What is Hyperthymic Temperament?

Introduction

Hyperthymic temperament, or hyperthymia, from Ancient Greek ὑπέρ (“over”, meaning here excessive) + θυμός (“spirited”), is a proposed personality type characterised by an exceptionally, or in some cases, abnormally positive mood and disposition.

Also known as Hyperthymic Personality-Type and Chronic Hypomania.

Refer to Bipolar Disorder.

Graph showing showing hyperthymia in comparison to other bipolar spectrum disorders.

Background

It is generally defined by increased energy, vividness and enthusiasm for life activities, as opposed to dysthymia. Hyperthymia is similar to but more stable than hypomania.

Characteristics of the hyperthymic temperament include:

  • Increased energy and productivity.
  • Short sleep patterns.
  • Vividness, activity extroversion.
  • Self-assurance, self-confidence.
  • Strong will.
  • Extreme talkativeness.
  • Tendency to repeat oneself.
  • Risk-taking/sensation seeking.
  • Breaking social norms.
  • Very strong libido.
  • Love of attention.
  • Low threshold for boredom.
  • Generosity and tendency to overspend.
  • Emotion sensitivity.
  • Cheerfulness and joviality.
  • Unusual warmth.
  • Expansiveness.
  • Tirelessness.
  • Irrepressibility, irresistible, and infectious quality.

The clinical, psychiatric understanding of hyperthymia is evolving. Studies have shown that hyperthymic temperament promotes efficient performance of complex tasks under time pressure or extreme conditions. Despite this positive characterisation, hyperthymia can be complicated with depressive episodes manifesting as a softer form of bipolar illness, such as cyclothymia. Research also suggests a familial genetic connection of the temperament to bipolar I.

Aside from references in historical and more recent writings on the spectrum of mood disorders, further literature on the temperament is lacking. There is a lack of agreement on its definition, implications or whether it is pathological. It is not known where to place hyperthymia on the affective spectrum.

Hyperthymia manifesting intermittently or in an unusual way may mask hypomania or another psychiatric disorder. Hyperthymia can be most accurately diagnosed by a psychologist or psychiatrist with the help of a patient’s family and/or close friends.

What are Racing Thoughts?

Introduction

Racing thoughts refers to the rapid thought patterns that often occur in manic, hypomanic, or mixed episodes.

While racing thoughts are most commonly described in people with bipolar disorder and sleep apnoea, they are also common with anxiety disorders, OCD, and other psychiatric disorders such as attention deficit hyperactivity disorder. Racing thoughts are also associated with sleep deprivation, hyperthyroidism and the use of amphetamines.

Description

Racing thoughts may be experienced as background or take over a person’s consciousness. Thoughts, music, and voices might be zooming through one’s mind as they jump tangentially from one to the next. There also might be a repetitive pattern of voice or of pressure without any associated “sound”. It is a very overwhelming and irritating feeling, and can result in losing track of time. In some cases, it may also be frightening to the person experiencing it, as there is a loss of control. If one is experiencing these thoughts at night when going to sleep, they may suddenly awaken, startled and confused by the very random and sudden nature of the thoughts.

Racing thoughts differ in manifestation according to the individual’s perspective. These manifestations can vary from unnoticed or minor distractions to debilitating stress, preventing the sufferer from maintaining a thought.

Generally, racing thoughts are described by an individual who has had an episode where the mind uncontrollably brings up random thoughts and memories and switches between them very quickly. Sometimes they are related, as one thought leads to another; other times they seem completely random. A person suffering from an episode of racing thoughts has no control over their train of thought, and it stops them from focusing on one topic or prevents sleeping.

Associated Conditions

The causes of racing thoughts are most often associated with anxiety disorders, but many influences can cause these rapid, racing thoughts. There are also many associated conditions, in addition to anxiety disorders, which can be classified as having secondary relationships with causing racing thoughts. The conditions most commonly linked to racing thoughts are bipolar disorder, anxiety disorder, attention deficit hyperactivity disorder, sleep deprivation, amphetamine dependence, and hyperthyroidism.

