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Impulsive behaviors play an important role in both bipolar and substance abuse disorders. However, results of studies investigating this link are often ambiguous, in part, due to the multidimensional nature of the impulsivity construct and the fact that many studies use a single measurement technique. We describe a model of impulsivity characterized by three components: response initiation, response inhibition and consequence sensitivity. How these components differ from one another in terms of their use, behavioral theory and biological function is discussed, along with measurement techniques.
Impulsivity is a prominent characteristic of both bipolar disorder (BD) (Swann et al., 2003, 2001) and substance abuse disorder (SA) (Moeller and Dougherty, 2002). Furthermore, the comorbidity of BD with SA is a well-documented pattern of psychiatric presentation (e.g., Krishnan, 2005). The strength of this association has been attributed to common underlying biobehavioral processes of impulsivity in BD and SA (Dougherty et al., 2004; Swann et al., 2004). However, each of these psychiatric conditions may also involve separate aspects of impulsivity (Moeller et al., 2001), which underscores the necessity for assessment of multiple characteristics of both trait-dependent and state-dependent impulsive behavior to truly appreciate the contribution of impulsivity to BD and SA (Dougherty et al., 2003b).
Impulsivity Across Bipolar Phase and Substance Abuse
An excellent example of the importance of considering the type of impulsivity assessment within psychiatric disorders is Swann and colleagues' (2004) report on the use of both self-report and laboratory behavioral measures of impulsivity in individuals with comorbid and independent diagnoses of BD and SA compared to controls. The Barratt Impulsiveness Scale (BIS) (Patton et al., 1995) was the self-report measure of trait-dependent aspects of impulsivity, while the Immediate and Delayed Memory Task (IMT/DMT) (Dougherty et al., 2002) was the behavioral measures of state-dependent aspects of impulsivity. The patients with BD were classified into one of four groups based on phase of their BD (manic or euthymic) and presence or absence of SA history (SA+ or SA-) (Swann et al., 2004). These patients were compared to two additional groups recruited from the community: adults with and without a history of SA (SA-only and controls). The result was a comparison of trait-dependent and state-dependent impulsivity between six groups: manic/SA+, manic/SA-, euthymic/SA+, euthymic/SA-, SA-only and controls.
Trait-dependent impulsivity (BIS total scores). While global impulsive behavior of people with euthymic and manic BD has shown essentially identical elevations of trait-dependent impulsivity compared to controls (Swann et al., 2003), the study being examined here compares trait-dependent impulsivity in euthymic patients with and without SA to impulsivity in SA-only individuals and controls (Swann et al., 2004) (Figure 1, left). Levels of trait-dependent impulsive behaviors reported by individuals in the euthymic/SA- and SA-only groups were essentially identical; however, comorbidity of these two disorders (euthymic/SA+) appeared to have an additive effect on trait-dependent impulsive behavior. Collectively, this indicates that elevated trait-dependent impulsivity is dependent on both SA and BD regardless of the phase of illness.
State-dependent impulsivity (IMT). Alternatively, the profile for state-dependent impulsivity provides a different assessment of these groups (Swann et al., 2004) (Figure 1, right). Comparing people with euthymic BD with and without SA to SA-only and controls showed that state-dependent impulsive performance of the euthymic-only patients (euthymic/SA-) presented a profile similar to the controls, while individuals with comorbid euthymic phase BD and SA (euthymic/SA+) presented a profile of performance similar to SA-only. This indicates that elevated state-dependent impulsive behavior is dependent on SA during the euthymic phase of BD. A more detailed examination illustrates that while differentiation of state-dependent impulsivity in the euthymic phase is dependent on comorbidity with SA, the manic phase of BD produces elevated state-dependent impulsive behavior regardless of SA comorbidity (Figure 2). Therefore, elevated state-dependent impulsive behavior is also dependent on the phase of the BD.
These examples demonstrate how measurements using different modes of impulsivity assessment lead to different profiles of impulsive behavior (Swann et al., 2004). The trait-dependent measure showed that euthymic and manic BD, as well as SA impulsivity profiles, are different from controls but not from each other. This trait-dependent assessment also showed that the impulsivity profile is dependent on the comorbidity of these disorders in the euthymic phase. Conversely, the state-dependent measure clearly showed that current impulsive tendencies were dependent both on SA history and BD phase of illness.
