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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. Diagnosis for BP-II requires that the individual must never have experienced a full manic episode. Otherwise, one manic episode meets the criteria for bipolar I disorder (BP-I).

Signs and symptoms
Bipolar disorder is characterized by marked swings in mood, activity, and behavior. BP-II is characterized by periods of hypomania, which may occur before, after, or independently of a depressive episode. Hypomania Hypomania is the signature characteristic of BP-II, defined by an experience of elevated mood. A patient's mood is typically cheerful, enthusiastic, euphoric, or irritable. Hypomania is distinct from mania. During a typical hypomanic episode, patients may present as upbeat, may show signs of poor judgment or display signs of increased energy despite lack of sleep, but do not meet the full criteria for an acute manic episode. For these reasons, hypomania commonly goes unnoticed. Individuals often will only seek treatment during a depressive episode, and their history of hypomania may go undiagnosed. Although hypomania may increase functioning, episodes require treatment as they may indicate increasing instability and can precipitate a depressive episode. Patients characteristically experience a depressed mood and may describe themselves as feeling sad, gloomy, down in the dumps, or hopeless, for most of the day, nearly every day. In children, this can present with an irritable mood. Most patients report significant fatigue, loss of energy, or tiredness. Patients or their family members may note diminished interest in usual activities such as sex, hobbies, or daily routines. Many patients report a change in appetite along with associated weight change. Sleep disturbances may be present, and can manifest as problems falling or staying asleep, frequent awakenings, excessive sleep, or difficulties getting up in the morning. Around half of depressed patients develop changes in psychomotor activity, described as slowness in thinking, speaking, or movement. Conversely, they may also present with agitation, with inability to sit still or wringing their hands. Other signs and symptoms include changes in posture and facial expression, slowed speech, poor hygiene, unkempt appearance, feelings of guilt, shame, or helplessness, diminished ability to concentrate, nihilistic thoughts, and suicidal ideation. For example, a patient with depression with mixed features may have a depressed mood, but has simultaneous symptoms of rapid speech, increased energy, and flight of ideas. Conversely, a patient with hypomania with mixed features will present with the full criteria for a hypomanic episode, but with concurrent symptoms of decreased appetite, loss of interest, and low energy. Episodes with mixed features can last up to several months. They occur more frequently in patients with an earlier onset of bipolar disorder, are associated with higher frequency of episodes, and are associated with a greater risk of substance use, anxiety disorders, and suicidality. In addition, they are associated with increased treatment resistance compared to non-mixed episodes. Symptoms of psychosis include delusions, hallucinations, or both. Delusions are more common than hallucinations in bipolar disorder. In general, having psychotic episodes means the illness is more severe. People with psychosis have poor insight and more agitation, anxiety, and hostility. In contrast to bipolar II, in bipolar I, more than 50% of people have experienced psychosis. Psychosis is more common during manic episodes than depressive episodes, so psychotic symptoms are more common in bipolar type I compared to bipolar type II. == Causes ==
Causes
Multiple factors contribute to the development of bipolar spectrum disorders, although there have been very few studies conducted to examine the possible causes of BP-II specifically. 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. 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. ==Diagnosis==
Diagnosis
BP-II is diagnosed according to the criteria established in the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5). The diagnostic criteria are established from self-reported experiences from patients or their family members, the psychiatric assessment, and the mental status examination. In addition, Screening instruments like the Mood Disorders Questionnaire are helpful tools in determining a patient's status on the bipolar spectrum. In addition, certain features have been shown to increase the chances that depressed patients have a bipolar disorder, including atypical symptoms of depression like hypersomnia and hyperphagia, a family history of bipolar disorder, medication-induced hypomania, recurrent or psychotic depression, antidepressant refractory depression, and early or postpartum depression. These symptoms cannot be explained by other diagnoses such as: • Cyclothymia The occurrence rate of psychiatric illness in first degree relatives of BP-II patients was 26.5%, versus 15.4% in BP-I patients. ==Management==