Anxiety Disorders

Racing thoughts associated with anxiety disorders can be caused by many different conditions, such as obsessive-compulsive disorder (OCD), panic disorder, generalised anxiety disorder, or posttraumatic stress disorder.

In people with OCD, racing thoughts can be brought on by stressors, or triggers, causing disturbing thoughts in the individual. These disturbing thoughts, then, result in compulsions characterising OCD in order to lower the stress and gain some sort of control over these stressful, racing thoughts.

Panic disorder is an anxiety disorder characterised by repeated panic attacks of fear or nervousness, lasting several minutes. During these panic attacks, the response is out of proportion to the situation. The racing thoughts may feel catastrophic and intense, but they are a symptom of the panic attack and must be controlled in order to soothe the panic and minimise the panic attack.

Generalised anxiety disorder (GAD) is a neurological anxiety disorder that involves uncontrollable and excessive worrying about irrational topics or problems. These stressful thoughts must be present for at least six months in order to be diagnosed as GAD. Along with other symptoms, racing thoughts is one of the most common ones. With GAD, there is an inability to relax or let thoughts or worries go, persistent worrying and obsessions about small concerns that are out of proportion to the result, and even worrying about their excessive worrying.

Bipolar Disorder

Racing thoughts can be brought on by bipolar disorder, defined by mood instability that range from extreme emotional highs, mania, to severe depression. During the manic phase of bipolar disorder is when racing thoughts usually occur. Disjointed, constantly changing thoughts with no underlying theme can be a sign of the manic phase of bipolar disorder. Manic thoughts can prevent performance of daily routines due to their rapid, unfocused and overwhelming nature. Racing thoughts in people with bipolar disorder are generally accompanied with other symptoms associated with this disorder.

Amphetamines

Amphetamines are used as a stimulant to trigger the central nervous system, increasing heart rate and blood pressure while decreasing appetite. Since amphetamines are a stimulant, use of these drugs result in a state that resembles the manic phase of bipolar disorder and also produces similar symptoms, as stated above.

Attention Deficit Hyperactivity Disorder

Racing thoughts associated with ADHD is most common in adults. With ADHD, racing thoughts can occur and tend to cause insomnia. Racing thoughts in people with ADHD tend to be rapid, unstable thoughts which do not follow any sort of pattern, similar to racing thoughts in people with bipolar disorder. Medications used to treat ADHD, such as Adderall or Methylphenidate, can be prescribed to patients with ADHD to calm these racing thoughts, most commonly in the morning when people wake up but just as well in the evening before sleep.

Lack of Sleep

Racing thoughts, also referred to as “racing mind”, may prevent a person from falling asleep. Chronic sleep apnoea and prolonged disturbed sleep patterns may also induce racing thoughts. Treatment for sleep apnoea and obstructive airway disorder can improve airflow and improve sleep resulting in improved brain and REM (rapid eye movement) function and reduced racing thought patterns.

Hyperthyroidism

Hyperthyroidism is a condition in which the thyroid gland produces too much thyroid hormone, thyroxin. This overabundance of thyroxin causes irregular and rapid heartbeat, irritability, weight loss, nervousness, anxiety and racing thoughts. The anxiety and inability to focus is very common in hyperthyroidism and leads to racing thoughts, as well as panic attacks and difficulty concentrating.

Frequency

Anxiety disorder, the most common mental illness in the United States, affects 40 million people, ages 10 and older; this accounts for 18% of the US population. Most people suffering from anxiety disorder report some form of racing thoughts symptom.

The prevalence of OCD in every culture studied is at least 2% of the population, and the majority of those have obsessions, or racing thoughts. With these reports, estimates of more than 2 million people in the United States (as of 2000) suffer from racing thoughts.

