شناخت اجرایی عصبی، سیستم های حافظه و اختلال شخصیت مرزی

Borderline Personality Disorder (BPD) is a common, disabling, and burdensome psychiatric condition. It is characterized by turbulent fluctuations of negative emotions and moods, unstable and conflictual interpersonal relationships, an incoherent and often contradictory sense of self, and impulsive, potentially lethal self-injurious behaviors. The neurobehavioral facets of BPD have not been extensively studied. However, clinical theoreticians and researchers have proposed that the symptoms and behaviors of BPD are, in part, associated with disruptions in basic neurocognitive processes. This review summarizes and evaluates research that has investigated the relationship between executive neurocognition, memory systems, and BPD. Three historical phases of research are delineated and reviewed, and the methodological and conceptual challenges this body of investigation highlights are discussed. Laboratory-based assessment of executive neurocognition and memory systems is integral to an interdisciplinary approach to research in BPD. Such an approach holds promise in elucidating the neurobehavioral facets, development, diagnostic boundaries, prevention, and optimal interventions for this debilitating and enigmatic disorder.

Borderline personality disorder (BPD; Diagnostic and Statistical Manual, 4th Edition; DSM-IV; American Psychiatric Association, 1994) is characterized by turbulent, anxious, angry, and depressive emotional states, unstable interpersonal relationships, an incoherent and often contradictory self-concept, and impulsive and often dangerous behaviors such as self-injury and drug abuse. Following the pioneering clinical descriptions of borderline personality ( Grinker et al., 1968 and Kernberg, 1967), empirical research of BPD has progressed over the last 20 years. Based on recent population prevalence estimates (0.3–0.7%), between six-hundred thousand and 1.4 million adults in the United States meet diagnostic criteria for BPD ( Lenzenweger et al., 1997, Samuels et al., 2002 and Torgersen et al., 2001). The suicide rate for BPD individuals is about 10% ( Paris, 2002 and Stone, 1993), comparable to the other psychiatric disorders such as schizophrenia and major depression. In addition, 69% to 75% of individuals with BPD engage in self-injurious behaviors ( Clarkin et al., 1983 and Cowdry et al., 1985), and the frequency of self-injurious behaviors is more than in any other psychiatric diagnosis ( Stanley, Winchel, Molcho, Simeon, & Stanley, 1992). Individuals with BPD exhibit high drop out rates and variable improvement in psychotherapy ( Clarkin, 1996), and respond only partially to psychopharmacological therapies ( Soloff, 2000). Additionally, this diagnostic group utilizes health care services more frequently than any other psychiatric group ( Bender et al., 2001). Despite this troubling clinical picture, BPD has not received research attention and widespread clinical focus commensurate with the suffering and mortality it causes. There is considerable reason to suspect that there are disruptions in basic executive neurocognition and memory processes in BPD. Central to the symptoms of BPD is unstable and dysregulated inhibitory control over behavior, emotion, and cognition. The acquisition of executive neurocognition is inextricably linked to emotion and personality development, and inhibitory capacity influences the acquisition of prosocial behaviors, affect regulation, and problem solving abilities (Derryberry & Reed, 1994 and Posner & Rothbart, 2000). These capacities are commonly impaired in BPD. From a clinical perspective, neurocognitive function predicts response to intervention in other clinical groups (e.g., Smith, Hull, Romanelli, Fertuck, & Weiss, 1999). Should BPD individuals, or subgroups of them, evidence a characteristic constellation of inhibitory and memory characteristics, treatment could be tailored to complement them, leading to improved treatment planning and interventions. From a scientific vantage point, BPD is a diagnostic entity that can be used to elaborate the understanding of basic cognitive and affective processes. The study of emotion, mood, temperament, affect regulation, and their relationship with personality, cognition, and psychopathology are at the center of rapid, exciting developments in cognitive (Gazzaniga, 2000) and affective science (Davidson, Scherer, & Goldsmith, 2003). Previous reviews have emphasized the clinical implications of neurocognitive functioning in BPD and other personality disorders (see Gorton et al., 1999 and O'Leary & Cowdry, 1994). This review, by contrast, focuses on research that has attempted to systematically characterize executive neurocognition and memory systems in BPD. First, we define the types and subtypes of executive neurocognition and memory of relevance to BPD. A historical review of three phases of research in executive neurocognition, memory, and BPD follows. Finally, then we discuss the literature in this area as it relates to the neurobiology and neuroscience, development, and clinical understanding BPD.

In distillation, the main findings of this review are: (1) Well-characterized groups of BPD subjects appear to exhibit non-specific deficits in multiple domains of executive neurocognitive and memory performance in comparison to psychiatric and non-clinical groups. On a cautionary note, complicating factors such as co-occurring conditions, state-dependent effects, omnibus measurement, small sample sizes, and a limited number of studies implore us to be tentative about this pattern of findings. (2) Phase III studies, while also limited in number and unreplicated, consistently suggest that motivational influences and negative affects have a disorganizing and disruptive influence on executive neurocognitive and memory performance in BPD compared to comparison groups. There are a few observations regarding overall the state of investigation in executive neurocognition, memory, and BPD, and promising areas for future investigation. First, it appears that the more emotional stimuli are specifically tailored to the phenomenology of BPD the greater the impact on cognitive and memory systems (e.g., Korfine & Hooley, 2000). Second, while there are associations between task performance on certain cognitive and memory laboratory tasks and the diagnosis of BPD, very few researchers have taken the next step and related the task performance to actual social behavior (e.g., social behavior in dyadic relationships, suicidality, etc.). Additionally, longitudinal designs that assess the stability and validity of associations between neurocognition, symptomatology, affectivity, and social behavior are called for, given the emerging longitudinal data on the instability of the diagnosis, and the rapidly shifting, state-dependent aspects of BPD. As a final point, it could be argued that the main findings of the review are not surprising or illuminating, as the notion that affects have a disorganizing effect on cognition and memory in BPD is what clinicians have been describing for decades. While this is accurate, what is promising is that clinically relevant phenomena can be rigorously operationalized and assessed in an experimental laboratory context. The promise of the perspective of experimental psychopathology is that the features and symptoms of devastating clinical phenomena–even multi-faceted and heterogeneous conditions like BPD–can be assessed and related to basic biological and psychological mechanisms and systems (Lenzenweger & Hooley, 2003). With collaboration and cross-fertilization, this translational effort should eventually de-mystify and de-stigmatize this enigmatic disorder. Most importantly, firmer scientific foundation in BPD research will inform more effective, research-based interventions. As a result, there is compelling reason for hope that the devastating suffering that BPD causes to individuals and their families can be mitigated as the neurobehavioral facets of the disorder are increasingly understood.