Effects of borderline personality disorder features and a family history of alcohol or drug dependence on P300 in adolescents
Introduction
Over the last 20 years, a large research literature has developed implicating the P300 event-related electroencephalographic potential (ERP) as a potential biological marker for alcoholism risk. Several studies have reported P300 decrements among alcoholic patients and their biological relatives (Begleiter et al., 1984, Begleiter et al., 1987, Hill et al., 1988, Porjesz and Begleiter, 1990, Berman et al., 1993, Hill and Steinhauer, 1993, Polich et al., 1994, Hill et al., 1995a, Hill et al., 1995b, Porjesz and Begleiter, 1998, Ramsey and Finn, 1997). However, a decrement in P300 amplitude is not unique to these individuals. P300 amplitude reductions are also associated with other psychological, psychiatric and substance use disorders which overlap with alcoholism, including impulsivity (Branchey et al., 1993, Bauer, 2001, McGue et al., 2001, Iacono et al., 2002), Antisocial Personality Disorder (ASPD; Bauer et al., 1994, O'Connor et al., 1994, Costa et al., 2000), Conduct Disorder (CD; Bauer and Hesselbrock, 1999a, Bauer and Hesselbrock, 1999b, Bauer and Hesselbrock, 2003), impulsive aggression (Barratt et al., 1997, Mathias and Stanford, 1999, Houston et al., in press), psychopathy (Kiehl et al., 1999), Attention-Deficit Hyperactivity Disorder (Klorman, 1991, Johnstone and Barry, 1996) and depression (Blackwood et al., 1987, Bruder et al., 1995, Houston et al., 2003). Recent studies have suggested that these overlapping disorders may mediate or explain, in part, the effects of a family history of alcoholism on P300 amplitude. For example, Bauer and Hesselbrock, 1999a, Bauer and Hesselbrock, 1999b demonstrated the significant impact of underlying behavioral/personality disorders, such as CD and ASPD, on P300 amplitude decrements among subjects with a family history of alcoholism. In addition, longitudinal work by Hill and Shen (2002) demonstrated differential developmental trajectories of P300 amplitude, with the lowest amplitude associated with a combination of both childhood psychopathology and a family history of alcoholism. The literature supports the recent suggestion that visual P300 amplitude might prove useful as a trait marker for a spectrum of disinhibiting psychiatric disorders and behaviors (Iacono et al., 2002).
The goal of the present study was to determine if P300 amplitude decrements could be detected within yet another disorder characterized by disinhibited behavior—Borderline Personality Disorder (BPD). It also examined whether the correlates of this disorder would be neurophysiologically similar to those of a family history of alcoholism. BPD is a severe, persistent pattern of behavior characterized by fluctuating affect, an unstable self-image, volatile interpersonal relationships and marked impulsivity. According to the DSM, BPD is one of four Cluster B personality disorders that are described as dramatic, emotional or erratic. Thus, the BPD diagnosis shares some behavioral or symptom patterns with the other Axis II Cluster B diagnoses, particularly ASPD. In fact, there has been some suggestion that these two diagnoses could reflect different manifestations of similar underlying psychopathology (Coccaro et al., 1989, Zanarini et al., 1989, Zanarini et al., 1990, Paris, 1997).
The literature on P300 findings in BPD is sparse. The few existing studies are consistent in showing reduced P300 amplitude and prolonged P300 latency in adult BPD patients. These studies have utilized a simple auditory oddball task (Blackwood et al., 1986, Kutcher et al., 1987, Kutcher et al., 1989, Drake et al., 1991) and have not examined the responsiveness of BPD patients to visual stimuli or to challenging cognitive tasks. It is important to note that the patients in these studies were principally recruited from inpatient treatment programs, which are typically inhabited by severely ill patients with multiple disorders. It is unclear whether co-morbid Axis I pathology was always taken into consideration.
The present study endeavored to complement and extend previous P300 research on BPD in several different ways. In contrast to the aforementioned studies of BPD, which used adult subjects, we examined the P300 in a large sample of adolescents. Although the BPD pattern typically manifests in young adulthood, a substantial body of work has recognized the features and/or precursors of the disorder during childhood and adolescence (Bleiburg, 2000, Paris, 2000). In addition, recent research has demonstrated the continuity of BPD features across adolescence (Crawford et al., 2001). Furthermore, the BPD diagnosis in adolescents may precede a diffuse range of adult psychopathology (Becker et al., 2000). Thus, deficits in neurophysiological processing related to BPD features during adolescence may prove useful for studying the development and treatment of adult psychopathology.
