Impulsivity as a common process across borderline personality and substance use disorders

Clinical Psychology Review 25 (2005) 790 – 812

Impulsivity as a common process across borderline personality and substance use disorders Marina A. Bornovalovaa, C. W. Lejuez a,T, Stacey B. Daughtersa, M. Zachary Rosenthalb, Thomas R. Lynchc a

Department of Psychology, University of Maryland, College Park, MD 20742, United States. b Duke University Medical Center, United States c Duke University and Duke University Medical Center, United States

Abstract Borderline personality disorder (BPD) is a significant public health problem characterized by persistent problems with emotional, behavioral, cognitive, and interpersonal functioning. Research indicates an especially high rate of comorbidity between BPD and Substance Use Disorders (SUD). In trying to better understand, and therefore improve the assessment, prevention, and treatment of these disorders, researchers have considered the role of impulsivity. Indeed, impulsivity consistently has been shown to be a biologically-based, heritable characteristic with emergent psychological properties linked to the development and maintenance of BPD and SUD. Following from a previous review of the comorbidity between BPD and SUD (Trull, T. J., Sher, K. J., Minks-Brown, C., Durbin, J., & Burr, R. (2000). Borderline personality disorder and substance use disorders: A review and integration. Clinical Psychology Review, 20, 235–253), the current manuscript revisits the role of impulsivity as a common process across these disorders with a specific focus on the multidimensional nature of impulsivity and its interaction with trait and state negative affectivity. D 2005 Published by Elsevier Ltd.

1. Impulsivity as a common process across borderline personality and substance use disorders Borderline personality disorder (BPD) is a significant public health problem with substantial adverse consequences for individuals, families, and society at large. BPD is characterized by T Corresponding author. Tel.: +1 301 405 5932; fax: +1 301 314 9566. E-mail address: [email protected] (C.W. Lejuez). 0272-7358/$ - see front matter D 2005 Published by Elsevier Ltd. doi:10.1016/j.cpr.2005.05.005

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persistent problems with emotional (e.g., anger), behavioral, (e.g., self–injury), cognitive (e.g., dissociation), and interpersonal (e.g., chaotic relationships) functioning (APA, 1994). Although the exact factors underlying the etiology and course of BPD are unknown, it is hypothesized that BPD is the result of both biological vulnerabilities (e.g., genetic predisposition, temperament) and environmental events (e.g., emotional, physical, and/or sexual trauma) (Linehan, 1993). Although BPD frequently co-occurs with a number of Axis I conditions such as mood (Bunce & Caccaro, 1999; Zanarini et al., 1998), anxiety (Nurnberg, Raskin, Levine, Pollack, 1989) and eating disorders (Wonderlich, Swift, Slomik, & Goodman, 1990), research indicates an especially high rate of comorbidity between BPD and Substance Use Disorders (SUDs; Trull, Sher, Minks-Brown, Durbin, & Burr et al., 2000). Indeed, up to 57.4% of individuals with BPD meet criteria for a SUD (cf. Trull et al., 2000) and an estimated 5–32% of substance-abusing populations meet criteria for BPD (Brooner, King, Kidorf, Schmidt, & Bigelow, 1997; Weiss, Mirin, Griffin, Gunderson, & Hufford, 1993). Additionally, individuals diagnosed with BPD are likely to initiate substance use and abuse at a younger age than non-BPD individuals, ensuring a more pervasive and problematic course of SUDs such as more severe physical dependence and more adverse social, emotional, and legal consequences (Linehan et al., 1999; Links, Heslegrave, Mitton, van Reekum, & Patrick, 1995; Ross, Dermatis, Levounis, & Galanter, 2003). Finally, the presence of cormorbid BPD and SUD presents a host of complications for treatments focused specifically on BPD (Van Den Bosch, Verheul, Schippers, & Van Den Brink, 2002), SUD (Martinez-Raga, Marshall, Keaney, Ball, & Strang, 2002), or both disorders simultaneously (Dimeff, Rizvi, Brown, & Linehan, 2000; Ross et al., 2003). Impulsivity has been implicated in the development of BPD (Lieb, Zanarini, Schmahl, Linehan, & Bohus, 2004; Linehan, 1993; Links et al., 1995; Siever, Torgersen, Gunderson, Livesley, & Kendler, 2002), SUD (e.g., Kirby, Petry, & Bickel, 1999; Krueger, Caspi, & Moffitt, 1996; Krueger et al., 2002; Moeller et al., 2001, 2002), and their comorbidity (Casillas & Clark, 2002; Nace, 1989; Trull et al., 2000). Unfortunately, a complete understanding of the role of impulsivity in these disorders and their comorbid presentation is limited by a lack of attention to the complex, multidimensional nature of the construct (e.g., Evenden, 1999). To address this issue, we review empirical data that relates impulsivity to the independent presentations of BPD and SUD, across multiple dimensions of the construct. Although we will consider variables such as family history of psychopathology, neurobiological vulnerability, traumatic stress, maladaptive family environments, and state and trait negative affectivity, we will do so only insofar as available theory or data provide insight into the role of impulsivity in BPD and SUD (see Trull et al., 2000 as well as Linehan, 1993 for a comprehensive review of these other factors). In considering the relationship of more specific dimensions and measurement approaches of impulsivity to BPD, SUD, and their comorbidity, we will consider impulsivity across four empirically investigated dimensions including: (a) traditional trait conceptualizations of impulsivity including action without planning as well as engagement in maladaptive behaviors without attention to potential harm (Eysenck, Pearson, Easting, & Allsopp, 1985; Patton, Stanford, & Barratt, 1995; Whiteside & Lynam, 2001); (b) impulsive aggression (Pally, 2002; Siever & Davis, 1991); (c) the inability to delay gratification or discount a reward as a function of delay (Ainslie, 1975; Mischel, Shoda, & Rodriquez, 1989); and (d) poor response inhibition and passive avoidance (Logan, 1994; Newman, Patterson, & Kosson, 1987).

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2. Traditional trait conceptualizations The broad construct of impulsivity has been characterized traditionally as a stable and enduring trait. Widely used trait-based self-report measures include the Barrett Impulsivity Scale (BIS-11; Patton et al., 1995), the Eysenck Impulsiveness Scale (I-7; Eysenck & Eysenck, 1977), and the Temperament and Character Inventory (TCI; Cloninger, Svrakic, and Przybeck, 1993), which followed from the Tridimensional Personality Questionnaire (TPQ; Cloninger, Svrakic, & Przybeck, 1991). Although somewhat overlapping, the precise aspects of impulsivity differ somewhat across these measures. Specifically, the BIS-11 is designed to measure attentional, motor (acting without thinking), and nonplanning subtypes of impulsivity. The I-7 provides a single impulsivity factor score but is considered to be composed of non-planning, risk-taking, and liveliness subscales of impulsivity. In contrast, the TCI and TPQ are designed to measure biologically influenced temperament traits such as novelty seeking, harm avoidance, reward dependence, and persistence, as well as more complex and broad character dimensions including self-directedness, cooperativeness, and self-transcendence. 2.1. BPD Traditional measures of impulsivity have been used to identify BPD symptom severity, diagnosis, and poor BPD treatment prognosis (e.g., Ball, Tennen, Poling, Kranzler, & Rounsaville, 1997; Forman et al., 2004; Henry et al., 2001; Koenigsberg et al., 2001; Lejuez et al., 2003; Morey, Warner, & Boggs, 2002; Morey et al., 2003; Svrakic, Whitehead, Przybeck, & Cloninger, 1993; Trull, 1992). For example, in a study assessing impulsivity with the BIS in patients with BPD, bipolar II disorder, and individuals with other personality disorders, individuals with BPD scored significantly higher than the other two groups on impulsiveness (Henry et al., 2001). Similarly, Fossati et al. (2004) reported that impulsivity as measured by the BIS was positively correlated with the number of BPD symptoms in 747 undergraduate students. Furthermore, in two studies by van Reekum et al. (Van Reekum et al., 1994; Van Reekum, Links, Mitton, Fedorov, & Patrick, 1996), inattentiveness and a tendency toward action without anticipating consequences, as measured by the BIS-11, was reported to underlie impulsivity exhibited by individuals with BPD. Similar results have been found when using other measures of impulsivity and general personality functioning. Both Ball et al. (1997) and Svrakic et al. (1993) reported that the TCI predicted BPD symptom severity. Specifically, symptom severity was positively related to novelty seeking and harm avoidance, and negatively related to persistence and self-directedness. Lejuez et al. (2003) found that elevated scores on the I-7 predicted BPD symptom severity, and expanding on this study, Cheavens et al. (2005) found the I-7 was positively correlated with several features of BPD, including chronic thought suppression, parental criticism, interpersonal sensitivity, and impulsive aggression. 2.2. SUD As with BPD, traditional measures of impulsivity have been used to identify substance use vulnerability, severity, social and emotional consequences, and dependence (e.g., Allen, Moeller, Rhoades, & Cherek, 1998; Fishbein, Lozovsky, & Jaffe, 1989; King et al., 1991; Moeller et al., 2001, 2002; Monterosso, Ehrman, Napier, O’Brien, & Childress, 2001; Patton et al., 1995; Petry, 2001). For instance, Allen et al. (1998) reported that individuals with a history of drug dependence scored

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significantly higher on the BIS than individuals without a history of drug use. Higher scores on the BIS also have been associated with increased severity of cocaine use (Moeller et al., 2001). The association between the BIS and cocaine severity was strongest for the motor impulsivity subscale, which was significantly correlated with self-reported cocaine use, craving, and withdrawal symptoms. The BIS also has been associated with increased severity of alcohol consumption among incarcerated individuals (Fishbein et al., 1989). Furthermore, Moeller et al. (2002) found that cocaine dependent individuals continued to display significantly higher levels of impulsivity on the BIS compared to healthy controls, even after controlling for antisocial personality disorder and lifetime history of aggression. The findings of elevated impulsivity in SUD individuals compared to controls have been demonstrated with other self report measures as well. Soloff, Lynch, and Kelly (2000) reported that the I-7 differentiates substance-using and non-using populations. Further, Petry (2001) assessed selfreported levels of impulsivity in pathological gambling substance abusers, non-pathological gambling substance abusers, and non-clinical controls, finding that both substance abuse and pathological gambling had an additive effect on levels of impulsivity across measures. Finally, individuals with dependence on alcohol (Ball et al., 1997) and illicit drugs (Ball, Tennen, & Kranzler, 1999) scored significantly higher on measures corresponding to impulsivity on TPQ and TCI.