Treatment

There are various treatments available to calm racing thoughts, some of which involve medication. One type of treatment involves writing out the thoughts onto paper. Some treatments suggest using activities, such as painting, cooking, and other hobbies, to keep the mind busy and distract from the racing thoughts. Exercise may be used to tire the person, thereby calming their mind. When racing thoughts are anxiety induced during panic or anxiety attacks, it is recommended that the person wait it out. Using breathing and meditation techniques to calm the breath and mind simultaneously is another tool for handling racing thoughts induced by anxiety attacks. Mindfulness meditation has also shown to help with racing thoughts by allowing practitioners to face their thoughts head-on, without reacting.

While all of these techniques can be useful to cope with racing thoughts, it may prove necessary to seek medical attention and counsel. Since racing thoughts are associated with many other underlying mental illnesses, such as bipolar disorder, anxiety disorder, and ADHD, medications used commonly to treat these disorders will help calm racing thoughts in patients.

Treatment for the underlying causes of racing thoughts is helpful and useful in order to calm the racing thoughts more permanently. For example, in people with ADHD, medications used to promote focus and calm distracting thoughts, will help them with their ADHD.

Some obstructive airway disorders may be relieved with nasal septoplasty which can improve sleep and lead to a reduction of racing mind. Insomnia may increase racing thoughts and those effected will find sleep apnoea treatment and nasal surgery helpful to eliminate their racing thoughts.

It is important to look at the underlying defect that may be causing racing thoughts in order to prevent them in the long-term.

What is the Hypomania Checklist?

Introduction

The Hypomania Checklist (HCL-32) is a questionnaire developed by Dr. Jules Angst to identify hypomanic features in patients with major depressive disorder in order to help recognise bipolar II disorder and other bipolar spectrum disorders when people seek help in primary care and other general medical settings.

It asks about 32 behaviours and mental states that are either aspects of hypomania or features associated with mood disorders. It uses short phrases and simple language, making it easy to read. The University of Zurich holds the copyright, and the HCL-32 is available for use at no charge. More recent work has focused on validating translations and testing whether shorter versions still perform well enough to be helpful clinically. Recent meta-analyses find that it is one of the most accurate assessments available for detecting hypomania, doing better than other options at recognising bipolar II disorder.

Development and Brief History

The Hypomania Checklist was built as a more efficient screening measure for hypomania, to be used both in epidemiological research and in clinical use. Existing measures for bipolar disorder focused on identifying personality factors and symptom severity instead of the episodic nature of hypomania or the possible negative consequences in behavioural, affective, or cognitive changes associated. These measures were mostly used in non-clinical populations to identify individuals at risk and were not used as screening instruments. The HCL-32 is a measure intended to have high sensitivity to direct clinicians from many countries to diagnosing individuals in a clinical population with bipolar disorder, specifically bipolar II disorder.

Initially developed by Jules Angst and Thomas Meyer in German, the questionnaire was translated into English and translated back to German to ensure accuracy. The English version of the HCL has been used as the basis for translation in other languages through the same process. The original study that used the HCL in an Italian and a Swiss sample noted the measure’s high sensitivity and a lower sensitivity than other used measures.

The scale includes a checklist of 32 possible symptoms of hypomania, each rated yes or no. The rating “yes” would mean the symptom is present or this trait is “typical of me,” and “no” would mean that the symptom is not present or “not typical” for the person.

Limitations

The HCL suffers from the same problems as other self-report inventories, in that scores can be easily exaggerated or minimised by the person completing them. Like all questionnaires, the way the instrument is administered can influence the final score. If a patient is asked to fill out the form in front of other people in a clinical environment, for instance, social expectations may elicit a different response compared to administration via a postal survey.

