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Bipolar II disorder (BP-II) is a mood disorder on the bipolar spectrum, defined by at least one hypomanic episode and one episode of major depression, without any full manic episodes. Hypomania is a milder form of mania lasting at least four days, lacking psychosis but potentially causing significant life impairment. BP-II often involves more frequent and severe depressive episodes compared to bipolar I disorder, and is associated with higher risk of suicidal behaviors. Diagnosis is challenging as hypomanic symptoms may be mistaken for high-functioning behavior or missed entirely, leading to frequent misdiagnosis as unipolar depression. Co-occurring substance use disorders and mixed depression complicate accurate assessment. Proper diagnosis is crucial for effective treatment and avoiding worsening symptoms from antidepressant use without mood stabilizers.

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Causes

Multiple factors contribute to the development of bipolar spectrum disorders,28 although there have been very few studies conducted to examine the possible causes of BP-II specifically.29 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.30 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.31

Signs and symptoms

Bipolar disorder is characterized by marked swings in mood, activity, and behavior.32 BP-II is characterized by periods of hypomania, which may occur before, after, or independently of a depressive episode.33

Hypomania

Main article: 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.34 In addition, they can present with symptoms of inflated self-esteem or grandiosity, decreased need for sleep, talkativeness or pressured speech, flight of ideas or rapid cycling of thoughts, distractibility, increased goal-directed activity, psychomotor agitation, and/or excessive involvement in activities that have a high potential for painful consequences (engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments.)35

Hypomania is distinct from mania.3637 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.38 Patients may display elevated confidence, but do not express delusional thoughts as in mania. They can experience increase in goal-directed activity and creativity, but do not reach the severity of aimlessness and disorganization. Speech may be rapid, but interruptible. Patients with hypomania never present with psychotic symptoms and do not reach the severity to require psychiatric hospitalization.39

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.40 Although hypomania may increase functioning, episodes require treatment as they may indicate increasing instability and can precipitate a depressive episode.4142

Depressive episodes

It is during depressive episodes that BP-II patients often seek help. Symptoms may be syndromal or subsyndromal.43

Depressive episodes in BP-II can present similarly to those experienced in unipolar depressive disorders.44 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. Changes in posture, speech, facial expression, and grooming can be observed. 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.4546

Many experts in the field have attempted to find reliable differences between BP-II depressive episodes and episodes of major depressive disorder (MDD), but the data is inconsistent. However, some clinicians report that patients who came in with a depressive episode, but were later diagnosed as having bipolar disorder often presented with hypersomnia, increased appetite, psychomotor retardation, and a history of antidepressant-induced hypomania.4748 Evidence also suggests that unlike MDD depressive episodes, BP-II depressive episodes tend to include symptoms more commonly associated with atypical depression, such as overeating or oversleeping. Other factors that can distinguish BP-II from MDD are age of onset, which is lower for BP, the frequency of recurrence, which is greater for BP-II, and bipolar disorder family history (both type 1 and 2).49

Mood episodes with mixed features

A mixed episode is defined by the presence of a hypomanic or depressive episode that is accompanied by symptoms of the opposite polarity. This is commonly referred to as a mood episode with mixed features (e.g. depression with mixed features or hypomania with mixed features), but can also be referred to as mixed episodes or mixed states.50 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.51

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.52

Relapse

Bipolar disorder is a lifelong condition, and patients should be followed up regularly for relapse prevention.53 Although BP-II is thought to be less severe than BP-I in regard to symptom intensity, BP-II is associated with higher frequencies of rapid cycling and depressive episodes.54 In the case of a relapse, patients may experience new onset sleep disturbance, racing thoughts and/or speech, anxiety, irritability, and increase in emotional intensity. Family and/or friends may notice that patients are arguing more frequently with them, spending more money than usual, are increasing their binging on food, drugs, or alcohol, and may suddenly start taking on many projects at once. These symptoms often occur and are considered early warning signs.55

Psychosocial factors in a person's life can trigger a relapse in patients with BP-II. These include stressful life events, criticism from peers or relatives, and a disrupted circadian rhythm. In addition, the addition of antidepressant medications can trigger a hypomanic episode.56