3. Impulsive aggression Aggressive behavior is generally conceptualized by either premeditated aggression or impulsive (unplanned) aggression (cf. Stanford et al., 2003). A self-report measure, the Buss-Durkee Hostility Inventory (BDHI; Buss & Durkee, 1957) assesses seven major aggression dimensions: physical aggression, indirect aggression, irritability, negativism, resentment, suspiciousness, and verbal aggression, with the measure often used to indicate impulsive aggression (e.g., Soloff, Lynch, & Moss, 2000). Alternatively, given that impulsive aggression is hypothesized to be in part a biologically-based process with emergent psychological properties, a number of studies have focused on biological indicators, specifically levels of 5-HT (serotonin precursor). Indeed, a large body of literature demonstrates that low levels of 5-HT are correlated with high rates of aggressive behavior (e.g., Coccaro & Kavoussi, 1997). Other measurement approaches involve the in-vivo assessment of the actual behavior of impulsive aggression. Two such measures include the Point Subtraction Aggression Paradigm (PSAP; Cherek, 1981) and the Taylor Aggression Paradigm (Taylor, 1967). In brief, the PSAP measures an individual’s aggressive response (i.e., points taken away from fictitious opponent) to the periodic loss of a monetary reinforcer, with this loss being attributed to the behavior of the said fictitious other participant. The Taylor Aggression Paradigm is similar, except instead of subtracting points, subjects administer a shock to a fictitious subject. To our knowledge, the Taylor Aggression Paradigm has not been used in studies of BPD or SUD, and therefore will not be discussed further. 3.1. BPD In relation to BPD, impulsive aggression may be defined as a hair-trigger aggressive response to provocation with loss of behavioral control; either directed toward others in the form of violent acts and other inappropriate and uncontrolled expressions of anger or toward the self in the form of suicide,

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suicidal threats and gestures, and other self-damaging acts such as cutting (Dougherty, Bjork, Huckabee, Moeller, & Swann, 1999; Henry et al., 2001; Pally, 2002; Siever & Davis, 1991). Others have suggested that impulsive aggression also could contribute to a number of the interpersonal characteristics of BPD such as b. . .inappropriate anger, recurrent suicide gestures, and frantic efforts to avoid abandonment when separation is threatenedQ (Koenigsberg et al., 2001; p. 360). It is important to note that a propensity to engage in unprovoked aggression does not fall under impulsive aggression and is not considered to be a key feature of BPD. Compared to hospitalized depressed patients without BPD, patients with BPD have been shown to present with higher self-reported impulsive aggression (Benjamin & Wonderlich, 1994). One study has indicated that impulsive aggression (as measured by the BDHI) is an important factor in suicide attempts among individuals with a BPD diagnosis (Soloff, Lis, Kelly, Cornelius, & Ulrich, 1994). Further, several studies have examined the role of decreased serotonin activity as a marker for impulsive aggression in BPD individuals with a history of suicide attempts (Mann, Oquendo, Underwood, & Arango, 1999; Soloff et al., 2000). Additionally, Fossati et al. (2004) reported that physical, verbal, and indirect aggression as measured by the BDHI was significantly related to BPD symptoms. Similar findings regarding the relationship between the BDHI and BPD also have been reported elsewhere (Henry et al., 2001; Paris, Zweig-Frank, Bond, & Guzder, 1996; Soloff, Kelly, Strotmeyer, Malone, & Mann, 2003). Research also has demonstrated that BPD patients who display impulsive aggression, defined as angry outbursts and self-destructive behavior, have blunted responses to agents that enhance serotonergic activity (Stein et al., 1996; Coccaro et al., 1989). Furthermore, two neuroimaging studies have reported that patients with BPD demonstrate reduced serotonergic responsiveness of orbital frontal, ventral medial and cingulate areas of the prefrontal cortex after fenfluramine administration (New et al., 2002; Siever, Buchsbaum, & New 1999). These areas of the prefrontal cortex influence emotional responding via connections with the amygdala (Keightley et al., 2002), in turn hypothetically influencing the ability to regulate impulsive aggression. Correspondingly, prefrontal metabolic activity is significantly lower in borderline and antisocial patients with impulsive aggression, and the aforesaid areas of prefrontal cortex have shown decreased activation to serotonergic probes (Brown et al., 1982; New et al., 2002; Raine et al., 1994, 1997; Siever et al., 1999). Finally, evidence indicates that medications used to increase serotonergic functioning lead to reductions in impulsive aggression among BPD patients (Coccaro, Bergeman, Kavoussi, & Seroczynski, 1997; Figueroa & Silk, 1997). Beyond self-report and biological measures of impulsive aggression, in-vivo tasks such as the PSAP may be especially valuable for understanding both impulsivity in isolation and the degree to which it may be influenced by negative affect. Dougherty et al. (1999) compared women diagnosed with BPD with healthy controls on the PSAP and the BDHI. BPD patients responded to the money losses with significantly greater (approximately three times as many) aggressive responses as healthy controls, and had significantly higher scores on the BDHI. Further results suggest that self reported impulsivity, impulsive aggression, and affect dysregulation are not separate processes, but collectively contribute to the high frequency of interpersonal conflict, impulsive acts, and selfinjurious behavior that typify BPD. Specifically, when controlling for negative affect, the group differences in aggressive responding among BPD and non-BPD participants disappeared. In addition, the statistical significance of the group differences was reduced after controlling for self-reported impulsivity.

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3.2. SUD The relationship between substance use and impulsive aggression has been well documented, although the causal relationship between the two remains unclear. Specifically, it is difficult to determine whether underlying personality traits such as impulsive aggression predisposes an individual to engage in violent acts and substance use, or if substance use induces impulsive aggressive behavior. For instance, more than half of domestic violence perpetrators present with substance-related disorders (Maffli & Zumbrunn, 2003; Murphy, O’Farrell, Fals-Stewart, & Feehan, 2001; Stuart, Moore, Ramsey, & Kahler, 2003). Similarly, individuals with histories of violent crime initiate substance use earlier in life (Best, Hernando, Gossop, Sidwell, & Strang, 2003; Gordon, Kinlock, & Battjes, 2004; Kinlock, O’Grady, & Hanlon, 2003; Lennings, Copeland, & Howard, 2003). Finally, individuals with SUDs are more likely than controls to attempt suicide (Harris & Barraclough, 1997; Moscicki, 1997; Shaffer et al., 1996). In addition, men entering treatment for alcoholism are four to six times more likely than nonalcoholic men to have engaged in partner violence (O’Farrell & Murphy, 1995), and substance use is reported in approximately 40% of domestic assaults (Leonard, 1993) and 70% of domestic homicides (Slade, Daniel, & Heisler, 1991). Impulsive aggression is not limited to violence towards others among substance abusers. For example, Anderson, Howard, Walker, and Suchinsky (1995) reported that among 500,000 American military veterans, substance abusers were 7.5 times more likely than non-substance abusers to attempt suicides. Finally, the BDHI has been used to assess impulsive aggression in substance abusers, and a number of studies have indicated a positive relationship with substance use (Gerra et al., 2004; Johnson, Cloninger, Roache, Bordnick, & Ruiz, 2000; Koller, Preub, Bottlender, Wenzel, & Soyka, 2002; Petry, 2000). Similarly, in-vivo assessment of aggressive behavior has been conducted in SUD populations. For example, Allen et al. (1998) compared subjects with histories of drug use and history of no drug use, showing that SUD individuals evidence more aggressive responses in the PSAP. Gerra et al. (2001) found that aggressive responding on the PSAP was significantly higher in methadone patients than in healthy controls. To partial out the acute pharmacological effects of methadone, Gerra et al. (2001) also examined dosage and duration of methadone exposure, with findings indicating that aggression did not correlate with either; consequently, the authors concluded that impulsive aggression in methadone patients is a trait-like factor rather than the result of the acute effects of methadone.

4. Delay discounting and delay of gratification Delay discounting is based on the tenet that, as a reward is delayed, its value is systematically discounted such that impulsive individuals prefer smaller immediate rewards over larger delayed rewards (Ainslie, 1975, Kirby et al., 1999; Mischel, 1984; Rodriguez, Mischel, & Shoda., 1989). In this way, it is important to consider negative consequences in the same framework as rewards, with delayed larger consequences often preferred over immediate smaller consequences. Combining both positives and negatives, the impulsive individual likely will choose a small yet immediate reward with a large yet delayed negative consequence over a large yet delayed reward with a small yet immediate negative consequence (e.g., Ainslie, 1975; Cooper, Wood, Orcutt, & Albino, 2003). In line with this preference, impulsive individuals often place themselves in a position to sustain excessive long-term costs in exchange for modest short-term gains (e.g., Baumeister & Scher, 1988; Cooper et al., 2003; Kirby et al., 1999). Similar to delay discounting at a conceptual level, delay of gratification differs somewhat on a

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measurement level. Specifically, unlike delay discounting where one makes a permanent choice between an immediate smaller reward and a delayed larger reward, the primary interest in the delay of gratification procedure is the ability to sustain choice of the delayed reinforcer while the smaller, immediate reinforcer is continually available. Regarding measurement approaches, delay discounting procedures initially were developed for animal research (Ainslie, 1975; Richards, Mitchell, de Wit, & Seiden, 1997), and several variations have been developed for humans. A commonly used procedure was developed by Rachlin, Raineri, and Cross (1991), who asked participants to choose between monetary rewards (often ranging from $1 to $1000) obtained either immediately or following a series of delays (often ranging from 1 month to 50 years). For each delay, a computer program adjusts the amount of the immediate reward until the immediate and delayed rewards are of equivalent subjective value. The reduction in the amount of the immediate reward at the indifference point compared to its original amount provides a measure of the present subjective value of the delayed reward. Although this procedure provides quite precise data, it often can take a large number of trials and the long delays and large reward values require that the task involve hypothetical choices. In response to the length of the task, considerably shorter versions using a preselected set of forced choices have been used (e.g., Kirby et al., 1999). Several modifications also have been made to limit the hypothetical nature of the task. Most commonly, smaller amounts of money and shorter delays are used with the further contingency that one of the trials will be randomly selected and the choice made by the participant will be executed. Thus, if a trial comparing $14 now and $25 in 19 days was selected randomly, the participant either would receive $14 at the end of the session or would be mailed a check for $25 in 19 days. Often, delay of gratification procedures have been used with children. Specifically, the participant is presented with a choice between a more preferred (larger or more favored) reinforcer and a less preferred reinforcer (e.g. Mischel & Mischel, 1983). Participants are instructed that they can have a larger reinforcer when the experimenter returns after an unspecified delay or that they can have a smaller reinforcer immediately. Further, even if the delayed larger reinforcer is selected initially, the participant has the continual option to sacrifice the larger delayed reinforcer and switch to the immediate smaller reinforcer. Therefore, delay of gratification then is measured by the latency to select the immediate smaller reinforcer. 4.1. BPD The concepts of delay discounting and delay of gratification could be used to understand the occurrence of a variety of maladaptive behaviors central to BPD. For example, self-harm can be conceptualized as an impulsive behavior chosen because of the immediate benefits of temporary emotional distraction and relief from intense negative affect, despite a variety of long-term consequences (Linehan, 1993; Wagner & Linehan, 1999). Indeed, Brown, Comtois, and Linehan (2002) assessed the self-reported reasons for suicide attempts and non-suicidal self injury among BPD women. Findings indicated that subjects reported engaging in the behavior to reduce aversive internal states; further, the self-destructive behavior often was intended to regain normal feelings and distract oneself from negative affect. Despite the intuitive appeal of this approach, only one study has directly examined this question and has found no difference in response preferences on a delayed gratification task between BPD and non-BPD individuals (Dougherty et al., 1999). Similarly, Lejuez et al. (2005) examined persistence on a psychological stressor task in forty females with elevated BPD symptom severity who were receiving inpatient substance abuse treatment. The task