Management
Although BP-II is a prevalent condition associated with morbidity and mortality, there has been an absence of robust clinical trials and systematic reviews that investigate the efficacy of pharmacologic treatments for the hypomanic and depressive phases of BP-II. Medications (Lamictal) is an anticonvulsant that can be used as a mood stabilizer to treat BP-II. The most common pharmacologic agents utilized in the treatment of BP-II includes mood stabilizers, atypical antipsychotics, and antidepressants, though antidepressant use in bipolar disorder is controversial. There is strong evidence that lithium is effective in treating both the depressive and hypomanic symptoms in BP-II, along with the reduction of hypomanic switch in patients treated with antidepressants. Furthermore, lithium is the only mood stabilizer to demonstrate a decrease in suicide and self-harm in patients with mood disorders. In addition to preventing suicide, lithium also decreases death from all causes in people with mood disorders. Due to lithium's narrow therapeutic index, lithium levels must be monitored regularly for prevention of lithium toxicity. There is also evidence that the anticonvulsants valproate, lamotrigine, carbamazepine, and topiramate are effective in the reduction of symptoms of hypomanic and depressive episodes of bipolar disorder. Potential mechanisms contributing to these effects include a decrease in brain excitation due to blockage of low-voltage sodium-gated channels, decrease in glutamate and excitatory amino acids, and potentiation of levels of GABA. There is evidence that lamotrigine decreases the risk of relapse in rapid-cycling BP-II. It is more effective in BP-II than BP-I, suggesting that lamotrigine is more effective for the treatment of depressive rather than manic episodes. Doses ranging from 100 to 200 mg have been reported to have the most efficacy, while experimental doses of 400 mg have rendered little response. A large, multicenter trial comparing carbamazepine and lithium over two and a half years found that carbamazepine was superior in terms of preventing future episodes of BP-II, although lithium was superior in individuals with BP-I. There is also some evidence for the use of valproate and topiramate, although the results for the use of gabapentin have been disappointing. Antipsychotics (Seroquel) is an atypical antipsychotic that is used to treat acute BP-II depression Atypical antipsychotics are utilized as a second line option for hypomanic episodes, typically indicated patients who do not respond to mood stabilizers. Other atypical antipsychotics that are used to treat BP-II include lurasidone, olanzapine, cariprazine, aripiprazole, asenapine, paliperidone, risperidone, ziprasidone. First generation antipsychotics used for treatment are haloperidol and chlorpromazine. As a class, the first generation antipsychotics are associated with movement disorders, along with anticholinergic side effects compared to second generation antipsychotics (atypical antipsychotics). Antidepressants There is evidence to support the use of SSRI and SNRI antidepressants in BP-II, but the use of these treatments is controversial. Potential risks of antidepressant pharmacotherapy in patients with bipolar disorder include increased mood cycling, development of rapid cycling, dysphoria, and switch to hypomania. In addition, the evidence for their efficacy in bipolar depression is mixed. Thus, in most cases, antidepressant monotherapy in patients with BP-II is not recommended. However, antidepressants may provide benefit to some patients when used in addition to mood stabilizers and atypical antipsychotics, as these drugs reduce the risk of manic/hypomanic switching. However, relapse can still occur, despite continued medication and therapy. People with bipolar disorder may develop dissociation to match each mood they experience. For some, this is done intentionally, as a means by which to escape trauma or pain from a depressive period, or simply to better organize one's life by setting boundaries for one's perceptions and behaviors. ==Prognosis==
Prognosis
There is evidence to suggest that BP-II has a more chronic course of illness than BP-I. This constant and pervasive course of the illness leads to an increased risk in suicide and more hypomanic and major depressive episodes with shorter periods between episodes than BP-I patients experience. Their recurrent depression results in personal distress and disability. Another facet of this illness that is associated with a poorer prognosis is rapid cycling, which denotes the occurrence of four or more major Depressive, Hypomanic, and/or mixed episodes in a 12-month period. To improve a patient's prognosis, long-term therapy is most favorably recommended for controlling symptoms, maintaining remission and preventing relapses. With treatment, patients