Across the past decade there has been a rather dramatic increase in interest in Bipolar II Disorder. Once viewed as a relatively minor and unreliably diagnosed variant of the ‘real’ illness, BP II and other depressions grouped within the so-called ‘softer’ end of the bipolar spectrum are now considered by some experts as the more prevalent forms of manic depressive illness (see, for example, Angst and Cassano, 2005). Not only is BP II much more common than previously appreciated, there is good evidence that the depressive episodes – which can consume one half of an afflicted adult's lifetime (Judd et al., 2003) – can have devastating effects on psychosocial vocational functioning that at least match those of the ‘major’ form of the illness (Judd et al., 2005). Such findings underscore the more pernicious and protracted nature of the depressive episodes of bipolar disorder, as well as the need for better antidepressant therapies for people who experience hypomanic episodes.

As people with BP II almost never seek treatment for the hypomanic episodes, clinicians often do not make the diagnosis of BP II until after the patient has received some sort of antidepressant therapy for some duration. Once the diagnosis is made, he or she must answer only one fundamental question when fashioning a treatment: ‘Is the risk of a treatment-emergent affective switch (TEAS) sufficiently high to warrant the use of a mood stabiliser?