focus on different types of information processing, controlled and automatic, is crucial for an integrated understand of BPD. Further, an integrated approach that includes neurobiology, neurocognition, personality traits, and interpersonal characteristics in BPD may inform the development of more effective treatments for this debilitating, multifaceted disorder. Borderline Personality Disorder (BPD) (1) has “come of age” as a condition warranting concerted and rigorous empirical study and specific treatment (2). Evidence supports BPD as a syndrome with differing risk factors, course, phenomenology, and treatment response compared to Post-Traumatic Stress Disorder, Bipolar Disorder, and Major Depressive Disorder (3,4). BPD exhibits serious morbidity and mortality. The completed suicide rate is comparable to Major Depression and Schizophrenia (5) and it is associated with the highest rate of non-suicidal self-injury (6). Finally, BPD is associated with high health care utilization that is more frequent than other personality disorders and Major Depression (7). Simultaneously, BPD exhibits some of the greatest challenges to psychopathology and treatment researchers given its heterogeneous combination of traits, behaviors, symptoms, and interpersonal and personality characteristics. Questions that preoccupied investigators of BPD in the recent past, revolving around polarized nature vs. nurture dichotomies, are currently giving way to more generative lines of inquiry. These include: What environmental, psychological, biological, and genetic risk factors combine to pave the way for the development of BPD? What are the mechanisms that subserve the phenotypic features of the disorder (8,9)? How might we sub-type the disorder for differential treatment planning? With these questions, a prior Cartesian dualism in the study of BPD has evolved into approaches that integrate the social, neurocognitive, and the neurobiological to inform a mechanistic understanding of the disorder (10). For instance, Depue and Lenzenweger (11,12) propose a contemporary, neuroscience-influenced behavioral model that may ultimately prove more useful in understanding the disorder than mere reliance on manifest/phenotypic attributes. Lenzwenweger & Clarkin’s (Eds.) 2nd Edition of Major Theories of Personality Disorder (13) is a source for descriptions of current theoretical models of personality disorders. The study of neurocognition in BPD is crucial to an integrated, interdisciplinary approach. By definition, neurocognitive and neuropsychological approaches are at the intersection of psychological processes (such as memory and executive neurocognition) and the neural structures and circuits that subserve them (such as the hippocampus and frontal cortices). Disruptions in basic neurocognitive processes may underly many of the phenotypic features of BPD (see Table 1). We have published a review of experimental studies that used neurocognitive instruments to assess executive neurocognition and memory in BPD (16). In this review, three phases of research were identified (see Table 2). Phase I (1967-1980) began to establish BPD as a coherent syndrome, and pioneering researchers attempted to employ traditional IQ and personality tests to document indicators of the diagnosis. While this phase had promising findings, methodological and measurement limitations (e.g., lack of reliable diagnostic instruments) make the results from this phase dubious. Phase II began with the advent of the DSM-III (17) definition of BPD, which allowed for more reliable and standardized diagnosis based on symptom and behavioral indicators through semi-structured diagnostic interview. At the same time, neuropsychological tests developed on individuals with neurological disorders began to be applied to psychiatric disorders such as BPD. The extant studies from Phase II indicate that individuals with BPD exhibit non-specific deficits in multiple areas of neuropsychological performance including spatial and verbal working memory, delayed memory, attention, and executive neurocognition. However, confounding factors such as depression severity, state levels of negative emotion such as anxiety, and potential IQ differences between BPD and control groups invites a cautious interpretation of these apparent multiple, non-specific deficits. Studies from Phase II are still underway, as a definitive characterization of BPD – with greater control of confounding variables – using conventional neuropsychological tests remains an unfinished but important endeavor. Phase III studies (1999-present) have widened the scope of neurocognitive inquiry, and attempted to use instruments and study designs that are more closely tied to the phenomenology of BPD. The greater ecological validity and methodological rigor of most of these studies has led to a more differentiated set of preliminary findings. A summary of Phase III findings are that (a) there is impaired executive neurocognition in BPD without current mood disorder (18,19,20,21). Other forms of neurocognition such as attention and working memory appear unimpaired, suggesting a relative specificity to executive neurocognitive deficits. Lenzenweger et al. (19) report that executive neurocognitive performance is associated with the personality trait of “constraint” in the BPD group. Informed by a neurobehavioral model, this study, moves beyond characterization of neurocognitve impairment by linking such