have been shown to present a decreased risk of suicide (especially when treated with lithium) and a reduction of frequency and severity of their episodes, which in turn moves them toward a stable life and reduces the time they spend ill. To maintain their state of balance, therapy is often continued indefinitely, as around 50% of the patients who discontinue it relapse quickly and experience either full-blown episodes or sub-syndromal symptoms that bring significant functional impairments. It has been suggested that symptom interference in relation to social and interpersonal relationships in BP-II is worse than symptom interference in other chronic medical illnesses such as cancer. The impact on a patient's psychosocial functioning stems from the depressive symptoms (more common in BP-II than BP-I). An abnormal semantic memory organization can manipulate thoughts and lead to the formation of delusions and possibly affect speech and communication problems, which can lead to interpersonal issues. Treatment often lasts after remission is achieved, and the treatment that worked is continued during the continuation phase (lasting anywhere from 6–12 months) and maintenance can last 1–2 years or, in some cases, indefinitely. One of the treatments of choice is lithium, which has been shown to be very beneficial in reducing the frequency and severity of depressive episodes. Mortality Several studies have shown that the risk of suicide is slightly higher in patients who have BP-II than those with BP-I. In results of a summary of several lifetime study experiments, it was found that 32.4% of BP-I patients experienced suicidal ideation or suicide attempts compared to 36% in BP-II patients. Bipolar disorders, in general, are the third leading cause of death in 15- to 24-year-olds. BP-II patients were also found to employ more lethal means and have more complete suicides overall. BP-II patients have several risk factors that increase their risk of suicide. The illness is very recurrent and results in severe disabilities, interpersonal relationship problems, barriers to academic, financial, and vocational goals, and a loss of social standing in their community, all of which increase the likelihood of suicide. Mixed symptoms and rapid-cycling, both very common in BP-II, are also associated with an increased risk of suicide. As a result of the high suicide risk for this group, reducing the risk and preventing attempts remains a main part of the treatment; a combination of self-monitoring, close supervision by a therapist, and faithful adherence to their medication regimen will help to reduce the risk and prevent the likelihood of suicide. == Epidemiology ==
Epidemiology
The global estimated lifetime prevalence of bipolar disorder among adults range from 1 to 3 percent. The annual incidence is estimated to vary from 0.3 to 1.2 percent worldwide. Other meta-analyses have found lifetime prevalence of BP-II up to 1.57%. 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%. 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. In addition, BP-II is underdiagnosed in practice, and it is easy to miss milder forms of the condition. Comorbid conditions Comorbid conditions are extremely common in individuals with BP-II. In fact, individuals are twice as likely to present a comorbid disorder than not. == History ==
History
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'". The first diagnostic distinction to be made between manic-depression involving mania and involving hypomania came from Carl Gustav Jung in 1903. 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." ==Society and culture==
Society and culture
John Adams, president of the United StatesHeath Black revealed in his autobiography, Black, that he has been diagnosed with BP-II. • Maria Bamford has been diagnosed with BP-II. • Geoff Bullock, singer-songwriter, was diagnosed with BP-II. • Mariah Carey was diagnosed with BP-II in 2001. In 2018, publicly revealed and actively seeking treatment in the form of therapy and medication. • Charmaine Dragun, former Australian journalist/newsreader. Inquest concluded she had BP-II. • Joe Gilgun has been diagnosed with BP-II. • Shane Hmiel has been diagnosed with BP-II. • Jesse Jackson Jr. has been diagnosed with BP-II. • Thomas Eagleton received a diagnosis of BP-II from Dr. Frederick K. Goodwin. • Carrie Fisher had been diagnosed with BP-II. • Demi Lovato has been diagnosed with BP-II. • Evan Perry, subject of the documentary Boy Interrupted, was diagnosed with BP-II. • Richard Rossi, filmmaker, musician, and maverick minister was diagnosed with BP-II. • Rumer has been diagnosed with BP-II. • Catherine Zeta-Jones received treatment for BP-II after dealing with the stress of her husband's throat cancer. According to her publicist, Zeta-Jones made a decision to check into a mental health facility for a brief stay. • Chappell Roan has been diagnosed with BP-II. == See also ==
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