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was a stressful math test in which participants were given points for correct answers which would influence the amount of money they would receive at the end of the session, but also the option to terminate the task at any point in the last 7 min of the task. Self-report indicated that the task produced elevated levels of negative affect across participants suggesting its utility as a psychological stressor task. Further, BPD symptom severity, with a focus on self-destructive behavior (Borderline Symptom List; Bohus et al., 2001) was negatively related to persistence on the task. The results can be applied to the delayed discounting and the delay of gratification dimensions of impulsivity because terminating the task can be conceptualized as taking the immediate reward of relief from the stressful task over the more long-term benefit of greater financial payment and the sense of satisfaction that might accompany completing the task. Although speculative, this finding could be taken to identify a potential mechanism for self-destructive behaviors which provide an escape from acute negative affect despite the obvious long-term consequences. 4.2. SUD A large body of studies indicate that both licit and illicit substance-using samples evidence substantially high rates of delay discounting, compared to normal controls (e.g., Kollins, 2003; Baker, Johnson, & Bickel, 2003; Petry, 2001; Monterosso et al., 2001). For example, Coffey, Gudleski, Saladin, and Brady (2003) compared impulsivity in crack/cocaine users and normal controls by presenting hypothetical immediate and delayed rewards (i.e., money). Crack/cocaine users were found to discount delayed rewards at a higher rate than a control group. Using a similar design and measures, this effect also was found in heroin users (Kirby et al., 1999). Interestingly, when heroin users were presented with delay discounting scales concerning drugs or money, these individuals discounted delayed heroin significantly more than delayed money (Madden, Petry, Badger, & Bickel, 1997). Finally, this effect is generalizable to licit drug groups as well. Petry (2002) compared normal controls to alcoholic individuals who were either in the active or remission phase of alcoholism. Results evidenced that active alcoholics discounted at a rate significantly higher than normal controls and alcoholics in remission. However, those in remission were found to discount significantly higher than normal controls. This last finding is especially relevant in demonstrating that delay discounting may be conceptualized as trait-like (albeit enhanced by environmental influences), and not simply due to substance dependence. Less clear findings have been provided using the delay of gratification procedure (e.g., Wagner, 1993).

5. Response inhibition and passive avoidance An emerging body of literature has suggested that impulsivity may include deficits in ability to inhibit prepotent responding, with much of this work utilizing Logan’s (1994) Stop Signal Task and the Go/No Go Task (e.g., Newman et al., 1990). Although performance on both tasks reflects inhibitory control, the two tasks may measure relatively distinct aspects of impulsivity: the Stop Signal Task is believed to measure inhibition of prepotent motor responding, whereas the Go/No Go paradigm measures passive avoidance, or the ability to learn to inhibit punished responses. Procedurally, the Stop-Signal Task requires inhibition of an already planned motor response (i.e., pressing a key in response to a visual stimulus), where a signal of bgoQ is converted to a bstopQ (the latter generally indicated by a short sound). In a typical Stop Signal Task, subjects are to respond appropriately to the presentation of either an X or

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an O in the center of the computer screen. On 25% of the trials (25% of the X trials and 25% of the O trials), a tone (stop signal) sounds after the presentation of the X or O. Subjects are instructed to refrain from pressing any keys when they hear the sound. Thus, the task provides a measure of four potential dependent variables including: the latency to respond to the letter presentation, the individual’s accuracy in responding appropriately to the go signal (X or O), the percentage of trials on which the individual fails to inhibit the response when the stop signal is presented, and the time needed to refrain from responding. Conversely, in the Go/No Go paradigm, a motor response is selectively executed or inhibited depending on whether a dGoT or dGoT stimulus appears on a computer screen (e.g., Rubia et al., 1998). In a common version of Newman’s (Newman et al., 1990) paradigm, participants learn to press or to not press a button as a consequence of positive or negative feedback received during a trial-and-error earning task. Correct presses are rewarded with positive feedback (and, often, a small monetary gain); incorrect presses are punished with negative feedback (and a small monetary loss). While engaged in this task, participants are able to voluntarily regulate the length of time that the contingent positive or negative feedback remains available for on-screen reflection and consideration. A smaller yet emerging body of literature indicates that individuals with impulse-control problems demonstrate a significant reduction in reflection on the negative feedback and a significant increase in the number of passive-avoidance errors committed on the task, implying an inability to take sufficient time to pause and reflect on one’s errors (e.g., Newman et al., 1987, 1990). This reduced reflection on negative feedback then decreases the opportunity to evaluate and correct one’s responses, in turn increasing the likelihood of future maladaptive behavior. 5.1. BPD Although no studies to date have utilized the Stop Signal Task with borderline individuals, the Go/No Go task has provided preliminary evidence of deficits in passive avoidance. For example, Hochhausen, Lorenz, and Newman (2002) assessed incarcerated females on levels of passive avoidance using the Go/ No Go Task, as well as for BPD diagnostic status. The authors reported that BPD individuals committed significantly more passive avoidance errors than controls. Leyton (2001) compared BPD subjects to healthy controls on the Go/No Go Task. Compared to the healthy subjects, the subjects with BPD made significantly more punishment-reward commission errors, which is similar to findings reported by Leyton et al. (1999). Finally, Vo¨llum, Richarson, and Stirling (2004) demonstrated that different neural networks are activated during the Go/No Go Task in subjects with BPD compared to healthy volunteers, suggesting that individuals with BPD may utilize different cortical resources in efforts to inhibit responding. 5.2. SUD Both the Stop Signal and Go No/Go Tasks have been studied in SUD individuals. Specifically, disinhibition was examined in cocaine users and age matched controls using the Stop Signal Task. Cocaine users displayed a significantly poorer ability to inhibit their behavioral responses than did controls such that they required more time to inhibit responses to stop signals and displayed a lower probability of inhibiting their responses (Fillmore & Rush, 2002). In addition, Fillmore, Rush, and Hays (2002) examined the acute effects of cocaine abuse on an individual’s ability to inhibit behavior using

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the Stop Signal Task. Current cocaine administration was found to reduce subjects’ ability to inhibit responses to the stop signals. With regard to passive avoidance, Colder and O’Conner (2002) reported that among undergraduates frequent alcohol use was associated with disinhibition during the GoNo/Go task. Likewise, Fillmore and Vogel-Sprott (1999) compared healthy controls and opiate-dependent individuals on the Go No/Go task, finding significantly poorer performance in opiate dependent individuals. Interestingly, the researchers also examined neural correlates of such poor performance, suggesting the role of dysfunction (i.e., attenuated response) in the anterior cingulate cortex. Finally, in a more recent study, Forman et al. (2004) reported that opiate addicts demonstrated poorer performance and attenuated anterior cingulate activation on the Go/No Go Task compared to healthy controls.

6. The role of impulsivity in the comorbidity of BPD and SUD In the previous sections, we have outlined the independent relationships of several dimensions of impulsivity with both BPD and SUD. Following from the commonalities in the relationship of impulsivity with each of these disorders, we now turn to the role of impulsivity in the comorbidity of BPD and SUD. Studies have indicated that individuals with both disorders evidence higher levels of impulsivity than those with either disorder alone (e.g., Links et al., 1995; Trull, Waudby, & Sher, 2004). Specifically, studies comparing substance abusing patients with and without BPD found that those with BPD are at higher risk for behavioral dyscontrol and self-destructive behaviors. Although this work makes conceptual sense and indicates an important vulnerability associated with comorbid BPD and SUD, these studies all are cross-sectional in nature and provide little in terms of understanding the pathways underlying this comorbidity. In addition, this gap also leaves little in terms of informing assessment, prevention, and treatment efforts. In an effort to address such issues, Trull et al. (2000) outlined several theoretical directional models to account for the development and maintenance of comorbid BPD and SUD. Limiting our discussion to his pathways including impulsivity, the most plausible class of models outlined by Trull begins with the presence of a family history of mood/disinhibitory psychopathology and a genetic/biological predisposition to impulsivity serving as important etiological factors likely underlying the SUD/BPD comorbidity. In support of this suggestion, recent evidence strongly indicates the heritability of impulsivity (e.g., Siever et al., 2002), with several studies implicating serotonin deficiencies (e.g., Goveas, Csernansky, & Coccaro, 2004; Paris et al., 2004; Siever et al., 1999; Skodol, Siever, & Livesley et al., 2002; Stein et al., 1996; Torgersen, 2000). Given the link between serotonin deficiencies and impulsive aggression (e.g., Coccaro et al., 1997; New & Siever, 2002), it is reasonable to conclude that impulsive aggression is at least one specific aspect with a strong genetic basis that can be evidenced in laboratory behavioral assessments and on self-report instruments (Coccaro et al., 1997; New & Siever, 2002; Skodol et al., 2002). Relatedly, an abundance of literature has determined that poor performance on the Go No/Go Task and response inhibition dimensions of impulsivity (the latter unfortunately not focusing on humans) is in part genetically determined (Brush, Gendron, & Isaacson, 1999; LeMarquand, Benkelfat, Pihl, Palmour, & Young, 1999; Crean, Richards, & de Wit, 2002), with poor performance on both tasks linked to low levels of 5-HT (i.e., Leyton, 2001; Harrison, Everitt, & Robbins, 1999; Overtoom, Verbaten, Kemner, Kenemans, & van Engeland, 2003; see LeMarquand, 1999 for similar results). In contrast to these findings, research investigating the hereditary and/or

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biological basis of delay discounting has shown that low levels of serotonin after tryptophan (i.e., serotonin precursor) depletion in individuals with a family history of substance use were not associated with a change in rates of discounting (Crean et al., 2002; Winstanley, Dalley, Theobald, & Robbins, 2004). Taken together, it is reasonable to conclude from these studies that biological substrates with emergent psychological properties (i.e., temperament, personality dispositions) may account, in part, for the development of impulsive behavior in BPD and SUD. A second possible pathway to the development of comorbid BPD and SUD includes the reciprocal relationship among impulsivity and environmental influences including family conflict, problematic parenting, and childhood trauma (Danielson, Moffitt, Caspi, & Silva, 1998; Leonard et al., 2000; Loukas, Zucker, Fitzgerald, & Krull, 2003; Trull et al., 2000; Wall, Wekerle, & Bissonnette, 2000). Specifically, a number of studies have shown that childhood trauma (e.g., witnessing violence, experiencing child physical, sexual, or emotional abuse) is associated with 5-HT deficiencies (Rinne, de Kloet, & Wouters et al., 2002). Low levels of serotonin in part underlie impulsive responding on measures of impulsivity in general (e.g., Rinne et al., 2002; Soloff et al., 2003), as well as measures of impulsive aggression specifically (e.g., New et al., 2002; Soloff, Lynch, & Kelly, 2002). Finally, a number of studies have suggested that childhood trauma may underlie impulsive and self-destructive (i.e., self-harm) behavior (Soloff et al., 2002; Sansone, Gaither, & Songer, 2002; Yates, 2004). Relatedly, impulsivity may develop through processes of social learning in childhood. For example, a large body of literature addresses the relationship of childhood aggressive behavior and a history of violence (e.g., Buka, Stichick, Birdthistle, & Earls, 2001). For instance, studies have shown that many adolescents who experience persistent traumatic experiences (i.e., physical and sexual abuse) from family members run away from home, resulting in high rates of (a) continued traumatic stress (Tyler, 2002), (b) self-harm (Tyler, Whitbeck, Hoyt, & Johnson, 2003), and (c) substance use (McClanahan, McClelland, Abram, & Teplin, 1999; Whitbeck, Hoyt, Danny, & Ackley, 1997). In this case, impulsivity may be influenced by traumatic childhood experiences in the home, but exacerbated through stressors outside the home (e.g., experiencing violence and rape, trading of sex for money, food, or shelter). For these individuals, substance use involvement may function as a type of coping strategy in line with the delay discounting dimension of impulsivity (Votta & Manion, 2004), where the immediate benefits of alleviating negative affect outweigh the long-term consequences. Similarly, these individuals may engage in substance use as a result of having learned that their chaotic social environment makes it unlikely that a delay in gratification will ever be actualized. Unfortunately, no studies have addressed other aspects of impulsivity (e.g., passive avoidance, response inhibition) in relation to traumatic childhood and adolescent experiences, and this may be a fruitful ground for future research. Trull et al. (2000) further suggest that the behavioral manifestations of impulsivity may be somewhat dependent on the presence of other variables. Specifically, the authors propose that impulsivity enters into a reciprocal relationship with negative affect and poor ability to tolerate negative affect, leading to both the independent and comorbid presentation of BPD and SUD. This framework allows for the possibility that the two disorders may develop independently from each other, as well as the possibility that if one develops first, increased levels of impulsivity and affective instability may contribute to the development of the second disorder. Finally, it is possible that both disorders are likely to continue once they develop (in the absence of treatment) and may have continued effects on each other over time. Some suggestive evidence stems from a series of studies that examine risk factors for deviant behavior in adolescence (Cooper, Agocha, & Sheldon, 2000, Cooper et al., 2003). Results of these studies suggest that substance use serves as a coping strategy in times of negative affect, with level of impulsivity (as