neurocognitive performance to a personality trait highly relevant to the impulsivity dimension of BPD. (b) There is impaired capacity to cognitively inhibit the encoding of negatively valenced emotional stimuli in BPD (22). This suggests enhanced attention to negative and potentially threatening stimuli that cannot be readily extinguished from working memory. (c) Adding an element of reward and punishment to an executive neurocognitive task appears to further impair performance in BPD relative to controls (18,23,24,25). Moreover, poorer performance in reward and punishment influences on executive neurocognitive performance is associated with behavioral indices of impulsivity in BPD (24). Concordantly, adding an affective component to a cognitive interference tasks (the emotional Stroop task) contributes to poorer Stroop performance in BPD and other personality disorder participants compared to controls (26). (d) With regard to episodic memories, if negatively valenced, they are less specific in individuals with BPD than in control participants (27). Moreover, greater specificity in the recall of episodic memories predicts increases in the frequency of suicide and parasuicidal behaviors in BPD (28). (e). Finally, BPD subjects in an episode of major depression appear similar in neurocognitive performance to MDD without personality disorder (29,30). However, in this comparison, the BPD with depression participants are more affectively aroused than MDD without personality disorder. Elevated anxiety, when controlled for in BPD, highlights that BPD subjects perform better than MDD in psychomotor, attentional, and performance IQ. This finding suggests that the mechanisms that subserve cognitive impairment in MDD and BPD may be different, even while there is overlapping symptomatology and neuropsychological profile. Building on this body of work, current and future research is attempting to model BPD based on a mechanistic understanding, with increased attention to on social neurocognition and neuroimaging. The Role of Social Neurocognition in BPD. Individuals with BPD have impairments and biases in processing social stimuli, or, in social neurocognition. Individuals with BPD have less capacity to make coherent interpretations of others intentions and mental states than other psychiatric groups if they have experienced childhood trauma (31). They tend to appraise social situations in polarized ways (32), and are biased to attribute the negative intentions in the behaviors of others (33,34.35; see also 36 for review). Individuals with BPD are prone to assume that others are untrustworthy and to view themselves as overly needy and weak (37), suggesting a high level of rejection sensitivity (38). Human Face Appraisal and Attribution in BPD, Childhood Maltreatment, and Attachment. The human face is a prime source of information in social interactions that is consistent across cultures and that has been conserved in human evolution (39). Consequently facial expressions are of particular importance in the investigation of social neurocognition in BPD. The influences of the quality of face appraisals include attachment, childhood maltreatment, and BPD features. Attachment research has identified a secure form and two insecure forms of attachment: avoidant and anxious-ambivalent (40). Secure attachment is characterized by generally positive experiences and expectations in relationships with significant others. Avoidant attachment is characterized by a defensive disengagement from others out of concerns over acceptance and rejection. Fearful-ambivalent attachment is characterized by intense concern about the support and availability of significant others and exaggerated attempts to maintain proximity and engagement with significant others. In a non-clinical adult population, these attachment dimensions influence facial appraisals (41). Participants observed faces morph over time from a negative emotional expression to a neutral expression, and they were instructed to indicate when the face looked neutral. During a stressful experimental condition, insecurely attached individuals took longer to stop perceiving negative facial expressions than did the secure individuals. Among the insecure subtypes of attachment, the fearful-ambivalent attached individuals took the longest to stop perceiving negative expressions. A fearful-ambivalent attachment style is the most common attachment type in BPD groups (42). A history of chronic maltreatment, which is commonly reported by individuals with BPD, may also instill a propensity to anticipate rejection and hurtful motives on others. This maltreatment may lead to insecure and unstable relationships and high levels of rejection sensitivity. Studies have documented that children with a history of maltreatment have biases in processing facial stimuli, such as a propensity to perceive anger in relatively neutral faces (cf. 43). In the first study to assess individuals with BPD in face perception and appraisal, faces of varying emotional expressions were shown to a BPD and control group (44). The BPD group was less accurate than controls in identifying the emotions on the faces. A second study found that individuals with BPD (with a history of childhood abuse) were as accurate as controls, but were biased in interpreting negative expressions to neutral faces (45). These findings are consistent with a neuroimaging study that found greater amygdala activation