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Mania Symptoms of and Symptoms


The genetic contribution to mania is strong, underscoring the need to consider biological factors. Mania appears to fit nicely into the theoretical framework that employs appetitive and aversive motivational systems, as seen in Depue’s attempt to specify a biological substrate for mania within a neurobehavioral framework. With respect to motivational systems, the symptoms of mania suggest that appetitive motivation is activated noncontingently, unrestrained by the BIS. These symptoms include an elevated, expansive mood, an increase in motor activity, engaging in activities with a high potential for painful consequences that is not recognized, and inflated selfesteem and overconfidence. The manic strongly seeks rewards (i.e., behavioral activation) in an unrestrained manner, confidently expects to achieve them due to insensitivity to the risks of punishment and frustrative nonreward, and enjoys a positive mood and high self-esteem in anticipation of attaining those rewards. Activation of the BAS in Gray’s model should produce this covariation of behavioral activation, reward-seeking behavior, and positive mood. The breakdown of restraint of the BAS by the BIS would result in lack of awareness of potential risks and a minimal impact of actual failures.

The strength of the activation of the BAS seen in mania suggests that the primary problem is excessive activation of the BAS, as opposed to simple lack of restraint by the BIS, but it is difficult to be certain. This author has suggested elsewhere that the irritability that arises when the manic is thwarted could represent a response to frustration that violates social norms as a result of the lack of control by the BIS. Depue and his colleagues proposed a neurobiological theory of bipolar affective disorder that bears many similarities to the perspective adopted here. Also consistent with the theme of this chapter, Depue and Iacono emphasize the importance of placing neurobiological hypotheses within a neurobehavioral framework that allows relating neurochemical deficits to the behaviors critical for diagnosis. At the level of a behavioral theory, the behavioral facilitation system (BFS) described by these authors is strikingly similar to the BAS. The BFS facilitates behavior via activation of locomotor activity and reward-incentive motivation, just as the BAS does. Similarly, Depue and Iacono conclude that the mesolimbic DA system is critically involved in the BFS, especially the projections of the A10 DA cell group in the ventral tegmental area to the nucleus accumbens (mesolimbic DA pathway) and the prefrontal cortex (mesocortical DA pathway). Depue describe mania as exhibiting high levels of the multiple manifestations of activity in the BFS: high motor activity (hyperactivity, rapid and pressured speech, and expressive facies), high incentive reward activation (excessive interest and pleasure, desire for excitement), a positive mood (elation, euphoria), high nonspecific arousal (manifested in changes in appetite, energy level, need for sleep, thought, attention, and sensory vividness), and cognitive changes (increased optimism and feelings of self-worth). Bipolar depression represents the opposite of mania, an absence of activity in the BFS (e.g., retardation—an absence of motor activity, anhedonia—no interest or pleasure, etc.). Depue et al. propose that the fundamental deficit in bipolar disorder is a failure to regulate the BFS (trait variability), which is different from the trait level of the strength of the BFS. Individual differences in the strength of the BFS (trait level) will affect the severity of manic episodes when regulation fails. A strong unregulated BFS will more often reach clinical severity for mania, and the manic component will be prominent. In contrast, a weak unregulated BFS is much less likely to result in a clear manic syndrome—producing a clinical picture of unipolar depression, even though the underlying etiology is the same as for bipolar disorder. This model is one of the few that can account for the appearance of unipolar depression among the relatives of bipolar probands, as is found in the genetics literature. This account explains the partial effectiveness of the traditional antipsychotic medications in treating mania because these drugs block dopaminergic activity in the mesolimbic and mesocortical pathways. In this theory, the drugs would not address the problem of dysregulation, but they would weaken the BAS and thereby reduce manic behavior. To summarize, Depue’s theory of the etiology of bipolar disorder invokes an appetitive motivational system almost identical to the BAS. A failure of regulation of this system is the primary etiological factor that allows it to swing from excessive activation in mania and an absence of activation in bipolar depression (and some unipolar depressions).

Implicating the mesolimbic and mesocortical dopamine pathways as central to this motivational system parallels Wise’s concept of psychomotor activation in response to reward in ubstance abuse, as well as Gray’s own suggestion for the BAS. Thus, the role of dopamine pathways for this appetitive motivational system is strongly documented. The dopamine projections from the ventral tegmental area to the nucleus accumbens are cited by all authors, whereas those to the prefrontal cortex are not always mentioned.

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