In addition, the adolescent sample used in the present study was recruited from the community rather than an inpatient treatment facility. As a result, the subjects did not possess a severe or acute level of psychopathology. They also lacked the complications of multiple co-occurring disorders, including substance dependence, psychosis or bipolar disorder and had never been medicated for a psychiatric problem.
As noted previously, we also examined the relationship between the P300 waveform and a family history of alcohol or substance dependence in this sample. Previous work has shown that the family members of BPD patients exhibit a higher than expected rate of alcohol and drug abuse (Widiger and Trull, 1993). Considering the large body of research implicating the P300 as a neurobiological risk marker for alcoholism, the current study adds to the literature by focusing on the potential relationship between BPD features and a family history of alcohol or substance dependence.
Contrary to the earlier P300 studies on BPD that used auditory tasks, we employed a modified version of the Stroop color-word task. The Stroop task elicits the P300 in the visual modality, which may be more appropriate for detecting subtle impairment (Polich et al., 1994). Furthermore, the Stroop task measures response disinhibition and dysregulation, which may be more clinically significant and disabling than a disturbance in attention. Thus, it may be an ideal measure for revealing the cognitive disturbances associated with disinhibited psychopathology, particularly those that place individuals at risk for developing personality disorders and/or substance use problems. The Stroop task has been used extensively as a neuropsychological measure in samples characterized by a lack of behavioral control (Grodzinsky and Diamond, 1992, Chevalier et al., 2000, Fishbein, 2000, Kim et al., 2001). Other ERP investigations using the Stroop task have reported cognitive deficits associated with disinhibited psychopathology including Conduct Disorder (Bauer and Hesselbrock, 1999a) and Attention Deficit Hyperactivity Disorder (Miller et al., 1996).
Section snippets
Subjects
Subjects in the present study were 175 males (n=79) and females (n=96), aged 14–20 years. They were recruited as part of a larger study of conduct problems and familial risk factors for alcoholism and drug abuse. Most subjects were recruited from the greater Hartford area via advertisements or presentations directed at their parents. The remainder was recruited through presentations before high school classes or guidance counselors, YMCA/YWCA organizations, police athletic leagues or similar
Demographic results
Table 1 summarizes the demographic characteristics of subjects assigned to each group. Analyses of the demographic data did indicate minor but statistically significant group differences in age and education. For age, there was a significant main effect for FH group [F(2,159)=3.48, P<0.05], with post-hoc tests indicating that subjects with a paternal history of cocaine or opiate dependence (FHD) were slightly younger than those with no paternal history (P<0.05). There were no significant age
Discussion
The demonstration of reduced P300 amplitude in BPD+ subjects is consistent with previous work suggesting an inverse relationship between disinhibited behavior and P300 amplitude. The P300 decrement associated with BPD is further supported by the behavioral performance finding of poorer response accuracy in the BPD+ group. Interestingly, the P300 reduction in BPD+ subjects appeared to be independent of a family history of alcohol or substance dependence in this sample. Although the absence of a
Acknowledgments
This research was supported, in part, by PHS Grants T32AA07290 and P50AA03510.
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2012, Neuroscience and Biobehavioral ReviewsCitation Excerpt :In all of these oddball paradigms, subjects are required to actively discriminate a target from a standard stimulus and consequently, the P300 amplitude is elicited by the infrequent target stimuli (P3b amplitude). Studies that did not use one of these methodologies (Bauer et al., 1994b; Berman et al., 2006, 1993; Ehlers and Wilhelmsen, 2007; Houston et al., 2004), or studies in which data were obtained from passive ERP procedures (Hada et al., 2000, 2001; Rodriguez Holguin et al., 1999a,b), were excluded. The subject samples used in the study included adequate SUD+ or FH+ groups.
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2007, Pharmacology Biochemistry and BehaviorP3 components and adolescent binge drinking in Southwest California Indians
2007, Neurotoxicology and TeratologyCitation Excerpt :Although not all studies agree, changes in both the amplitude and latency of the P300 component of the ERP have been reported in alcoholics and in subjects with a family history of alcoholism (for reviews see [64,66,107,108,109]). There is also a literature suggesting that P300 amplitude deficits are associated with conduct disorder/antisocial personality disorder [6–12,26,29,76,100] as well as other psychiatric disorders related to and/or comorbid with alcoholism [13,72,73]. It has also been suggested that lowered P300 amplitude may be a general measure of CNS disinhibition [16] or frontal executive dysfunction [52,82].
Borderline personality disorder features in adolescent girls: P300 evidence of altered brain maturation
2005, Clinical Neurophysiology