in BPD relative to control in when viewed neutral faces (46; reviewed below). Individuals with BPD in this imaging study also appeared to infer negative intentions and untrustworthiness in the neutral faces. Finally, in a recent study (47) BPD features in a non-clinical sample were associated with a higher degree of anxious (fearful) attachment, which, in turn, was associated with a tendency to perceive rejection and negativity in neutral faces. In sum, studies of face processing in BPD, childhood maltreatment, and attachment have found consistent biases in the perception of faces. There are is a lack of consensus with regard to overall accuracy of emotional appraisal, which may be accounted for by such factors as the response format of testing (timed or untimed) or levels of affective arousal. However, there is some consistency in the bias to interpret negative emotion to relatively neutral faces in physically abused children, adult BPD, and in non-clinical adults with fearful attachment style. At this point it is unclear if social neurocognitive deficits are specific to BPD, or are the primary consequence of early maltreatment or insecure attachment. Further, state-trait distinctions are important, since social neurocognitive differences in BPD may be most apparent during periods of intense negative affect. Controlled and Automatic Information Processing. From a mechanistic perspective, a guiding distinction is between automatic and controlled information processing mechanisms (10,20). Controlled information processing requires conscious effortf, is deliberative, and is usually voluntary. Self-regulation of emotion, cognition, and behavior are the sum of controlled processing mechanisms. An example is one’s deliberate attempt to resolve a conflict with someone important in one’s life. By contrast, automatic information processing operates without conscious effort, it is implicit, and is non-deliberative. Reflexive, spontaneous emotional reactions are automatic processes. One’s automatic feeling of emotional pain in response to a critical, angry facial expression is an example of an automatic process. There are cognitive processes that are automatic as well, such as certain subtypes of attention that guide one’s perception (e.g., alerting and orienting; 48). As will be illustrated, this distinction has compelling implications for neuroimaging and neurocognitive study of BPD. The Neural Circuitry of Social Neurocognition: Implications for Neuroimaging in BPD: A review of the circuitry of emotion and its relation to impulsivity and aggression (49), provides a model for approaching the neural circuitry of interpersonal dysfunction in BPD. The model also relies upon the relationship between controlled and automatic processes. The human amygdala plays a crucial role in regulating attention to potentially threatening social cues and the valence of social expressions (cf. 50). Accordingly, threatening stimuli (including socially relevant cues to rejection) automatically activate the amygdala. Subsequently, the anterior cingulate (ACC) and prefrontal cortex are activated. The ACC is crucial for the cognitive evaluation of conflicting stimuli, emotion regulation, perception of social exclusion, and pain perception (see 50,51 for reviews). The orbital frontal cortex (OFC) may modulate aggression by inhibiting amygdala activation. Other frontal regions implicated in controlled emotional evaluation, modulation, and/or appraisal include the dorsolateral prefrontal cortex (DLPFC), and the ventromedial prefrontal cortex (VPFC). Of particular salience to rejection sensitivity and interpersonal dysfunction, is evidence for a social distress circuit (52,53). In this circuit, the dorsal anterior cingulate (dACC) is an emotional “alarm bell” for social exclusion. In an fMRI study, activation in the dACC after an experience of rejection was associated with self-reported distress. Further, activation of the Right Ventral Prefrontal Cortex (RVPFC) during rejection was associated with less distress, suggesting that this region is involved in the regulation of social distress (53). Neuroimaging Studies in BPD. Neuroimaging studies in BPD have implicated key brain structures and circuits that may subserve interpersonal dysfunction in BPD. These areas are associated with controlled (frontal cortices) and automatic processes (limbic brain areas). Three structural imaging studies in individuals with BPD (54,55,56) found relative reductions in the volumes of the hippocampus, amygdala, and right ACC, all limbic structures. Additionally, Tebartz van Elst et al., (56) found relative reduction of the left OFC, a frontal structure, in individuals with BPD. There have been several functional imaging studies of BPD, all supporting impairments in circuits and structures subserving controlled and automatic information processing. A Positron Emission Tomography (PET) study of individuals with BPD and controls found that executive neurocognitive impairment (which was higher in BPD) was associated with altered serotonin functioning in the medial frontal gyrus, ACC, temporal gyrus, and striatum (57). A PET study of neural response to personalized memories of abandonment and neglect (58) found greater increases in blood flow in bilateral DLPFC and right cuneus in women with BPD compared to controls during distressing memories. Additionally, there were greater decreases in blood flow in right ACC area in BPD