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.57 These include anxiety, eating, personality (cluster B), and substance use disorders.5859 For BP-II, the most conservative estimate of lifetime prevalence of alcohol or other substance use disorders is 20%. In patients with comorbid substance use disorder and BP-II, episodes have a longer duration and treatment compliance decreases. Preliminary studies suggest that comorbid substance use is also linked to increased risk of suicidality.60

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).61 In addition, alternative diagnostic criteria is established in the World Health Organization's International Classification of Diseases-11th Revision (ICD-11)].62 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.63

DSM-5 criteria

According to the DSM-5, a patient diagnosed with BP-II will have experienced at least one hypomanic episode, at least one major depressive episodes, and no manic episode. Furthermore, the occurrence of the mood episodes are not better explained by schizoaffective disorder, schizophrenia, delusional disorder, or other specified or unspecified schizophrenia spectrum and other psychotic disorder. The final criteria that must be met is that the mood episodes cause clinically significant distress or impairment in social, occupational, or other important areas of functioning (from the depressive symptoms or the unpredictability of cycling between periods of depression and hypomania).64

A hypomanic episode is established if a patient's symptoms last for most of the day each day for at least four days. Furthermore, three or more of the following symptoms must be present: Inflated sense of self-esteem or grandiose thoughts, feeling well rested despite getting low amounts of sleep (3 hours), talkativeness, racing thoughts, distractibility, and increase in goal-directed activity or psychomotor agitation, or excessive involvement in activities with high risk of painful consequences. Per DSM-5 criteria, a major depressive episode consists of the presence of a depressed mood or loss of interest/pleasure in activities (anhedonia). In addition to the former symptoms, five out of the nine following symptoms must occur for more than two weeks (to the extent in which it impairs functioning): weight loss/gain, insomnia or hypersomnia, psychomotor agitation or retardation, fatigue, feelings of worthlessness/inappropriate guilt, decreased concentration, or thoughts of death/suicide.65

Specifiers:

  • With current or most recent episode hypomanic or depressed
  • With partial remission or full remission
  • With mild, moderate, or severe severity
  • With anxious distress
  • With catatonic features
  • With mood congruent psychotic features
  • With peripartum onset
  • With seasonal pattern (applies only to the pattern of major depressive episodes)
  • With rapid cycling.

ICD-11

According to the ICD-11, a BP-II patient will have experienced episodic experiences of one or more hypomaniac episodes and one or more major depressive episodes, and no history of a manic episode or mixed episode.66 These symptoms cannot be explained by other diagnoses such as:

The specifiers are the same as the DSM-5 with the exception of catatonic features and if symptoms have occurred with or without psychosis about 6 weeks after childbirth.75

Differential diagnoses

The signs and symptoms of BP-II may overlap significantly with those of other conditions. Thus, a comprehensive history, medication review, and laboratory work are key to diagnosing BP-II and differentiating it from other conditions. The differential diagnosis of BP-II is as follows: unipolar major depression, borderline personality disorder, posttraumatic stress disorder, substance use disorders, and attention deficit hyperactivity disorder.76: 1653–7 

Major differences between BP-I and BP-II have been identified in their clinical features, comorbidity rates and family histories. During depressive episodes, BP-II patients tend to show higher rates of psychomotor agitation, guilt, shame, suicidal ideation, and suicide attempts. BP-II patients have shown higher lifetime comorbidity rates of phobias, anxiety disorders, substance use, and eating disorders. In addition, there is a higher correlation between BP-II patients and family history of psychiatric illness, including major depression and substance-related disorders compared to BP-I.77 The occurrence rate of psychiatric illness in first degree relatives of BP-II patients was 26.5%, versus 15.4% in BP-I patients.7879

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. Thus, the current treatment guidelines for the symptoms of BP-II are derived and extrapolated from the treatment guidelines in BP-I, along with limited randomized controlled trials published in the literature.8081: 1697 

The treatment of BP-II consists of the following: treatment of hypomania, treatment of major depression, and maintenance therapy for the prevention of relapse of hypomania or depression. As BP-II is a chronic condition, the goal of treatment is to achieve remission of symptoms and prevention of self-harm in patients.82 Treatment modalities of BP-II include medication-based pharmacotherapy, along with various forms of psychotherapy.83

Medications

The most common pharmacologic agents utilized in the treatment of BP-II includes mood stabilizers, antipsychotics, and antidepressants.84

