Another system that has been considered as a possible site of pathology in bipolar disorder is the behavioural activation system (BAS). The concept of the BAS was derived from investigations of the motivational effects of appetitive and aversive stimuli upon the behaviour of animals (Gray, 1982). The BAS governs approach behaviour, such that it is activated by, and seeks to bring the animal into contact with, conditioned and unconditioned positive incentive stimuli (Gray, 1990). Exposure to reward elicits behavioural patterns associated with BAS activity, such as approach, exploration and engagement, as well as activating underlying processes governed by the BAS. The latter includes incentive-reward motivation and the emotional states of desire and curiosity. Cognitive activity will also be affected, as increased interaction with the environment will produce the need for increased evaluation.
Depue and colleagues (Depue et al., 1987; Goplerud & Depue, 1985) have suggested that in bipolar-spectrum disorders the BAS is poorly regulated, such that the limits that define the extent of BAS variation are weak in these individuals. They note the correspondence between the features that characterise high levels of BAS activity (for example, high non-specific arousal, positive emotion, and engagement in goal-directed activity), and the symptoms of a hypomanic state, as well as observing that disengagement from reward-seeking activities, anhedonia and psychomotor retardation often characterise bipolar depression. In a study of the effects of naturally occurring stress on BAS level, Goplerud and Depue (1985) found that, after a stressful event, cyclothymic individuals took longer than did normal controls to return to baseline levels of BAS functioning. This suggests that in bipolar spectrum disorders, BAS dysregulation may exist not in terms of the initial appearance of a mood state, but in the inability of the system to return the mood state to its set point.
However, the development of a bipolar episode from a prolonged period of abnormal BAS level would seem to rely upon more than delayed achievement of homeostasis. One possibility is that associated changes in cognition may act to excite or depress the system further. Meyer et al. (2001) have investigated the link between BAS functioning and symptom onset: using a scale designed to measure the extent to which the BAS becomes activated after exposure to reward or potential reward (the Reward Responsiveness Scale of the BIS/BAS sensitivity scale) (Carver & White, 1994), they found that responsivity to reward not only correlates with levels of manic symptoms, but is also predictive of increases in manic symptoms, even when baseline levels of manic symptoms are controlled for.
Thus, while elevated BAS levels are a normal part of reaction to reward, it is possible that bipolar individuals show oversensitivity to rewarding events once in this state. There is some evidence of increased expectation of reward in bipolar-spectrum individuals following initial success: Stern and Berrenberg (1979) found that, after success feedback, individuals with a history of hypomanic symptoms were more likely to expect success on future laboratory tasks than were control participants, a difference that was not apparent when feedback was less positive. Such a tendency to focus upon—and overestimate—potential for reward in the environment constitutes a cognitive bias that may promote further-reward seeking behaviour, thus exciting the system further. Figure 12.2 illustrates the BAS model in the case of mood and BAS elevation.
With regard to the relationship between BAS dysregulation and bipolar depression, Depue and colleagues have proposed that bipolar depression represents extreme underactivity of the BAS, and there is some biological evidence to support this view. Several studies have found a relative decrease in left-frontal cortical activity in currently depressed individuals as compared with a non-depressed sample, and in previously depressed as compared with never depressed individuals (Allen et al., 1993; Henriques & Davidson, 1990; 1991), and relative level of activity in this area has been found to correlate positively with BAS sensitivity to reward as measured by Carver and White's (1994) scale (Harmon-Jones & Allen, 1997).
In keeping with the above approach, it could be postulated that at low levels of BAS activity, the BAS is abnormally sensitive to frustrative non-reward in bipolar individuals, such that it is easily subdued by failure to attain reward. A similar suggestion has been made
by Strauman (1999), and Carver and Scheier (1998), who postulate that depression results from a failure to attain approach goals. A need for further work investigating the relationship between frustrative non-reward, BAS level and symptoms of depression is indicated. Figure 12.3 illustrates the BAS model in the case of a decrease in mood and BAS activity.
In summary, the BAS model proposes that weak regulatory mechanisms within a biological system constitute the biological vulnerability in bipolar disorder, and that associated
changes in cognition—specifically, changes in the processing of signals of reward—act to maintain this dysregulation by channelling behaviour towards or away from further reward. Figure 12.2 illustrates this model in the case of mood and BAS elevation, while Figure 12.3 depicts this cycle in the case of a decrease in mood and in BAS activity.
It should be noted that increased BAS level in this model may be triggered not only by the occurrence of a rewarding event but also by the opportunity for reward or success. Such an opportunity may arise from apparently negative circumstances depending upon the particular values and goals of the individual: for example, the end of a romantic relationship may be perceived as an opportunity to pursue relationship or career prospects that were previously not possible. Stressful events may also affect daily rhythms such as sleep-wake patterns: as mentioned previously, disruption of this kind has been linked to the onset of mood disturbance. This disruption may provide a separate path by which stressful negative events could trigger mania or depression, augmenting the direct effect of the event on the BAS system.
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