Highlighting Bipolar II Disorder

Until recently, epidemiologic studies put the lifetime risk of manic-depressive illness, or bipolar disorder (BD), at 1 % to 2%. Now many clinicians are observing a considerable increase in bipolar II disorder (BD II), though in the absence of any concomitant increase in bipolar I disorder (BD I) referrals. If such observations are valid, how can they be explained? In this section several key issues are pursued (1,2). First, has there been a true increase in BD II, or has detection merely improved? second, considering the lengthy delays between onset and diagnosis of BD II, what strategies might further improve detection? Third, how should BDI and BDII be best modelled and distinguished-along a continuum or as distinct entities? Fourth, what neurobiological processes underpin BDII, and do they differ from those underpinning BD I? Fifth, might the management of BD II require different strategies than the current armamentarium used for managing BD I, whether these disorders differ dimensionally or categorically? As clinical observation is clearly open to numerous biases, is there more formalized evidence indicating that BD may be increasing? If this is a true phenomenon, an increased incidence in community studies would be anticipated over time; There is evidence for such an increase, at least in the overall bipolar class. When we compare the lifetime rate of mania in the 1984 Epidemiological Catchment Area (ECA) Community Study (3) and in the 1994 National Comorbidity Survey (4), respective rates (that is, 0.9% and 1.6%) suggest a doubling over the decade. Additionally, if BD is increasing, we would expect a cohort effect (for example, higher rates in younger people). Turning again to ECA data, we find that the rates for those aged 18 to 24 years were 1.3%, compared with 1.6% for those aged 25 to 44 years, 0.4% for those aged 45 to 64 years, and 0.1% for those aged 65 years or over. Such data support but do not prove a change in prevalence. Alternatively, changed rates might simply reflect changes in diagnostic approaches. As detailed by Hadjipavlou and colleagues (2), the application of and diagnostic criteria in a Zurich study is illuminating (5). In that cohort, the rates for BDI were 0.5% and 0.5% for hard and soft diagnostic assignment, respectively, and were identical to the DSM-IV decision rule-assigned rate. For BDII, the prevalence rate was 5.3% for diagnostic assessment and 11.9% for diagnostic assignment, with both well exceeding the DSM-IV rate of 1.6%. Study results indicate that the impact of differing assessment methods is more likely to apply to BD II than to BD I and that DSM-IV rates tend to be lower than cliniciandriven rates. Such differences are likely to be distinctly influenced by the DSM-IV requirement that a hypomanic state last at least 4 days. Other artefactual determinants of higher prevalence estimates include a widening of the definition of BD. The old diagnostic label of manic-depressive psychosis was rarely applied and is logically inappropriate in instances of milder bipolar states. As we are now seeing a broader subsection of the population, the rates of those with BD II may not necessarily correspond with those coming to clinical attention before and after mood disorder destigmatization. Again, redefinition or reconceptualization of certain diagnostic categories (for example, cyclothymia) has effectively broadened the spectrum of BDs. If there has been a real increase in BD II, a wide set of possible determinants invite speculation. Genetic changes would need to be considered. Environmental influences include increased use of illicit stimulant drugs and even increased use of prescribed antidepressants, because of their suggested capacity to cause switching. Another environmental candidate intriguing our research team is an omega-3 fatty acid (O3FA) contribution with several indirect lines of evidence. Several studies have shown striking associations (with correlations exceeding 0. …

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