These comparisons demonstrate that trait-dependent measures provide a different profile of impulsivity than state-dependent measures in BD and SA and research employing concurrent use of more than one type of impulsivity measure can lead to a more thorough characterization of underlying behavioral mechanisms. Continued and more detailed efforts are needed to provide a more comprehensive view of how various aspects of impulsivity interact within BD and SA and in impulse control disorders in general.
Behavioral Impulsivity and Modes of Measurement
Previous research and theory has conceptualized impulsivity as a multifaceted construct requiring multiple modes of measurement for accurate assessment (Barratt and Patton, 1983; Dougherty et al., 2003b). One definition that takes this complexity into account defines impulsive behavior as "a predisposition toward rapid, unplanned reactions to internal or external stimuli without regard to the negative consequences of these reactions to the impulsive individual or to others" (Moeller et al., 2001). This definition can be dissected to yield core components of impulsive behavior that provide a framework for research examining impulsive behaviors.
The definition of impulsivity described above can be conceptualized as having three primary component processes that influence the stimulus-response relationship (Figure 3). The first part of the impulsivity definition--"rapid, unplanned reactions to ... stimuli"--corresponds to the core component processes of response initiation, where impulsive behavior can be defined as responding that occurs prior to complete processing and evaluation of a stimulus and response inhibition, where impulsive behavior can be defined as a failure to inhibit an already initiated response. The second part of this definition--"reactions ... without regard to the negative consequences"--corresponds to the component process related to consequence sensitivity, where impulsivity is defined as responses that persist despite negative or less than optimal consequences (e.g., punishment or smaller reward). This three-component model provides a framework for better characterization of the underlying mechanisms of impulsive behavior, because while the impulsivity observed in different individuals may be expressed as similar behaviors, the underlying processes that determine these behaviors may be very different.
This theoretical distinction between these component processes of impulsivity is supported by both behavioral theory and biological function. For example, both Gray (1987, 1982) and Logan (1994) proposed models of behavior that contrast opposing forces of response initiation and inhibition. Further, neuroimaging studies have shown activation of separate neuroanatomical regions. During response initiation tasks, brain activation occurs in the middle frontal cortex and the inferior parietal cortex (Garavan et al., 1999). During response inhibition tasks, brain activation occurs in the right medial and mesial frontal cortex, as well as in the left caudate nucleus (Rubia et al., 2001). During consequence sensitivity (reward) tasks, brain activation occurs in the orbitofrontal cortex, as well as in the striatum (Rogers et al., 2004). The neurological differentiation of these three component processes illustrates how use of this model may lead to identification of underlying biological mechanisms involved in the etiology and treatment of different impulse control disorders.
This component model of impulsive behavior would be useful for capturing differences in impulsive behavior related to distinct underlying mechanisms, despite the evident similarity of the impulsive behaviors observed across impulse control disorders. For instance, simultaneous testing of the components of this model could yield important information about the underlying biobehavioral mechanisms of impulsivity expressed during the manic phase of BD. Perhaps, although these individuals may appreciate the negative consequences resulting from their impulsive behaviors, the drive to emit those behaviors (response initiation) overwhelms their capacity to inhibit responses. Conversely, the capacity to inhibit their impulsive behaviors (response inhibition) may be diminished such that the drive to emit these behaviors cannot be circumvented. Similarly, initiation and maintenance of SA behaviors may be the result of a bias for seeking appetitive stimuli regardless of the cost (insensitivity to consequences), which then overrides the inhibitory capacity (Moeller et al., 2001).
Previous research has shown that both adolescents with disruptive behavior disorders and their parents demonstrate a unique profile of behavioral responding across these three components compared to controls. In a single study comparing the three components of impulsivity, response initiation and response inhibition paradigms were more sensitive to elevated impulsive performance than consequence sensitivity paradigms in adolescents with disruptive behavior disorders compared to matched controls (Dougherty et al., 2003a). In another study, parents of adolescents with disruptive behavior disorders showed elevated trait-dependent impulsivity and laboratory impulsive responding during a response initiation paradigm compared to controls, but performance during a consequence sensitivity paradigm was not different between the groups (Swann et al., 2002). In that same study, the presence of an Axis I or Axis II psychiatric disorder was also related to trait-dependent impulsivity and laboratory response initiation, while consequence sensitivity was not.