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measured by more traditional self-report measures) often greatly impacting this relationship. For example, Cooper et al. (2000) found that, in concert with extroversion, impulsivity (defined as extent to which one typically acts quickly and without forethought; Eysenck, 1967) moderated the relationship between neuroticism and alcohol use as an affect regulation strategy. Additionally, the prospective study of Cooper et al. (2003) demonstrated that affective instability and impulsivity (NEO Personality Inventory, NEO-PI; Costa & McCrae, 1985, addressing the bacting without thinkingQ and binability to resisting urgesQ dimension of impulsivity) prospectively predicted initial or increasing involvement in risk behavior among those participants who evidenced little or no risk involvement at baseline assessment. Further defining affect-related problems to include avoidance coping (maladaptive coping method evidenced in both BPD and SUD; Gratz & Roemer, 2004; Simons, Ducette, Kirby, Stahler, & Shipley, 2003), Cooper et al. (2003) expanded on the finding that negative affect predicted onset of substance use among individuals who evidenced little or no substance use at baseline, and proposed that negative affect contributes to involvement in risk in situations where avoidance coping is activated. Although informative, these studies did not longitudinally evaluate the role of negative affect in the etiology of BPD. Thus, caution should be taken in applying these results to BPD until similar work more directly focused on BPD is conducted. In addition to studies examining a vulnerability to BPD and SUD, several studies using individuals with an explicit BPD and/or SUD diagnosis have focused on the rationale that if impulsive behaviors are evident when BPD individuals are in a state of intense negative affect, they will be more likely to evidence a destructive pattern of drug/alcohol use (i.e., binge drinking). Yet to date, few studies have examined substance use patterns in at-risk individuals, and only one study has examined drug/alcohol use patterns in BPD. Specifically, several studies have shown that alcohol-dependent individuals with high trait-negative affect (trait generally characterizing individuals with BPD, e.g., Linehan, 1993; Skodol, Gunderson et al., 2002, Skodol, Siever et al., 2002), are significantly more likely to abuse alcohol during negative affective states (determined by the Inventory of Drinking Situations, IDS) compared to alcohol-dependent individuals evidencing trait-positive affect (Cannon, Leeka, Patterson, & Baker, 1990; Cannon et al., 1992). Similarly, Skinstad, Laberg, and Ellertsen (1998) demonstrated that BPD individuals in treatment evidenced patterns of alcohol use that were more sporadic and binge-like than non-BPD individuals. Relatedly, Kruedelbach et al. (1993) examined BPD individuals in substance use treatment, finding that BPD subjects were (a) more likely to cope with problems in an escape-avoidance method (including via substance use and abuse) and (b) reported having more cravings for substances secondary to states of negative affect during treatment. Although most studies focused on comorbid BPD and SUD have utilized traditional self-report conceptualizations of impulsivity, other dimensions may provide fruitful venues for further developing the synergistic relationship of impulsivity and negative affectivity. For example, from a delay discounting or delay of gratification approach, one can hypothesize that impulsive behaviors such as self-harm function as maladaptive methods of altering state negative affect (e.g., Brown et al., 2002; Fromme & Rivet, 1994, Linehan, 1993; Wagner & Linehan, 1999). Substance abuse, then, may be yet another method of immediately avoiding or terminating negative affect, and the behavior of substance abuse being negatively reinforced despite the long-term adverse consequences. Alternatively, substance use may function as an outlet for uncontrollable anger, thereby limiting engagement in aggressive behaviors aimed inward or towards others. Conversely, substance use may be a method of coping with negative affect resulting from social rejection stemming from inappropriate aggressive

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responses (Bagge et al., 2004; Trull, Useda, Conforti, & Doan, 1997; Eisenberg et al, 1995). Finally, although no work has been conducted in relation to the interaction between performance on Go/NoGo and response inhibition tasks and negative affect, it is possible that performance on bemotionalQ versions of these tasks (measuring responses to neutral and negatively valanced words) may change across affective states, with implications for interpersonal functioning under states of negative affect. This latter statement is of course speculative, but may be yet another avenue for future investigations. Taken together, recent work suggests that considering impulsivity across its various dimensions in an interactive role with trait and state negative affectivity may begin to address the complex nature of comorbid BPD and SUD.

7. Methodological and theoretical considerations 7.1. Methodological considerations Given the significant public health concerns associated with BPD, SUD, and their co-occurrence, it becomes increasingly necessary to understand the development and maintenance of these disorders to improve assessment, prevention, and treatment. Focusing on specific mechanisms likely will be critical in the success of such efforts. Following from suggestive findings in the literature, it is clear that impulsivity, across its various dimensions, plays a role in BPD, SUDs, and their comorbidity. However, the complex nature of both this construct and the disorders of interest continue to leave far fewer answers than questions. Indeed, despite the existence of multiple assessment modalities, it is yet not clear how to define and study impulsivity as a unitary, overarching construct. One relevant example is a recent longitudinal study demonstrating that the impulsive symptoms of BPD are the most likely to dissipate for remitted borderline patients (Zanarini, Frankenburg, Hennen, & Silk, 2003). In contrast, affective symptoms of BPD remained constant despite remission from the diagnosis. However, Zanarini et al. (2003) defined impulsivity via presence and severity of behavioral acts (e.g., self-mutilation, substance use). In contrast, chronic anger and angry acts were included under the baffective problemsQ cluster. This finding further highlights the importance of the assessment method of impulsivity. Indeed, because impulsivity was measured by using discrete behavioral topographies, it is difficult to discern whether results from this suggest that (a) BPD individuals indeed became less impulsive over time, or (b) rather than remitting completely, the behavioral topography of impulsivity in BPD changed over time. Relatedly, the above study highlights the importance of recognizing and measuring impulsivity as a multi-dimensional construct (Campbell & Fiske, 1959). Although notable exceptions exist (e.g., Monterosso et al., 2001), researchers typically do not cross modalities of measurement (e.g., behavioral laboratory as well as self-report assessments, cf. Stanford, Greve, Boudreaux, Mathias, & Brumbelow, 1996), making it difficult to (a) interpret the generalizability of results across other dimensions of impulsivity and (b) understand how specific components of impulsivity are related to BPD, SUDs, and their comorbidity. Moreover, when the same mode of assessment is employed to index a construct of interest as is often the practice with trait research (e.g., multiple self-report methodologies to assess impulsivity), one potential problem is the exaggeration of correlation coefficients across questionnaires, such that the correlation coefficients are due in large part to the influence of the same modality of measurement (e.g., Cohen, 1988). Additionally, behaviors that are representative of a trait may vary across ethnic or cultural groups and may not be applicable to some ethnic minorities (Kagan, 1998). Self-

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report also may be affected by automatic (e.g., failure to remember) and/or strategic (e.g., lying) distortions in responding (e.g., Leigh & Stall, 1993). Finally, due to the effects of chronic drug use, some drug users may lack the insight or cognitive ability to understand questions or provide an accurate report of their own behavior. Differences in assessment modality often are further complicated by associated differences in whether impulsivity is indexed as a trait or state. Indeed, self-report measures typically draw upon patterns of behavior which are expected to remain somewhat static across situations. Although behavioral measures may be used to measures impulsivity as a personality trait, they are also likely to be sensitive to affective, drug, and other states. Several studies described above have shown that impulsive behavior may be in large part dependent on current affect (Bagge et al., 2004; Brown et al., 2002; Crean et al, 2002; Cooper et al., 2000, 2003; Dougherty et al., 1999; Lejuez et al, 2005; Lane, Cherek, Rhodes, Pietras, & Tcheremissine, 2003). This point is especially crucial, as researchers often attempt to generalize a bsnapshotQ of behavior across a variety of settings without specifying the context of testing. Given that both self-report and behavioral measures are somewhat limited, the correlations between self-report and behavioral measures may be expected to be relatively low (e.g., Lejuez et al., 2002; White et al., 1994; Mitchell, 1999; Monterosso et al., 2001; Lane et al., 2003). Although one available study has suggested that laboratory measures present distinct factors relative to rating scales of impulsive behavior problems, loadings on laboratory task factors (i.e., response inhibition and delay of reward) were relatively low, and several contemporary measures of impulsivity were not examined (Lane et al., 2003). Thus, it remains uncertain whether the various measures widely used today in the study of externalizing spectrum disorders truly reflect a single higher-order construct versus multiple measures of impulsive or disinhibitory tendencies. The heterogeneity of the impulsivity construct in itself, and the diversity of findings regarding this construct in BPD and SUD research, suggest the need to separate the underlying features of impulsivity and clarify the relationship between these features and manifested maladaptive behaviors (Hochhausen et al., 2002). 7.2. Theoretical considerations It is important to consider other potential obstacles to the interpretation of causality and/or directionality in this line of research. First, the symptom presentation of BPD across patients is extremely variable (e.g., Skodol et al., 2002). As a result of the polythetic diagnostic system, only 5 out of 9 diagnostic criteria are needed to meet criteria for a BPD diagnosis, resulting in 151 possible diagnostic presentations. Given this heterogeneity, it is difficult to determine which, if any, of the diagnostic criteria are basic or underlying across all presentations of BPD. Second, the diagnostic criterion for impulsivity in BPD can be met with impulsive substance use. As a salient example, the Revised Diagnostic Interview for Borderlines (DIB-R; Zanarini, Frankenburg, & Vujanovic, 2002) assesses impulsivity as a dimension of the borderline diagnosis according to the following impulsive features: substance abuse/ dependence; sexual deviance; self-mutilation; manipulative suicide efforts, and other impulsive patterns (e.g., binge eating, verbal outbursts, property damage). Similarly, the Structured Clinical Interview for DSM-IV (First, Spitzer, Gibbon, Williams, & Benjamin, 1995) defines impulsivity as incidents of substance use, risky sexual behavior (e.g., condom non-use), binge eating, and impulsive spending. As a result of this diagnostic overlap, it is difficult to differentiate substance use as a product of BPD from BPD-like symptoms resulting from the acute and chronic pharmacological effects of alcohol and illicit substances (Rounsaville et al., 1998; Trull et al., 2000).