Similar reliability scores were found when only using 16 item assessments versus the traditional 32-item format of the HCL-32. A score of at least 8 items was found valid and reliable for distinguishing Bipolar Disorder and Major Depressive Disorder. In a study, 73% of patients who completed the HCL-32 R1 were true bipolar cases identified as potential bipolar cases. However, the HCL-32 R1 does not accurately differentiate between Bipolar I and Bipolar II. However, the 16-item HCL has not been tested as a standalone section in a hospital setting. In addition, while the HCL-32 is a sensitive instrument for hypomanic symptoms, it does not distinguish between bipolar I and bipolar-II disorders. The HCL-32 has not been compared with other commonly used screening tools for bipolar disorder, such as the Young Mania Rating Scale (YMRS)and the General Behaviour Inventory (GBI). The online version of the HCL has been shown to be as reliable as the paper version.

What is a Mixed Affective State?

Introduction

A mixed affective state, formerly known as a mixed-manic or mixed episode, has been defined as a state wherein features unique to both depression and mania – such as episodes of despair, doubt, anguish, rage or homicidal ideation, suicidal ideation, splitting, racing thoughts, sensory overload, pressure of activity, and heightened irritability – occur either simultaneously or in very short succession.

Previously, the diagnostic criteria for both a manic and depressive episode had to be met in a consistent and sustained fashion, with symptoms enduring for at least a week (or any duration if psychiatric hospitalisation was required), thereby restricting the official acknowledgement of mixed affective states to only a minority of patients with bipolar I disorder. In current DSM-5 nomenclature, however, a “mixed episode” no longer stands as an episode of illness unto itself; rather, the symptomology specifier “with mixed features” can be applied to any major affective episode (manic, hypomanic, or depressive), meaning that they are now officially recognised in patients with, in addition to bipolar I disorder, bipolar II disorder and, by convention, major depressive disorder. A depressive mixed state in a patient, however, even in the absence of discrete periods of mania or hypomania, effectively rules out unipolar depression.

Diagnostic Criteria

As affirmed by the Diagnostic and Statistical Manual of Mental Disorders, fifth edition (DSM-5), the symptomology specifier “with mixed features” can be applied to manic episodes of bipolar I disorder, hypomanic episodes of either bipolar I disorder or bipolar II disorder and depressive episodes of either bipolar disorder or major depressive disorder, with at least three concurrent features of the opposite polarity being present. As a result, the presence of “mixed features” are now recognised in patients with bipolar II disorder and major depression; as earlier noted, however, although it is customary to withhold a diagnosis of a bipolar disorder until a manic or hypomanic episode appears, the presence of such features in a depressed patient even with no history of discrete mania or hypomania is strongly suggestive of the disorder.

Nevertheless, the DSM-5’s narrower definition of mixed episodes may result in fewer patients meeting mixed criteria compared to DSM-IV. A call was made by Tohen in 2017 for introducing changes from a currently phenomenological to a target oriented approach to DSM-5 mixed mood criteria in order to achieve more personalized medical attention.

Two features of both mania or hypomania and depression may superficially overlap and even resemble each other, namely “an increase in goal-directed activity” (psychomotor acceleration) vs. psychomotor agitation and “flight of ideas” and “racing thoughts” vs. depressive rumination. Attending to the patient’s experiences is very important. In the psychomotor agitation commonly seen in depression, the “nervous energy” is always overshadowed by a strong sense of exhaustion and manifests as purposeless movements (e.g. pacing, hand-wringing); in psychomotor acceleration, however, the excess in movement stems from an abundance of energy and is often channelled and purposeful. Likewise, in depressive rumination, the patient experiences the repetitive thoughts as heavy, leaden, and plodding; in psychic acceleration, however, (as seen in mania or hypomania) the thoughts move in a rapid progression, with many themes, rather than a singular one, being touched upon. Even when such experiences are accounted for on the basis of depression, the possibility does still exist, however, that the depressive episode may be complicated by other manic or hypomanic symptoms, in which case it is often prudent to attend to the patient’s personal and family history (e.g. family history of bipolar disorder, early age of onset) to determine whether or not the patient has bipolar disorder.