Mood stabilizers

Further information: mood stabilizer

Mood stabilizers used in the treatment of hypomanic and depressive episodes of BP-II include lithium, and the anticonvulsant medications valproate, carbamazepine, lamotrigine, and topiramate.85

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.86 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.87 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.88 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

Further information: Antipsychotic

Antipsychotics are utilized as a second line option for hypomanic episodes, typically indicated patients who do not respond to mood stabilizers.89 However, quetiapine is the only antipsychotic that has demonstrated efficacy in multiple meta-analyses of randomized controlled trials for treating acute BP-II depression, and is a first-line option for patients with BP-II depression.90: 1697 91 Other antipsychotics that are used to treat BP-II include lurasidone, olanzapine, cariprazine, aripiprazole, asenapine, paliperidone, risperidone, ziprasidone, haloperidol, and chlorpromazine.92 As a class, the first generation antipsychotics are associated with movement disorders, along with anticholinergic side effects compared with second generation antipsychotics.93

Antidepressants

Further information: Antidepressant

There is evidence to support the use of SSRI and SNRI antidepressants in BP-II, but the use of these treatments is controversial.9495 Potential risks of antidepressant pharmacotherapy in patients with bipolar disorder include increased mood cycling, development of rapid cycling, dysphoria, and switch to hypomania.96 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 antipsychotics, as these drugs reduce the risk of manic/hypomanic switching.97 However, the risk still exists, and should be used with caution.98

Non-pharmaceutical therapies

Further information: Therapy and Psychotherapy

Although medication therapy is the standard of care for treatment of both BP-I and BP-II, additional non-pharmaceutical therapies can also help those with the illness. Benefits include prevention of relapse and improved maintenance medication adherence. These include psychotherapy (e.g. cognitive behavioral therapy, psychodynamic therapy, psychoanalysis, interpersonal therapy, behavioral therapy, cognitive therapy, and family-focused therapy), social rhythm therapy, art therapy, music therapy, psychoeducation, mindfulness, and light therapy. Meta-analyses in the literature has shown that psychotherapy plus pharmacotherapy was associated with a lower relapse rate compared with patients treated with pharmacotherapy alone.99 However, relapse can still occur, despite continued medication and therapy.100 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.101

Prognosis

There is evidence to suggest that BP-II has a more chronic course of illness than BP-I.102 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.103 The natural course of BP-II, when left untreated, leads to patients spending the majority of their lives with some symptoms, primarily stemming from depression.104 Their recurrent depression results in personal distress and disability.105

This disability can present itself in the form of psychosocial impairment, which has been suggested to be worse in BP-II patients than in BP-I patients.106 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.107 Rapid cycling is quite common in those with BP-II, much more so in women than in men (70% vs. 40%), and without treatment leads to added sources of disability and an increased risk of suicide.108 Women are more prone to rapid cycling between hypomanic episodes and depressive episodes.109 To improve a patient's prognosis, long-term therapy is most favorably recommended for controlling symptoms, maintaining remission and preventing relapses.110 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.111 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.112

Functioning

The deficits in functioning associated with BP-II stem mostly from the recurrent depression that BP-II patients experience. Depressive symptoms are much more disabling than hypomanic symptoms and are potentially as, or more disabling than mania symptoms.113 Functional impairment has been shown to be directly linked with increasing percentages of depressive symptoms, and because sub-syndromal symptoms are more common—and frequent—in BP-II, they have been implicated heavily as a major cause of psychosocial disability.114 There is evidence that shows the mild depressive symptoms, or even sub-syndromal symptoms, are responsible for the non-recovery of social functioning, which furthers the idea that residual depressive symptoms are detrimental for functional recovery in patients being treated for BP-II.115 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.116 This social impairment can last for years, even after treatment that has resulted in a resolution of mood symptoms.117

The factors related to this persistent social impairment are residual depressive symptoms, limited illness insight (a very common occurrence in patients with BP-II), and impaired executive functioning.118 Impaired ability in executive functions is directly tied to poor psychosocial functioning, a common side-effect in patients with BP-II.119

The impact on a patient's psychosocial functioning stems from the depressive symptoms (more common in BP-II than BP-I).120 An increase in these symptoms' severity seems to correlate with a significant increase in psychosocial disability.121 Psychosocial disability can present itself in poor semantic memory, which in turn affects other cognitive domains like verbal memory and (as mentioned earlier) executive functioning leading to a direct and persisting impact on psychosocial functioning.122