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Yet another problem in investigating the BPD–SUD directionality is that BPD symptoms that develop within the context of drug dependence may be difficult to disentangle and may persist long into treatment, precluding an accurate diagnosis even after prolonged abstinence (Rounsaville et al., 1998). Similarly, it is possible that one disorder may result from the other. Because it is difficult to isolate causal processes, especially where a long history of substance use is present, some researchers have advocated for simply removing diagnostic criteria that are relevant to SUD when attempting to diagnose BPD (e.g., Nace, Saxon, & Shore, 1986). Interestingly, the removal of the SUD-related criteria from the original diagnostic criteria might result in dramatically decreased prevalence rates of BPD (Carroll et al., 1993, but see Weiss et al., 1993 for a counterexample); unfortunately, these vastly different groups may also differ on basic processes underlying the disorder. As directional models are developed and tested, these issues must be of critical concern. Finally, gender differences across the dimensions of impulsivity, as well as BPD and SUD diagnoses may produce several confounds, as rates of BPD are considerably higher in females compared to males, whereas rates of SUDs and levels of impulsivity are considerably higher in males compared to females (APA, 1994; Grilo et al., 1996; Johnson et al., 2003; Magura, Kang, Rosenblum, Handelsman, & Foote, 1998).

8. Conclusions and future directions As has been stressed through this paper and the extant literature, simple explanations are only marginally useful in providing more than a basic understanding of the relationships at hand. One clear conclusion that may be drawn is that when assessing a multi-dimensional construct such as impulsivity, a multi-trait, multi-method approach similar to the approach suggested by Campbell and Fiske (1959) brings about greater understanding of behavioral processes and provides a more comprehensive framework than a single modality alone. Relatedly, given the state-dependent nature of impulsive behavior, negative affectivity should be accounted for when examining impulsivity and comorbid BPD and SUD. Indeed, the above evidence for the engagement in impulsive behaviors in the presence of negative affect in BPD individuals suggests the possibility that (a) impulsivity may increase during an aversive affective state, and (b) impulsive behaviors may serve as a maladaptive method of altering negative affect behaviorally, (c) impulsive behavior may produce further changes in negative affect, entering into a reciprocal and/or synergistic relationship leading to further problematic behavior and associated negative consequences. In addition to conceptual advances, a better understanding of impulsivity in BPD and SUD can have important implications for prevention and treatment of the disorders. In particular, if impulsivity is exacerbated by current negative mood or trait affective instability then standard drug counseling may require modification. For example, Linehan, Davison, Lynch, and Sanderson (in press) have recommended that due to the emotional instability associated with BPD, an emphasis should be placed on helping the patient learn to tolerate and respond to negative affect in a manner that does include impulsive behavior. One potentially useful treatment is dialectical behavior therapy (DBT), which has been found to be efficacious for the treatment of BPD in seven well controlled randomized clinical trials conducted across four independent research teams (see Lieb et al., 2004 for review), with some evidence specific to comorbid BPD and SUD (Dimeff et al., 2000; Linehan et al., 1999). However, future studies are needed to demonstrate whether a focus in treatment on affect dysregulation is critical to reducing impulsive behavior.

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Impulsivity is clearly a crucial variable in understanding BPD, SUD, and the comorbidity of the two disorders. Extending previous conceptualizations of these relationships, the current manuscript has attempted to stress the multidimensional nature of impulsivity, as well as the potential interactive role of impulsivity with state and trait affective variables. In this way, we argue for further exploration of models of BPD/SUD comorbidity that examine how the combination of impulsivity across its various dimensions work in concert with negative affect, leading to the development of comorbid BPD and SUDs. In turn, the two disorders may be maintained in a reciprocal fashion, illustrating the dynamic nature of this relationship. Although future theory and research will need to consider a wide range of other relevant variables including family history of psychopathology, neurobiological vulnerability, traumatic stress, and maladaptive family environments, we hope the current work will lead to a more comprehensive framework to guide research that considers the complex role of impulsivity in BPD, SUD, and their comorbidity.

References Ainslie, G. (1975). Specious reward: A behavioral theory of impulsiveness and impulse control. Psychological Bulletin, 82, 463 – 509. Allen, T. J., Moeller, F. G., Rhoades, H. M., & Cherek, D. R. (1998). Impulsivity and history of drug dependence. Drug and Alcohol Dependence, 50, 137 – 145. American Psychiatric Association (1994). Diagnostic and statistical manual of mental disorders. (4th ed.). Washington, DC7 Author. Anderson, B. A., Howard, M. O., Walker, R. D., & Suchinsky, R. T. (1995). Characteristics of substance-abusing veterans attempting suicide: A national study. Psychological Reports, 77, 1231 – 1242. Bagge, C., Nickell, A., Stepp, S., Durrett, C., Jackson, K., & Trull, T. (2004). Borderline personality disorder features predict negative outcomes 2 years later. Journal of Abnormal Psychology, 113, 279 – 288. Baker, F., Johnson, M. W., & Bickel, W. K. (2003). Delay discounting in current and never-before cigarette smokers: Similarities and differences across commodity, sign, and magnitude. Journal of Abnormal Psychology, 112, 382 – 392. Ball, S. A., Tennen, H., & Kranzler, H. R. (1999). Factor replicability and validity of the Temperament and Character Inventory in substance-dependent patients. Psychological Assessment, 11, 514 – 524. Ball, S. A., Tennen, H., Poling, J. C., Kranzler, H. R., & Rounsaville, B. J. (1997). Personality, temperament, and character dimensions and the DSM-IV personality disorders in substance abusers. Journal of Abnormal Psychology, 106, 545 – 553. Baumeister, R. F., & Scher, S. J. (1988). Self-defeating behavior patterns among normal individuals: Review and analysis of common self-destructive tendencies. Psychological Bulletin, 104, 3 – 22. Benjamin, L. S., & Wonderlich, S. A. (1994). Social perceptions and borderline personality disorder: The relation to mood disorders. Journal of Abnormal Psychology, 103, 610 – 624. Best, D., Hernando, R., Gossop, M., Sidwell, C., & Strang, J. (2003). Getting by with a little help from your friends—The impact of peer networks on criminality in a cohort of treatment-seeking drug users. Addictive Behaviors, 28, 597 – 603. Bohus, M., Limberger, M. F., Frank, U., Sender, I., Gratwohl, T., & Stieglitz, R. (2001). Development of the Borderline Symptom List (BSL). Psychotherapie, Psychosomatik, Medizinische Psychologie, 51, 201 – 211. Brooner, R. K., King, V. L., Kidorf, M., Schmidt, C. W., & Bigelow, G. E. (1997). Psychiatric and substance use comorbidity among treatment seeking opioid abusers. Archives of General Psychiatry, 54, 71 – 80. Brown, G. L., Ebert, M. H., Goyer, P. F., Jimerson, D. C., Klein, W. J., Bunney, W. E., et al. (1982). Aggression, suicide, and serotonin: Relationships to CSF amine metabolites. American Journal of Psychiatry, 139, 741 – 746. Brown, M., Comtois, K. A., & Linehan, M. M. (2002). Reasons for suicide attempts and nonsuicidal self-injury in women with borderline personality disorder. Journal of Abnormal Psychology, 111, 198 – 202. Brush, F. R., Gendron, C. M., & Isaacson, M. D. (1999). A selective genetic analysis of the Syracuse high-and low-avoidance (SHA/Bru and SLA/Bru) strains of rats (Rattus norvegicus). Behavioural Brain Research, 106, 1 – 11.

806

M.A. Bornovalova et al. / Clinical Psychology Review 25 (2005) 790–812

Buka, S. L., Stichick, T. L., Birdthistle, I., & Earls, F. J. (2001). Youth exposure to violence: Prevalence, risks and consequences. American Journal of Orthopsychiatry, 71, 298 – 310. Bunce, S. C., & Coccaro, E. (1999). Factors differentiating personality-disordered individuals with and without a history of unipolar mood disorder. Depression and Anxiety, 10, 147 – 157. Buss, A. H., & Durkee, A. (1957). An inventory for assessing different kinds of hostility. Journal of Consulting Psychology, 21, 343 – 349. Campbell, D. T., & Fiske, D. W. (1959). Convergent and discriminant validation by the multitrait–multimethod matrix. Psychological Bulletin, 56, 81 – 105. Cannon, D. S., Leeka, J. K., Patterson, E. T., & Baker, T. B. (1990). Principal components analysis of the inventory of drinking situations: Empirical categories of drinking by alcoholics. Addictive Behaviors, 15, 265 – 269. Cannon, D. S., Rubin, A., Keefe, C. K., Black, J. L., Leeka, J. K., & Phillips, L. A. (1992). Affective correlates of alcohol and cocaine use. Addictive Behavior, 17, 517 – 524. Carroll, K. M., Ball, S. A., & Rousanville, B. J. (1993). A comparison of alternate systems for diagnosing antisocial personality disorder in cocaine abusers. Journal of Nervous and Mental Disorder, 181, 436 – 443. Casillas, A., & Clark, L. A. (2002). Dependency, impulsivity, and self-harm: Traits hypothesized to underlie the association between Cluster B personality and substance abuse disorders. Journal of Personality Disorders, 16, 424 – 436. Cheavans, J. S., Rosenthal, M. Z., Daughters, S. D., Novak, J., Kosson, D., Lynch, T. R., et al. (2005). An analogue investigation of the relationships among perceived parental criticism, negative affect, and borderline personality disorder features: The role of thought suppression. Behavior Research and Therapy, 43, 257 – 268. Cherek, D. (1981). Effects of smoking different doses of nicotine on human aggressive behavior. Psychopharmacology, 75, 339 – 345. Cloninger, C. R., Przybeck, T. R., & Svrakic, D. M. (1991). The tridimensional personality questionnaire: US normative data. Psychological Reports, 69, 1047 – 1057. Cloninger, C. R., Svrakic, D. M., & Przybeck, T. R. (1993). A psychobiological model of temperament and character. Archives of General Psychiatry, 50, 975 – 990. Coccaro, E. F., Bergeman, C. S., Kavoussi, R. J., & Seroczynski, A. D. (1997). Heritability of aggression and irritability: A twin study of the Buss-Durkee Aggression Scales in adult male twins. Biological Psychiatry, 41, 273 – 284. Coccaro, E. F., & Kavoussi, R. J. (1997). Fluoxetine and impulsive aggressive behavior in personality-disordered subjects. Archives of General Psychiatry, 54, 1081 – 1088. Coccaro, E. F., Siever, L. J., & Klar, H. M. (1989). Serotonergic studies in patients with affective and personality disorders. Archives of General Psychiatry, 46, 587 – 599. Coffey, S. F., Gudleski, G. D., Saladin, M. E., & Brady, K. T. (2003). Impulsivity and rapid discounting of delayed hypothetical rewards in cocaine-dependent individuals. Experimental and Clinical Psychopharmacology, 11, 18 – 25. Cohen, J. (1988). Statistical power analysis for the behavioral sciences. (2nd ed.). New Jersey7 Lawrence Erlbaum. Cooper, M. L., Agocha, V. B., & Sheldon, M. (2000). A motivational perspective on risky behaviors: The role of personality and affect regulation. Journal of Personality, 68, 1059 – 1088. Cooper, M. L., Wood, P. K., Orcutt, H. K., & Albino, A. W. (2003). Personality and the predisposition to engage in risky or problem behaviors during adolescence. Journal of Personality and Social Psychology, 84, 390 – 410. Crean, J., Richards, J. B., & de Wit, H. (2002). Impulsive behavior in men with and without a family history of alcoholism: Effects of tryptophan depletion. Behavioral Brain Research, 136, 349 – 357. Danielson, K. K., Moffitt, T. E., Caspi, A., & Silva, P. A. (1998). Comorbidity between abuse of an adult and DSM-III-R mental disorders: Evidence from an epidemiological study. American Journal of Psychiatry, 155, 131 – 133. Dimeff, L., Rizvi, S. L., Brown, M., & Linehan, M. M. (2000). Dialectical behavior therapy for substance abuse: A pilot application to methamphetamine-dependent women with borderline personality disorder. Cognitive and Behavioral Practice, 7, 457 – 468. Dougherty, D. M., Bjork, J. M., Huckabee, H. C. G., Moeller, F. G., & Swann, A. C. (1999). Laboratory measures of aggression and impulsivity in women with borderline personality disorder. Psychiatry Research, 85, 315 – 326. Eisenberg, N., Fabes, R. A., Murphy, B., Maszk, P., Smith, M., & Karbon, M. (1995). The role of emotionality and regulation in children’s social functioning: A longitudinal study. Child Development, 66, 1360 – 1384. Evenden, J. L. (1999). Varieties of impulsivity. Psychopharmacology, 146, 348 – 361. Eysenck, H. J. (1967). The biological basis of personality. Springfield, IL7 Charles C Thomas.