Treatment

Treatment of mixed states is typically based upon administration of mood stabilising medication, which may include anticonvulsants such as valproic acid; atypical antipsychotics such as quetiapine, olanzapine, aripiprazole, and ziprasidone; or first-generation antipsychotics such as haloperidol. There is question of lithium’s efficacy for treatment of mixed states due to conflicting conclusions drawn from various trials and research. Mood stabilisers work to reduce the manic symptoms associated with the mixed state, but they are not considered particularly effective for improving concurrent depressive symptoms.

What is Bipolar II Disorder?

Introduction

Bipolar II disorder is a bipolar spectrum disorder (refer to Bipolar I disorder) characterised by at least one episode of hypomania and at least one episode of major depression. Diagnosis for bipolar II disorder requires that the individual must never have experienced a full manic episode. Otherwise, one manic episode meets the criteria for bipolar I disorder.

Refer to Mixed Affective State.

Bipolar mood shifts.

Hypomania is a sustained state of elevated or irritable mood that is less severe than mania yet may still significantly affect quality of life and result in permanent consequences including reckless spending, damaged relationships and poor judegment. Unlike mania, hypomania is not associated with psychosis. The hypomanic episodes associated with bipolar II disorder must last for at least four days.

Commonly, depressive episodes are more frequent and more intense than hypomanic episodes. Additionally, when compared to bipolar I disorder, type II presents more frequent depressive episodes and shorter intervals of well-being. The course of bipolar II disorder is more chronic and consists of more frequent cycling than the course of bipolar I disorder. Finally, bipolar II is associated with a greater risk of suicidal thoughts and behaviours than bipolar I or unipolar depression. Although bipolar II is commonly perceived to be a milder form of Type I, this is not the case. Types I and II present equally severe burdens.

Bipolar 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 behaviour or simply attributed to personality, patients are typically not aware of their hypomanic symptoms. In addition, many people who suffer from Bipolar 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. Bipolar II is more common than Bipolar I, while Bipolar II and major depressive disorder have about the same rate of diagnosis. Of all individuals initially diagnosed with major depressive disorder, between 40% and 50% will later be diagnosed with either BP-I or BP-II. 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. Despite the difficulties, it is important that BP-II individuals be correctly assessed so that they can receive the proper treatment. Antidepressant use, in the absence of mood stabilisers, is correlated with worsening BP-II symptoms.

Brief 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'”. Narrower operational definitions of hypomania were developed from the 1960s/1970s.

The first diagnostic distinction to be made between manic-depression involving mania, and that involving hypomania, came from Carl Gustav Jung in 1903. In his paper, Jung introduced the non-psychotic version of the illness with the introductory 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.” Jung illustrated the hypomanic variation with five case histories, each involving hypomanic behaviour, occasional bouts of depression, and mixed mood states, which involved personal and interpersonal upheaval for each patient.

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 hospitalisation. It was proposed that the presentation of either the one state or the other differentiates two distinct diseases; the proposition was initially met with scepticism. However, studies since confirm that bipolar II is a “phenomenologically” distinct disorder.

Empirical evidence, combined with treatment considerations, led the DSM-IV Mood Disorders Work Group to add bipolar II disorder 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 Bipolar 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 Bipolar 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 stabilisers, may induce rapid cycling or mixed states.

Signs and Symptoms

Hypomanic Episodes

Hypomania is the signature characteristic of Bipolar II disorder. It is a state characterised by euphoria and/or an irritable mood. In order for an episode to qualify as hypomanic, the individual must also present three or more of the below symptoms, and last at least four consecutive days and be present most of the day, nearly every day.

