Mania and Depression have been recognized as independent entities for thousands of years. More recently, about 2 millennia ago, a link was described where melancholia (disabling depression) might be a from of mania. At this point we know that there is a heritable condition that is described as “bipolar spectrum disorder”. In 2008, Edvardsen found a “The ‘Bipolar Spectrum’ category consisting of Bipolar I disorder, Bipolar II disorder and Cyclothymia constitute one entity with high heritability without detectable shared family environmental effects. Future genetic and clinical work might consider that all variants of the bipolar spectrum are an expression of one underlying genetic liability.“
This is a real disease – it is not a style of behavior or simply a consequence of being exposed to erratic behavior during the developmental years.
We have numerous objective brain tests that show abnormalities of brain structure and brain function, and also have important evidence for cognitive dysfunction in people with bipolar spectrum disorder even when they are enjoying a period of remission from active mood disorder.
In 2007, Huxley reported that “As few as 1/3 of BPD (bipolar spectrum disorder) patients achieve full social and occupational functional recovery to their own premorbid levels.”
Some of this ongoing disability is related to ongoing emotional symptoms (mood swings & emotional lability), some is related to cognitive dysfunction (executive function, impulse control, and distractibility). Mason recently reported that in regard to risk taking “The bipolar disorder group showed the opposite pattern with preferential response to risky rewards.
In 2010 Berk taught us that “treating inflammation may be the best way to avoid progressive shortening of the inter-episode interval with each recurrence, {and perhaps related to} reduced probability of treatment response as the illness progresses. To this end, emerging data shows that these biomarkers may differ between early and late stages of BD in parallel with stage-related structural and neurocognitive alterations. This understanding facilitates identification of rational therapeutic targets, and the development of novel treatment classes. Additionally, these pathways provide a cogent explanation for the efficacy of seemingly diverse therapies used in BD, that appear to share common effects on oxidative, inflammatory and neurotrophic pathways.” Of note, all of the anti-manic medications have anti-inflammatory effects.