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.123 BP-II patients have also been shown to present worse cognitive functioning than those patients with BP-I, though they demonstrate about the same disability when it comes to occupational functioning, interpersonal relationships, and autonomy.124 This disruption in cognitive functioning takes a toll on their ability to function in the workplace, which leads to high rates of work loss in BP-II patient populations.125 After treatment and while in remission, BP-II patients tend to report a good psychosocial functioning but they still score less than patients without the disorder.126 These lasting impacts further suggest that a prolonged period of untreated BP-II can lead to permanent adverse effects on functioning.127

Recovery and recurrence

BP-II has a chronic relapsing nature.128 It has been suggested that BP-II patients have a higher degree of relapse than BP-I patients.129 Generally, within four years of an episode, around 60% of patients will relapse into another episode.130 Some patients are symptomatic half the time, either with full on episodes or symptoms that fall just below the threshold of an episode.131

Because of the nature of the illness, long-term therapy is the best option and aims to not only control the symptoms but to maintain sustained remission and prevent relapses from occurring.132 Even with treatment, patients do not always regain full functioning, especially in the social realm.133 There is a very clear gap between symptomatic recovery and full functional recovery for both BP-I and BP-II patients.134 As such, and because those with BP-II spend more time with depressive symptoms that do not quite qualify as a major depressive episode, the best chance for recovery is to have therapeutic interventions that focus on the residual depressive symptoms and to aim for improvement in psychosocial and cognitive functioning.135 Even with treatment, a certain amount of responsibility is placed in the patient's hands; they have to be able to assume responsibility for their illness by accepting their diagnosis, taking the required medication, and seeking help when needed to do well in the future.136

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.137 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.138 Lithium prevents mood relapse and works especially well in BP-II patients who experience rapid-cycling.139 Almost all BP-II patients who take lithium have a decrease in the amount of time they spend ill and a decrease in mood episodes.140

Along with medication, other forms of therapy have been shown to be beneficial for BP-II patients. A treatment called a "well-being plan" serves several purposes: it informs the patients, protects them from future episodes, teaches them to add value to their life, and works toward building a strong sense of self to fend off depression and reduce the desire to succumb to the seductive hypomanic highs.141 The plan has to aim high. Otherwise, patients will relapse into depression.142 A large part of this plan involves the patient being very aware of warning signs and stress triggers so that they take an active role in their recovery and prevention of relapse.143

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.144 Bipolar disorders, in general, are the third leading cause of death in 15- to 24-year-olds.145 BP-II patients were also found to employ more lethal means and have more complete suicides overall.146

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.147 Mixed symptoms and rapid-cycling, both very common in BP-II, are also associated with an increased risk of suicide.148 The tendency for BP-II to be misdiagnosed and treated ineffectively, or not at all in some cases, leads to an increased risk.149

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.150

Suicide is a common cause of death for many patients with severe psychiatric illness. The mood disorders (depression and bipolar) are by far the most common psychiatric conditions associated with suicide. At least 25% to 50% of patients with bipolar disorder also attempt suicide at least once. Aside from lithium—which is the most demonstrably effective treatment against suicide—little is known about contributions of specific mood-altering treatments to minimizing mortality rates in persons with either major mood disorders or bipolar depression specifically. Suicide is usually a manifestation of severe psychiatric distress that is often associated with a diagnosable and treatable form of depression or other mental illness. In a clinical setting, an assessment of suicidal risk must precede any attempt to treat psychiatric illness.151

Epidemiology

The global estimated lifetime prevalence of bipolar disorder among adults range from 1 to 3 percent.152 The annual incidence is estimated to vary from 0.3 to 1.2 percent worldwide.153 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%.154 Other meta-analyses have found lifetime prevalence of BP-II up to 1.57%.155 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%.156 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.157

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.158 In addition, BP-II is underdiagnosed in practice, and it is easy to miss milder forms of the condition.159

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'".160 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 1903.161162 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."163164 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.165

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.166

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.167

Society and culture

Main article: List of people with bipolar disorder

See also

  • Psychiatry portal
  • Psychology portal
  • Medicine portal

References

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