M.A. Bornovalova et al. / Clinical Psychology Review 25 (2005) 790–812

807

Eysenck, S. B. G., & Eysenck, H. J. (1977). The place of impulsiveness in a dimensional system of personality description. British Journal of Social and Clinical Psychology, 16, 57 – 68. Eysenck, S. B. G., Pearson, P. R., Easting, G., & Allsopp, J. F. (1985). Age norms for impulsiveness, venturesomeness and empathy in adults. Personality and Individual Differences, 6, 613 – 619. Figueroa, E., & Silk, K. R. (1997). Biological implications of childhood sexual abuse in borderline personality disorder. Journal of Personality Disorders, 11, 71 – 92. Fillmore, M. T., & Rush, C. R. (2002). Impaired inhibitory control of behavior in chronic cocaine users. Drug and Alcohol Dependence, 66, 265 – 273. Fillmore, M. T., Rush, C. R., & Hays, L. (2002). Acute effects of oral cocaine on inhibitory control of behavior in humans. Drug and Alcohol Dependence, 67, 157 – 167. Fillmore, M. T., & Vogel-Sprott, M. (1999). An alcohol model of impaired inhibitory control and its treatment in humans. Experimental and Clinical Psychopharmacology, 7, 49 – 55. First, M. B., Spitzer, R. L., Gibbon, M., Williams, J. B. W., & Benjamin, L. (1995). The Structured Clinical Interview for DSM-IV Personality Disorders (SCID-II). New York7 Biometrics Research Unit, New York State Psychiatric Institute. Fishbein, D. H., Lozovsky, D., & Jaffe, J. H. (1989). Impulsivity, aggression, and neuroendocrine responses to serotonergic stimulation in substance abusers. Biological Psychiatry, 25, 1049 – 1066. Forman, S. D., Dougherty, G. G., Casey, B. J., Siegle, G. J., Braver, T. S., Barch, D. M., et al. (2004). Opiate addicts lack errordependent activation of rostral anterior cingulated. Biological Psychiatry, 55, 531 – 537. Fossati, A., Barratt, E. S., Carretta, I., Leonardi, B., Grazioli, F., & Maffei, C. (2004). Predicting borderline and antisocial personality disorder features in nonclinical subjects using measures of impulsivity and aggressiveness. Psychiatry Research, 15, 161 – 170. Fromme, K., & Rivet, K. (1994). Young adults’ coping style as a predictor of their alcohol use in response to daily events. Journal of Youth and Adolescence, 23, 85 – 97. Gerra, G., Garofano, L., Bosari, S., Pellegrini, C., Zaimovic, A., Moi, G., et al. (2004). Analysis of monoamine oxidase A (MAO-A) promoter polymorphism in male heroin-dependent subjects: Behavioral and personality correlates. Journal of Neural Transmission, 11, 611 – 621. Gerra, G., Zaimovic, A., Raggi, M. A., Giusti, F., Delsignore, R., Bertacca, S., et al. (2001). Aggressive responding of male heroin addicts under methadone treatment: Psychometric and neuroendocrine correlates. Drug and Alcohol Dependence, 65, 85 – 95. Gordon, M. S., Kinlock, T. W., & Battjes, R. J. (2004). Correlates of early substance use and crime among adolescents entering outpatient substance abuse treatment. The American Journal of Drug and Alcohol Abuse, 30, 39 – 59. Goveas, J. S., Csernansky, J. G., & Coccaro, E. F. (2004). Platelet serotonin content correlates inversely with life history of aggression in personality-disordered subjects. Psychiatry Research, 126, 23 – 32. Gratz, K. L., & Roemer, L. (2004). Multidimensional assessment of emotion regulation and dysregulation: Development, factor structure, and initial validation of the Difficulties in Emotion Regulation Scale. Journal of Psychopathology and Behavioral Assessment, 26, 41 – 54. Grilo, C. M., Becker, D. F., Fehon, D. C., Walker, M. L., Edell, W. S., & McGlashan, T. H. (1996). Gender differences in personality disorders in psychiatrically hospitalized adolescents. American Journal of Psychiatry, 153, 1089 – 1091. Harris, E. C., & Barraclough, B. (1997). Suicide as an outcome for mental disorders. A meta-analysis. British Journal of Psychiatry, 170, 205 – 228. Harrison, A. A., Everitt, B. J., & Robbins, T. W. (1999). Central serotonin depletion impairs both the acquisition and performance of a symmetrically reinforced go/no-go conditional visual discrimination. Behavioural Brain Research, 100, 99 – 112. Henry, C., Mitropoulou, V., New, A. S., Koenigsberg, H. W., Silverman, J., & Siever, L. J. (2001). Affective instability and impulsivity in borderline personality and bipolar II disorders: Similarities and differences. Journal of Psychiatric Research, 35, 307 – 331. Hochhausen, N. M., Lorenz, A. R., & Newman, J. P. (2002). Specifying the impulsivity of female inmates with borderline personality disorder. Journal of Abnormal Psychology, 111, 495 – 501. Johnson, B. A., Cloninger, C. R., Roache, J. D., Bordnick, P. S., & Ruiz, P. (2000). Age of onset as a discriminator between alcoholic subtypes in a treatment-seeking outpatient population. American Journal on Addictions, 9, 17 – 27.

808

M.A. Bornovalova et al. / Clinical Psychology Review 25 (2005) 790–812

Johnson, D. M., Shea, M. T., Yen, S., Battle, C. L., Zlotnick, C., Sanislow, C. A., et al. (2003). Gender differences in borderline personality disorder: Findings from the Collaborative Longitudinal Personality Disorders Study. Comprehensive Psychiatry, 44, 284 – 292. Kagan, J. (1998). Three seductive ideas. Cambridge, MA7 Harvard University Press. Keightley, M. L., Winocur, G., Grahama, S. J., Mayberg, H. S., Hevenor, S. J., & Grady, C. L. (2002). An fMRI study investigating cognitive modulation of brain regions associated with emotional processing of visual stimuli. Neuropsychologia, 41, 585 – 596. King, R. A., Riddle, M. A., Chappell, P. B., Hardin, M. T., Anderson, G. M., Lombroso, P., et al. (1991). Emergence of selfdestructive phenomena in children and adolescents during fluoxetine treatment. Journal of the American Academy of Child and Adolescent Psychiatry, 30, 179 – 186. Kinlock, T. W., O’Grady, K. E., & Hanlon, T. E. (2003). The effects of drug treatment on institutional behavior. The Prison Journal, 83, 1 – 20. Kirby, K. N., Petry, N. M., & Bickel, W. K. (1999). Heroin addicts have higher discount rates for delayed rewards than nondrug-using controls. Journal of Experimental Psychology. General, 128, 78 – 87. Koenigsberg, H. W., Harvey, P. D., Mitropoulou, V., New, A. S., Goodman, M., Silverman, J., et al. (2001). Are the interpersonal and identity disturbances in the borderline personality disorder criteria linked to the traits of affective instability and impulsivity? Journal of Personality Disorders, 15, 358 – 370. Koller, G., Preub, U. W., Bottlender, M., Wenzel, K., & Soyka, M. (2002). Impulsivity and aggression as predictors of suicide attempts in alcoholics. European Archives of Psychiatry and Clinical Neuroscience, 252, 155 – 160. Kollins, S. H. (2003). Delay discounting is associated with substance use in college students. Addictive Behaviors, 28, 1167 – 1173. Kruedelbach, N., McCormick, R. A., Schulz, S. C., & Gruenreich, R. (1993). Impulsivity, coping styles, and triggers for craving in 773 substance abusers with borderline personality disorders. Journal of Personality Disorders, 7, 214 – 222. Krueger, R., Caspi, A., & Moffitt, T. E. (1996). Delay of gratification, psychopathology, and personality: Is low self-control specific to externalizing problems? Journal of Personality, 64, 107 – 129. Krueger, R. F., Hicks, B., Patrick, C. J., Carlson, S., Iacono, W. G., & McGue, M. (2002). Etiologic connections among substance dependence, antisocial behavior, and personality: Modeling the externalizing spectrum. Journal of Abnormal Psychology, 111, 411 – 424. Lane, S. D., Cherek, D. R., Rhodes, H. M., Pietras, C. J., & Tcheremissine, O. V. (2003). Relationships among laboratory and psychometric measures of impulsivity: Implications in substance abuse and dependence. Addictive Disorders & Their Treatment, 2, 33 – 40. Leigh, B. C., & Stall, R. (1993). Substance use and risky sexual behavior for exposure to HIV. Issues in methodology, interpretation, and prevention. American Psychologist, 48, 1035 – 1045. Lejuez, C. W., Daughters, S. B., Herna´ndez, G. D., Kosson, D., & Lynch, T. R. (2005). Distress tolerance, borderline symptom severity, and self harm in female inner-city residential treatment seeking drug users. Unpublished manuscript. Lejuez, C. W., Daughters, S. B., Nowak, J. A., Lynch, T., Rosenthal, M. Z., & Kosson, D. (2003). Examining the inventory of interpersonal problems as a tool for conducting analogue studies of mechanisms underlying Borderline Personality Disorder. Journal of Behavior Therapy and Experimental Psychiatry, 34, 313 – 324. Lejuez, C. W., Read, J. P., Kahler, C. W., Richards, J. B., Ramsey, S. E., Stuart, G. L., et al. (2002). Evaluation of a behavioral measure of risk-taking: The Balloon Analogue Risk Task (BART). Journal of Experimental Psychology: Applied, 8, 75 – 84. LeMarquand, D. G. (1999). Behavioral disinhibition induced by tryptophan depletion in nonalcoholic young men with multigenerational family histories of paternal alcoholism. American Journal of Psychiatry, 156, 1771 – 1779. LeMarquand, D. G., Benkelfat, C., Pihl, R. O., Palmour, R. M., & Young, S. N. (1999). Behavioral disinhibition induced by tryptophan depletion in nonalcoholic young men with multigenerational family histories of paternal alcoholism. American Journal of Psychiatry, 156, 1771 – 1779. Lennings, C. J., Copeland, J., & Howard, J. (2003). Substance use patterns of young offenders and violent crime. Aggressive Behavior, 29(5), 414 – 422. Leonard, K. (1993). Drinking patterns and intoxication in marital violence: Review, critique, and future directions for research. In S. Martin (Ed.), Alcohol and Interpersonal Violence: Fostering Multidisciplinary Perspectives. National Institute on Alcohol Abuse and Alcoholism (NIAAA) Research Monograph No. 24. National Institutes of Health (NIH) Publication No. 93-3496. The Institute: Rockville, MD, pp. 253–280.