Pharmacological manipulations also differentially influence performance across these different aspects of impulsivity. For example, alcohol consumption increased impulsive performance on a response initiation task (Dougherty et al., 2000), but reduced impulsive performance on a consequence sensitivity task (Ortner et al., 2003). Because of these differences, it is important to study how each of these processes contribute to impulsive behavior in a proposed sample. It is evident that documenting global trait-dependent impulsivity alone is insufficient and that accounting for the specific component processes of impulsivity will be necessary to explain underlying mechanisms of BD and SA. The three components of impulsivity discussed above are quantifiable using established laboratory behavioral measures.
Response initiation. Continuous performance tests (CPT) (Rosvold et al., 1956) have been used as measures of response initiation. The CPT requires participants to respond selectively to a series of rapidly presented stimuli (e.g., letters, numbers or abstract shapes; usually presentations and delays of
Response inhibition. Stop-signal tasks have been used extensively as measures of response inhibition, but mostly with young children (see Oosterlaan et al., 1998). In this task, participants are instructed to respond quickly to target stimuli when a "go" signal is presented, but to withhold responding when the "go" signal is unpredictably accompanied by a "stop" signal (e.g., auditory beep) (Logan, 1994). Impulsivity is defined as a failure to inhibit responding to an already initiated response and reflects response inhibition aspects of impulsivity.
Consequence sensitivity. Paradigms that measure consequence sensitivity originate within a vast body of literature describing operant behavior in animals (e.g., Ainslie, 1975) and humans (Rachlin, 2000). One of the most popular uses of insensitivity to consequences is defining impulsivity as making choices that are less than optimal and result in obtaining less than the maximum amount of reinforcement available. In this operant procedure, participants are typically given a choice between a smaller-sooner and a larger-later reinforcer. A disproportionate number of choices for the smaller-sooner reinforcer is considered impulsive because it results in consequences that are less than optimal.
Impulsivity is defined both by trait-dependent and state-dependent thoughts and behaviors. Our discussion has emphasized the importance of both impulsive traits and states as components to be studied across psychiatric disorders. To date, however, impulsive traits have been the principal focus of research. To more fully account for variance associated with impulsivity, a combination of indices is essential when attempting to understand impulsive behaviors (Carrillo de la Pena et al., 1993; Dougherty et al., 2003b). Multiple trait-dependent and state-dependent assessment tools are needed to more fully address questions about the role of impulsivity in BD and SA. Simultaneous assessment of multiple components of impulsivity provides direct benefits for future directions in psychiatric research, including prospective studies measuring onset of SA with BD and subsequent effects on core components of impulsivity, predicting treatment response with performance on different impulsivity measures, and development of individualized treatments for comorbid BD with SA, based on measures of impulsivity components. Measures from each of the core components of impulsivity (response initiation, response inhibition and consequence sensitivity) can ultimately provide convergent or divergent evidence that may supply important information as to the underlying mechanisms of these disorders.
This research was sponsored by grants from the National Institutes of Health (R01-MH065566 and R01-DA008425).
Dr. Dougherty is professor and vice chair of research for the department of psychiatry and behavioral medicine at Wake Forest University Health Sciences. Dr. Dougherty is a leading expert on the assessment of impulsivity and has developed several procedures for the assessment of state-dependent aspects of impulsivity.
Dr. Marsh is a research associate for the department of psychiatry and behavioral medicine at Wake Forest University Health Sciences. Dr. Marsh has been integral to the validation of recent measures of impulsivity assessment and particularly their relationship to biological measures.
Dr. Mathias is assistant professor for the department of psychiatry and behavioral medicine at Wake Forest University Health Sciences. Dr. Mathias has been integral to the validation of recent measures of impulsivity assessment and particularly their relationship to psychophysiological measures.
Dr. Swann is professor and vice chair of research for the department of psychiatry and behavioral sciences at the University of Texas Health Science Center at Houston. Dr. Swann is a psychiatrist specializing in bipolar disorder and has research expertise on treatment of impulsivity in psychiatric patients.
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