Bipolar II disorder
Bipolar II disorder (BP-II) is a mood disorder on the bipolar spectrum, characterized by at least one episode of hypomania and at least one episode of major depression.[1][2][3][4] Diagnosis for BP-II requires that the individual must never have experienced a full manic episode.[5] Otherwise, one manic episode meets the criteria for bipolar I disorder (BP-I).[2]
"BP-II" redirects here. For other uses, see BP2.Bipolar II disorder
BP-II, type two bipolar, bipolar type two
- Medication
- psychotherapy
Hypomania is a sustained state of elevated or irritable mood that is less severe than mania yet may still significantly affect the quality of life and result in permanent consequences including reckless spending, damaged relationships and poor judgment.[6]: 1651 Unlike mania, hypomania cannot include psychosis.[1][7] The hypomanic episodes associated with BP-II must last for at least four days.[2][8]
Commonly, depressive episodes are more frequent and more intense than hypomanic episodes.[2] Additionally, when compared to BP-I, type II presents more frequent depressive episodes and shorter intervals of well-being.[1][2] The course of BP-II is more chronic and consists of more frequent cycling than the course of BP-I.[1][9] Finally, BP-II is associated with a greater risk of suicidal thoughts and behaviors than BP-I or unipolar depression.[1][9] BP-II is no less severe than BP-I, and types I and II present equally severe burdens.[1][10]
BP-II is notoriously difficult to diagnose. Patients usually seek help when they are in a depressed state, or when their hypomanic symptoms manifest themselves in unwanted effects, such as high levels of anxiety, or the seeming inability to focus on tasks. Because many of the symptoms of hypomania are often mistaken for high-functioning behavior or simply attributed to personality, patients are typically not aware of their hypomanic symptoms. In addition, many people with BP-II have periods of normal affect. As a result, when patients seek help, they are very often unable to provide their doctor with all the information needed for an accurate assessment; these individuals are often misdiagnosed with unipolar depression.[1][2][9] BP-II is more common than BP-I, while BP-II and major depressive disorder have about the same rate of diagnosis.[11] Of all individuals initially diagnosed with major depressive disorder, between 40% and 50% will later be diagnosed with either BP-I or BP-II.[1] Substance use disorders (which have high co-morbidity with BP-II) and periods of mixed depression may also make it more difficult to accurately identify BP-II.[2] Despite the difficulties, it is important that BP-II individuals be correctly assessed so that they can receive the proper treatment.[2] Antidepressant use, in the absence of mood stabilizers, is correlated with worsening BP-II symptoms.[1]
Causes[edit]
Multiple factors contribute to the development of bipolar spectrum disorders,[12] although there have been very few studies conducted to examine the possible causes of BP-II specifically.[13] While no identifiable single dysfunctions in specific neurotransmitters have been found, preliminary data has shown that calcium signal transmission, the glutamatergic system, and hormonal regulation play a role in the pathophysiology of the disease.[14] The cause of Bipolar disorder can be attributed to misfiring neurotransmitters that overstimulate the amygdala, which in turn causes the prefrontal cortex to stop working properly. The bipolar patient becomes overwhelmed with emotional stimulation with no way of understanding it, which can trigger mania and exacerbate the effects of depression.[15]
Epidemiology[edit]
The global estimated lifetime prevalence of bipolar disorder among adults range from 1 to 3 percent.[62] The annual incidence is estimated to vary from 0.3 to 1.2 percent worldwide.[23] According to the World Mental Health Survey Initiative, the lifetime prevalence of BP-II was found to be 0.4%, with a 12-month prevalence of 0.3%.[63] Other meta-analyses have found lifetime prevalence of BP-II up to 1.57%.[64] In the United States, the estimated lifetime prevalence of BP-II was found to be 1.1%, with a 12-month prevalence of 0.8%.[63] The mean age of onset for BP-II was 20 years. Thus far, there have been no studies that have conclusively demonstrated that an unequal distribution of bipolar disorders across sex and ethnicity exists.[65]
A vast majority of studies and meta-analysis do not differentiate between BP-I and BP-II, and current epidemiology data may not accurately describe true prevalence and incidence.[66] In addition, BP-II is underdiagnosed in practice, and it is easy to miss milder forms of the condition.[63]
History[edit]
In 19th century psychiatry, mania covered a broad range of intensity, and hypomania was equated by some to concepts of 'partial insanity' or monomania. A more specific usage was advanced by the German neuro-psychiatrist Emanuel Ernst Mendel in 1881, who wrote "I recommend (taking under consideration the word used by Hippocrates) to name those types of mania that show a less severe phenomenological picture, 'hypomania'".[67] Narrower operational definitions of hypomania were developed from the 1960s/1970s.
The first diagnostic distinction to be made between manic-depression involving mania and involving hypomania came from Carl Gustav Jung in 1903.[68][69] In his paper, Jung introduced the non-psychotic version of the illness with the statement, "I would like to publish a number of cases whose peculiarity consists in chronic hypomanic behavior" where "it is not a question of real mania at all but of a hypomanic state which cannot be regarded as psychotic."[68][69] Jung illustrated the hypomanic variation with five case histories, each involving hypomanic behavior, occasional bouts of depression, and mixed mood states, which involved personal and interpersonal upheaval for each patient.[68]
In 1975, Jung's original distinction between mania and hypomania gained support. Fieve and Dunner published an article recognizing that only individuals in a manic state require hospitalization. It was proposed that the presentation of either the one state or the other differentiates two distinct diseases; the proposition was initially met with skepticism. However, studies since confirm that BP-II is a phenomenologically distinct disorder.[9]
Empirical evidence, combined with treatment considerations, led the DSM-IV Mood Disorders Work Group to add BP-II as its own entity in the 1994 publication. Only one other mood disorder was added to this edition, indicating the conservative nature of the DSM-IV work group. In May 2013, the DSM-5 was released. Two revisions to the existing BP-II criteria are anticipated. The first expected change will reduce the required duration of a hypomanic state from four to two days. The second change will allow hypomania to be diagnosed without the manifestation of elevated mood; that is, increased energy/activity will be sufficient. The rationale behind the latter revision is that some individuals with BP-II manifest only visible changes in energy. Without presenting elevated mood, these individuals are commonly misdiagnosed with major depressive disorder. Consequently, they receive prescriptions for antidepressants, which unaccompanied by mood stabilizers, may induce rapid cycling or mixed states.[70]