M.A. Bornovalova et al. / Clinical Psychology Review 25 (2005) 790–812

809

Leonard, K. E., Das Eiden, R., Wong, M. M., Zucker, R. A., Puttler, L. I., & Fitzgerald, H. E. (2000). Developmental perspectives on risk and vulnerability in alcoholic families. Alcoholism, Clinical and Experimental Research, 24, 238 – 240. Leyton, M. (2001). Brain regional alpha-[-sup-1-sup-1C]Methyl-l-tryptophan trapping in impulsive subjects with borderline personality disorder. American Journal of Psychiatry, 158, 775 – 782. Lieb, K., Zanarini, M. C., Schmahl, C., Linehan, M. M., & Bohus, M. (2004). Borderline personality disorder. The Lancet, 364, 453 – 461. Linehan, M., Davison, G., Lynch, T., & Sanderson, C. (in press). Principles of Therapeutic Change in the treatment of personality disorders. In Beutler, L., Castonguay, L. (Eds.), Identification of Principles of Therapeutic Change, Oxford University Press. Linehan, M. M. (1993). Cognitive-behavioral treatment for borderline personality disorder: The dialectics of effective treatment. New York7 The Guilford Press. Linehan, M. M., Schmidt, H., Dimeff, L. A., Craft, J. C., Kanter, J., & Comtois, K. A. (1999). Dialectical behavior therapy for patients with borderline personality disorder and drug-dependence. American Journal on Addictions, 8, 279 – 292. Links, P. S., Heslegrave, R. J., Mitton, J. E., van Reekum, R., & Patrick, J. (1995). Borderline personality disorder and substance abuse: Consequences of comorbidity. Canadian Journal of Psychiatry, 40, 9 – 14. Logan, G. D. (1994). On the ability to inhibit thought and action: A users’ guide to the stop signal paradigm. In D. Dagenbach, & T. H. Cart (Eds.), Inhibitory processes in attention, memory, and language. San Diego: Academic Press, pp. 189–239. Loukas, A., Zucker, R. A., Fitzgerald, H. E., & Krull, J. L. (2003). Developmental trajectories of disruptive behavior problems among sons of alcoholics: Effects of parent psychopathology, family conflict, and child undercontrol. Journal of Abnormal Psychology, 112, 119 – 131. Madden, G. J., Petry, N. M., Badger, G. J., & Bickel, W. K. (1997). Impulsive and self-control choices in opioid-dependent patients and non-drug-using control patients: Drug and monetary rewards. Experimental and Clinical Psychopharmacology, 5, 256 – 262. Maffli, E., & Zumbrunn, A. (2003). Alcohol and domestic violence in a sample of incidents reported to the police of Zurich City. Substance Use and Misuse, 38, 881 – 893. Magura, S., Kang, S. Y., Rosenblum, A., Handelsman, L., & Foote, J. (1998). Gender differences in psychiatric comorbidity among cocaine-using opiate addicts. Journal of Addictive Diseases, 17, 49 – 61. Mann, J. J., Oquendo, M. A., Underwood, M. D., & Arango, V. (1999). The neurobiology of suicide risk: A review for the clinician. Journal of Clinical Psychiatry, 60, 7 – 11. Martinez-Raga, J., Marshall, E. J., Keaney, F., Ball, D., & Strang, J. (2002). Unplanned versus planned discharges from in-patient alcohol detoxification: Retrospective analysis of 470 first-episode admissions. Alcohol and Alcoholism, 37, 277 – 281. McClanahan, S. F., McClelland, G. M., Abram, K. M., & Teplin, A. (1999). Pathways into prostitution among female jail detainees and their implications for mental health service. Psychiatric Services, 50, 1606 – 1613. Mischel, H. N., & Mischel, W. (1983). The development of children’s knowledge of self-control strategies. Child Development, 53, 603 – 619. Mischel, W. (1984). Convergences and challenges in the search for consistency. American Psychologist, 39, 351 – 364. Mischel, W., Shoda, Y., & Rodriquez, M. (1989). Delay of gratification in children. Science, 244, 933 – 938. Mitchell, S. H. (1999). Measures of impulsivity in cigarette smokers and non-smokers. Psychopharmacology, 146, 455 – 464. Moeller, F. G., Dougherty, D. M., Barratt, E. S., Oderinde, V., Mathias, C. W., Harper, R. A., et al. (2002). Increased impulsivity in cocaine dependent subjects independent of antisocial personality disorder and aggression. Drug and Alcohol Dependence, 68, 105 – 111. Moeller, F. G., Dougherty, D. M., Barratt, E. S., Schmitz, J. M., Swann, A. C., & Grabowski, J. (2001). The impact of impulsivity on cocaine use and retention in treatment. Journal of Substance Abuse Treatment, 21, 193 – 198. Monterosso, J., Ehrman, R., Napier, K. L., O’Brien, C. P., & Childress, A. R. (2001). Three decision-making tasks in cocainedependent patients: Do they measure the same construct? Addiction, 96, 1825 – 1837. Morey, L. C., Warner, M. B., & Boggs, C. D. (2002). Gender bias in the personality disorders criteria: An investigation of five bias indicators. Journal of Psychopathology and Behavioral Assessment, 24, 55 – 65. Morey, L. C., Warner, M. B., Shea, M. T., Gunderson, J. G., Sanislow, C. A., Grilo, C., et al. (2003). The representation of four personality disorders by the schedule for nonadaptive and adaptive personality dimensional model of personality. Psychological Assessment, 15, 326 – 332.

810

M.A. Bornovalova et al. / Clinical Psychology Review 25 (2005) 790–812

Moscicki, E. K. (1997). Identification of suicide risk factors using epidemiologic studies. Psychiatric Clinics of North America, 20, 499 – 517. Murphy, C. M., O’Farrell, T. J., Fals-Stewart, W., & Feehan, M. (2001). Correlates of intimate partner violence among male alcoholic patients. Journal of Consulting and Clinical Psychology, 69, 528 – 540. Nace, E. P. (1989). Personality disorder in the alcoholic patient. Psychiatric Annals, 19, 256 – 260. Nace, E. P., Saxon, J. J., & Shore, N. (1986). Borderline personality disorder and alcoholism treatment: A one-year follow-up study. Journal of Studies on Alcohol, 47, 196 – 200. New, A. S., Hazlett, E. A., Buchsbaum, M. S., Goodman, M., Reynolds, D., Mitropoulou, V., et al. (2002). Blunted prefrontal cortical FDG-PET response to meta-chlorophenylpiperazine in impulsive aggression. Archives of General Psychiatry, 59, 621 – 629. New, A. S., & Siever, L. J. (2002). Neurobiology and genetics of borderline personality disorder. Psychiatric Annals, 32, 329 – 336. Newman, J. P., Patterson, C. M., Howland, E. W., & Nichols, S. L. (1990). Passive avoidance in psychopaths: The effects of reward. Personality Individual Differences, 11, 1101 – 1114. Newman, J. P., Patterson, C. M., & Kosson, D. S. (1987). Response perseveration in psychopaths. Journal of Abnormal Psychology, 96, 145 – 148. O’Farrell, T. J., & Murphy, C. M. (1995). Marital violence before and after alcoholism treatment. Journal of Consulting and Clinical Psychology, 63, 256 – 262. Overtoom, C. C. E., Verbaten, M. N., Kemner, C., Kenemans, J. L., & van Engeland, H. (2003). Effects of methylphenidate, desipramine, and L-dopa on attention and inhibition in children with Attention Deficit Hyperactivity Disorder. Behavioural Brain Research, 145, 7 – 15. Pally, R. (2002). The neurobiology of borderline personality disorder: The synergy of bnature and nurtureQ. Journal of Psychiatric Practice, 8, 133 – 142. Paris, J., Zweig-Frank, H., Bond, M., & Guzder, J. (1996). Defense styles, hostility, and psychological risk factors in male patients with personality disorders. Journal of Nervous and Mental Disease, 184, 155 – 160. Paris, J., Zweig-Frank, H., Ng Ying Kin, N., Schwartz, G., Steiger, H., & Nair, N. (2004). Neurobiological correlates of diagnosis and underlying traits in patients with borderline personality disorder compared with normal controls. Psychiatry Research, 121, 239 – 252. Patton, J. H., Stanford, M. S., & Barratt, E. S. (1995). Factor structure of the Barratt Impulsiveness Scale. Journal of Clinical Psychology, 51, 768 – 774. Petry, N. (2000). Effects of increasing income on polydrug use: A comparison of heroin, cocaine and alcohol abusers. Addiction, 95, 705 – 717. Petry, N. M. (2001). Substance abuse, pathological gambling, and impulsivity. Drug and Alcohol Dependence, 63, 29 – 38. Petry, N. M. (2002). Discounting of delayed rewards in substance abusers: Relationship to antisocial personality disorder. Psychopharmacology, 162, 425 – 432. Rachlin, H., Raineri, A., & Cross, H. (1991). Subjective probability and delay. Journal of the Experimental Analysis of Behavior, 55, 233 – 244. Raine, A., Brennan, P., & Mednick, B. (1997). Interaction between birth complications and early maternal rejection in predisposing individuals to adult violence: Specificity to serious, early-onset violence. American Journal of Psychiatry, 154, 1265 – 1271. Raine, A., Buchsbaum, M. S., Stanley, J., Lottenberg, S., Abel, L., & Stoddard, J. (1994). Selective reductions in pre-frontal glucose metabolism in murderers. Biological Psychiatry, 36, 365 – 373. Richards, J. B., Mitchell, S., de Wit, H., & Seiden, L. (1997). Determination of discount functions in rats with an adjustingamount procedure. Journal of the Experimental Analysis of Behavior, 353 – 366. Rinne, T., de Kloet, E. R., & Wouters, L. (2002). Hyperresponsiveness of hypothalamic-pituitary-adrenal axis to combined dexamethasone/corticotropin-releasing hormone challenge in female borderline personality disorder subjects with a history of sustained childhood abuse. Biological Psychiatry, 52, 1102 – 1112. Rodriguez, M., Mischel, W., & Shoda, Y. (1989). Cognitive person variables in the delay of gratification of older children atrisk. Journal of Personality and Social Psychology, 57, 358 – 367. Ross, S., Dermatis, H., Levounis, P., & Galanter, M. (2003). A comparison between dually diagnosed inpatients with and without Axis II comorbidity and the relationship to treatment outcome. American Journal of Drug and Alcohol Abuse, 29, 263 – 279.

