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Fig. 1 | International Journal of Bipolar Disorders

Fig. 1

From: The existential crisis of bipolar II disorder

Fig. 1

ACE Model of mania. This schematic shows how manic drive, perhaps through differential action on different symptomatic domains can create a seemingly separate phenotype when in fact the difference in manifestation is largely because of the inherent properties of different neurocognitive schema and neural systems within the brain. In florid mania, manic drive (shown in yellow) is so extreme that irrespective of the inherent rigidity of various domains, they are all extended (akin to elastic bands) to the same extent. And so, activity, cognition and emotion are all impacted equally and symptoms from each of these domains are evident. However, when manic drive is more modest, those domains that are inherently more pliant are impacted first and hence why there is separation between emotion, cognition and activity. Emotion, by its very nature is more malleable and variable, whereas cognition succumbs more slowly, and activity is the most hard-wired and therefore requires significant manic drive before it is impacted. The figure also shows that lesser degrees of variation and more subtle changes lead to a more mixed presentation in which features of both mania and depression exist alongside each other, by virtue of belonging to independent domains (ACE). This schematic then explains how ‘bipolar II’ and other putative subtypes could perhaps be created and yet have the same underlying mechanisms and therefore, in essence, remain the same illness

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