vs. control during rejection memories. Another study used proton magnetic resonance spectroscopy to assess neuronal viability via metabolites in individuals with BPD versus controls (59). The BPD group exhibited relatively less metabolite concentration in the DLPFC cortex compared to controls, which is consistent with impaired controlled information processing. A review of [18 f]-fluorodeoxyglucose (FDG) uptake studies in BPD using PET (60) found support in 4 of 5 studies for reduced uptake of FDG in prefrontal regions (particularly the OFC) in individuals with BPD. One of these studies found an association between reduced FDG uptake and a history of aggression (Goyer et al., 1994). Two PET, fenfluramine (FEN) challenge studies found attenuated FEN response in OFC regions (61,62). Reduced FEN response is an indicator of blunted serotonin activity, and has been associated with impulsivity and depressive emotions, both features of BPD. In aggregate the FDG and FEN studies consistently find that individuals with BPD exhibit impaired frontal cortex (controlled) processing, which is needed modulate negative emotions such as aggression. There have been two published functional magnetic resonance imaging (fMRI) studies in BPD. The first compared neural activity in response to emotionally aversive stimuli in individuals with BPD compared to control individuals (63). There was greater bilateral amygdala activation in individuals with BPD relative to controls. In a more direct attempt to assess amygdala activation to social cues, a second fMRI study (46) compared BPD to non-clinical subjects on amygdala activation to neutral and happy, sad, and fearful faces. Individuals with BPD exhibited significantly greater left amygdala activation than non-clinical participants. This differential activation also occurred to neutral faces. Post-scan inquiry suggested that the individuals with BPD attributed negative attributes to the neutral faces (e.g., “They look like they are plotting something.”). Since facial expressions are stimuli that are rich in interpersonal cues, this study has important implications for understanding rejection sensitivity and interpersonal dysfunction. This study suggests that BPD individuals readily attribute negative, rejecting, and hostile intention to ambiguous social stimuli. As has been review previously, this attribution bias is consistent with other social cognitive studies reviewed previously (41,43,45,47). In sum, neuroimaging studies have implicated impairments in both controlled and automatic processes in BPD. Controlled processing difficulties are consistent with impaired and/or volumetric differences in orbitofrontal cortices, medial frontal cortex, and other regions of the prefrontal cortex. Consistent with impairments in automatic processes in BPD, smaller amygdala and hippocampal volumes have been demonstrated. Additionally, relatively increased neural activation of the ACC and amygdala suggest heightened attention and arousal in response to negative and neutral social stimuli. Further, individuals with BPD are biased to appraise these neutral faces more negatively, consistent with what would be expected to underly interpersonal dysfunction. Many of these brain areas are consistent with a proposed social rejection neural circuit (52,53). There have not been any fMRI studies in BPD that assessed both controlled and automatic processing of social stimuli. With concurrent investigation of both, we do not know if individuals with BPD are consciously attributing negative intentions to social stimuli, or automatically, non-consciously making such appraisals. Future Directions. Among the features of BPD, impulsive-aggression has received the most research attention (64,65). Emotional instability in BPD has also begun to receive considerable research focus. (60,66). In contrast to impulsive-aggression and emotional instability, the unstable interpersonal relationships feature of BPD has received the least research attention, particularly at the neural level. To address this gap in the BPD literature, a promising approach is one of social cognitive neuroscience (10). Consistent with a translational research perspective, social cognitive neuroscience investigates social behavior at the neural, neurocognitive, and behavioral levels. It uses the tools of modern neuroscience (such as fMRI) to link social and neurocognitive processes with the neural circuits and structures that subserve them. Treatment Implications. The most important outcome of a mechanistic understanding of neurocogntion in BPD is to apply such an understanding to the development of more effective treatments. In accord with the foregoing literature that strongly suggests social neurocognitive biases in BPD, we are developing a measure of the capacity to coherently infer the mental states of self and significant others (67). Specific forms of psychotherapy may foster this capacity in BPD (68,69), and lead to improvements in emotion regulation, impulsivity, and interpersonal functioning. A measure such as this, utilized in concert with social neurocognitive assessment during treatment, will allow for empirical assessment of what types of interventions promote this form of social cognition. Further, we will be able to empirically assess the theory that fostering this social neurocognitive capacity is associated with functional improvements in BPD.


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