M.A. Bornovalova et al. / Clinical Psychology Review 25 (2005) 790–812

811

Rounsaville, B. J., Kranzler, H. R., Ball, S. A., Tennen, H., Poling, J., & Triffleman, E. (1998). Personality disorders in substance abusers: Relation to substance use. Journal of Nervous and Mental Disease, 186, 87 – 95. Rubia, K., Oosterlaan, J., Sergeant, J. A., et al. (1998). Inhibitory dysfunction in hyperactive boys. Behavioural Brain Research, 94, 25 – 32. Sansone, R. A., Gaither, G. A., & Songer, D. A. (2002). The relationships among childhood abuse, borderline personality and self-harm behavior in psychiatric inpatients. Violence and Victims, 17, 49 – 56. Shaffer, D., Gould, M. S., Fisher, P., et al. (1996). Psychiatric diagnosis in child and adolescent suicide. Archives of General Psychiatry, 53, 339 – 348. Siever, L. J., Buchsbaum, M. S., & New, A. S. (1999). d,1-fenfluramine response in impulsive personality disorder assessed with [18F]fluorodeoxyglucose positron emission tomography. Neuropsychopharmacology, 20, 413 – 423. Siever, L. J., & Davis, K. L. (1991). A psychobiological perspective on the personality disorders. American Journal of Psychiatry, 148, 1647 – 1658. Siever, L. J., Torgersen, S., Gunderson, J. G., Livesley, W. J., & Kendler, K. S. (2002). The borderline diagnosis III: Identifying endophenotypes for genetic studies. Biological Psychiatry, 51, 964 – 968. Simons, L., Ducette, J., Kirby, K. C., Stahler, G., & Shipley, T. E. (2003). Childhood Trauma, Avoidance Coping, and Alcohol and Other Drug Use Among Women in Residential and Outpatient Treatment Programs. Alcoholism Treatment Quarterly, 21, 37 – 54. Skinstad, A. J., Laberg, J. C., & Ellertsen, B. (1998). A chart review study of male alcoholics differentiated by personality disorders. Nordic Journal of Psychiatry, 52, 5 – 13. Skodol, A. E., Gunderson, J. G., Pfohl, B., Widiger, T. A., Livesley, W. J., & Siever, L. J. (2002). The borderline diagnosis I: Psychopathology, comorbidity, and personaltity structure. Biological Psychiatry, 51, 936 – 950. Skodol, A. E., Siever, L. J., & Livesley, W. J. (2002). The borderline diagnosis II: Biology, genetics, and clinical course. Biological Psychiatry, 51, 951 – 963. Slade, M., Daniel, L. J., & Heisler, C. J. (1991). Application of forensic toxicology to the problem of domestic violence. Forensic Science, 36, 708 – 713. Soloff, P. H., Kelly, T. M., Strotmeyer, S. J., Malone, K. M., & Mann, J. J. (2003). Impulsivity, gender and response to fenfluramine challenge in borderline personality disorder. Psychiatry Research, 119, 11 – 24. Soloff, P. H., Lis, J. A., Kelly, T., Cornelius, J., & Ulrich, R. (1994). Risk factors for suicidal behavior in borderline personality disorder. American Journal of Psychiatry, 151, 1316 – 1323. Soloff, P. H., Lynch, K. G., & Kelly, T. M. (2002). Childhood abuse as a risk factor for suicidal behavior in borderline personality disorder. Journal of Personality Disorders, 16(3), 201 – 214. Soloff, P. H., Lynch, K. G., & Moss, H. B. (2000). Serotonin, impulsivity, and alcohol use disorders in the older adolescent: A psychobiological study. Alcoholism, Clinical and Experimental Research, 24, 1609 – 1619. Stanford, M. S., Greve, K. W., Boudreaux, J. K., Mathias, C. W., & Brumbelow, J. L. (1996). Impulsiveness and risk-taking behaviour: Comparison of high-school and college students using the Barrett Impulsiveness Scale. Personality and Individual Differences, 21, 1073 – 1075. Stanford, M. S., Houston, R. J., Mathias, C. W., Villemarette-Pittman, N. R., Helfritz, L. E., & Conklin, S. M. (2003). Characterizing Aggressive Behavior. Assessment, 10, 183 – 190. Stein, D. J., Trestman, R. L., Mitropoulou, V., Coccaro, E. F., Hollander, E., & Siever, L. J. (1996). Impulsivity and serotonergic function in compulsive personality disorder. Journal of Neuropsychiatry and Clinical Neurosciences, 8, 393 – 398. Stuart, G. L., Moore, T. M., Ramsey, S. E., & Kahler, C. W. (2003). Relationship aggression and substance use among women court-referred to domestic violence intervention programs. Addictive Behaviors, 28, 1603 – 1610. Svrakic, D. M., Whitehead, C., Przybeck, T. R., & Cloninger, C. R. (1993). Differential diagnosis of personality disorders by the seven-factor model of temperament and character. Achieves of General Psychiatry, 50, 991 – 999. Taylor, S. (1967). Aggressive behavior and physiological arousal as a function of provocation and the tendency to inhibit aggression. Journal of Personality, 35, 297 – 310. Torgersen, S. (2000). Genetics of patients with borderline personality disorder. Psychiatric Clinics of North America, 23, 1 – 8. Trull, T. J. (1992). DSM-III-R personality disorders and the five-factor model of personality: An empirical comparison. Journal of Abnormal Psychology, 101, 553 – 560. Trull, T. J., Sher, K. J., Minks-Brown, C., Durbin, J., & Burr, R. (2000). Borderline personality disorder and substance use disorders: A review and integration. Clinical Psychology Review, 20, 235 – 253.

812

M.A. Bornovalova et al. / Clinical Psychology Review 25 (2005) 790–812

Trull, T. J., Useda, J. D., Conforti, K., & Doan, B. T. (1997). Borderline personality disorderfeatures in nonclinical young adults: 2-year outcome. Journal of Abnormal Psychology, 106, 307 – 314. Trull, T. J., Waudby, C. J., & Sher, K. J. (2004). Alcohol, tobacco, and drug use disorders and personality disorder symptoms. Experimental and Clinical Psychopharmacology, 12, 65 – 75. Tyler, K. A. (2002). Social and emotional outcomes of childhood sexual abuse: A review of recent research. Aggression and Violent Behavior, 7, 567 – 589. Tyler, K. A., Whitbeck, L. B., Hoyt, D. R., & Johnson, K. D. (2003). Self-mutilation and homeless youth: The role of family abuse, street experiences, and mental disorders. Journal of Research on Adolescence, 13, 457 – 474. Van Den Bosch, L. M. C., Verheul, R., Schippers, G. M., & Van Den Brink, W. (2002). Dialectical behavior therapy of borderline patients with and without substance use problems: Implementation and long-term effects. Addictive Behaviors, 27, 911 – 923. Van Reekum, R., Links, P. S., & Fedorov, C. (1994). Impulsitivity in borderline personality disorder. In K. Silk (Ed.), Biological and neurobehavioral studies of borderline personality disorder. Washington, DC7 American Psychiatric Press, Inc. Van Reekum, R., Links, P. S., Mitton, M. J., Fedrov, C., & Patrick, J. (1996). Impulsitivity, defensive funcitoning, and borderline personality disorder. Canadian Journal of Psychiatry, 41, 81 – 84. Vo¨llum, B., Richarson, P., & Stirling, J. (2004). Neurobiological substrates of antisocial and borderline personality disorder: Preliminary results of a functional fMRI study. Criminal Behaviour and Mental Health, 14, 39 – 54. Votta, E., & Manion, I. (2004). Suicide, high-risk behaviors, and coping style in homeless adolescent males’ adjustment. Journal of Adolescent Health, 34, 237 – 243. Wagner, A. W., & Linehan, M. M. (1999). Recognition of facial expressions of emotion ability among women with borderline personality disorder. Journal of Personality Disorders, 13, 329 – 344. Wagner, E. F. (1993). Delay of gratification, coping with stress, and substance use in adolescence. Experimental and Clinical Psychopharmacology, 1, 27 – 43. Wall, A., Wekerle, C., & Bissonnette, M. (2000). Childhood maltreatment, parental acoholism, and beliefs about alcohol: Subgroup variation among alcohol-dependent adults. Alcoholism Treatment Quarterly, 18, 49 – 60. Weiss, R. D., Mirin, S. M., Griffin, M. L., Gunderson, J. G., & Hufford, C. (1993). Personality disorders in cocaine dependence. Comprehensive Psychiatry, 34, 145 – 149. Whitbeck, L. B., Hoyt, Danny, R., & Ackley, K. A. (1997). Abusive family backgrounds and later victimization among runaway and homeless adolescents. Journal of Research on Adolescence, 7, 375 – 392. White, J. L., Moffitt, T. E., Caspi, A., Bartusch, D. J., Needles, D. J., & Stouthamer-Loeber, M. (1994). Measuring impulsivity and examining its relationship to delinquency. Journal of Abnormal Psychology, 103, 192 – 205. Whiteside, S. P., & Lynam, D. R. (2001). The Five Factor Model and impulsivity: Using a structural model of personality to understand impulsivity. Personality and Individual Differences, 30, 669 – 689. Winstanley, C. A., Dalley, J. W., Theobald, D. E. H., & Robins, T. W. (2004). Fractionating impulsivity: Contrasting effects of central 5-HT depletion on different measures of impulsive behaviour. Neuropsychopharmacology, 29, 1331 – 1343. Wonderlich, S. A., Swift, W. J., Slomik, H. B., & Goodman, S. (1990). DSM-III-R personality disorders in eating-disorder subtypes. International Journal of Eating Disorders, 9, 607 – 616. Yates, T. M. (2004). The developmental psychopathology of self-injurious behavior: Compensatory regulation in posttraumatic adaptation. Clinical Psychology Review, 24, 35 – 74. Zanarini, M. C., Frankenburg, F. R., Dubo, E. D., Sickel, A. E., Trikha, A., Levin, A., et al. (1998). Axis II comorbidity of borderline personality disorder. Comprehensive Psychiatry, 39, 296 – 302. Zanarini, M., Frankenburg, F., Hennen, J., & Silk, K. (2003). The longitudinal course of borderline psychopathology: 6-year prospective follow-up of the phenomenology of borderline personality disorder. American Journal of Psychiatry, 160, 274 – 283.