  • Inflated self-esteem or grandiosity.
  • Decreased need for sleep (e.g. feels rested after only 3 hours of sleep).
  • More talkative than usual or pressure to keep talking.
  • Flight of ideas or subjective experience that thoughts are racing.
  • Distractability (i.e. attention too easily drawn to unimportant or irrelevant external stimuli), as reported or observed.
  • Increase in goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation.
  • Excessive involvement in activities that have a high potential for painful consequences (e.g., engaging in unrestrained buying sprees, sexual indiscretions, or foolish business investments).

It is important to distinguish between hypomania and mania. Mania is generally greater in severity and impairs function, sometimes leading to hospitalisation and in the most severe cases, psychosis. In contrast, hypomania usually increases functioning. For this reason, it is not uncommon for hypomania to go unnoticed. Often it is not until individuals are in a depressive episode that they seek treatment, and even then their history of hypomania may go undiagnosed. Although hypomania may increase functioning, episodes need to be treated because they may precipitate a depressive episode.

Depressive Episodes

It is during depressive episodes that BP-II patients often seek help. Symptoms may be syndromal or subsyndromal. Depressive BP-II symptoms may include five or more of the below symptoms (at least one of them must be either depressed mood or loss of interest/pleasure). In order to be diagnosed, they need to be present only during the same two-week period, as a change from previous hypomanic functioning:

  • Depressed mood most of the day, nearly every day, as indicated by either subjective report (e.g. feels sad, empty, or hopeless) or observation made by others (e.g. appears tearful). In children and adolescents, this could be irritable mood.
  • Markedly diminished interest or pleasure in all, or almost all, activities most of the day, nearly every day (as indicated by either subjective account or observation).
  • Significant weight loss when not dieting or weight gain (e.g. a change of more than 5% of body weight in a month), or decrease or increase in appetite nearly every day (e.g. in children, failure to make expected weight gain).
  • Insomnia or hypersomnia nearly every day.
  • Psychomotor agitation or retardation nearly every day (observable by others; not merely subjective feelings of restlessness or being slowed down).
  • Fatigue or loss of energy nearly every day.
  • Feelings of worthlessness or excessive or inappropriate guilt nearly every day (not merely self-reproach or guilt about being sick).
  • Diminished ability to think or concentrate, possible irritability or indecisiveness, nearly every day (either by subjective account or as observed by others).
  • Recurrent thoughts of death (not just fear of dying), recurrent suicidal ideation without a specific plan, a suicide attempt, or a specific plan for completing suicide.

Evidence also suggests that BP-II is strongly associated with atypical depression. Essentially, this means that many BP-II patients exhibit reverse vegetative symptoms. BP-II patients may have a tendency to oversleep and overeat, while typically depressed patients sleep and eat less than usual.

Mixed Depression

Depressive mixed states occur when patients experience depression and non-euphoric, usually subsyndromal, hypomania at the same time. As mentioned previously, it is particularly difficult to diagnose BP-II when a patient is in this state.

In a mixed state, mood is depressed, but the following symptoms of hypomania present as well:

  • Irritability.
  • Mental hyperactivity.
  • Behavioural hyperactivity.

Mixed states are associated with greater levels of suicidality than non-mixed depression. Antidepressants may increase this risk.

Relapse

In the case of a relapse, the following symptoms often occur and are considered early warning signs:

  • Sleep disturbance: patient requires less sleep and does not feel tired.
  • Racing thoughts and/or speech.
  • Anxiety.
  • Irritability.
  • Emotional intensity.
  • Spending more money than usual.
  • Binge behaviour, including food, drugs, or alcohol.
  • Arguments with family members and friends.
  • Taking on many projects at once.

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 organise one’s life by setting boundaries for one’s perceptions and behaviours.

Studies indicate that the following events may also precipitate relapse in BP-II patients:

  • Stressful life events.
  • Relatives’ or peers’ criticism.
  • Antidepressant use.
  • Disrupted circadian rhythm.

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. These include anxiety, eating, personality (cluster B), and substance use disorders. For bipolar II disorder, 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. The question of which condition should be designated the index and which the comorbid condition is not self-evident and may vary in relation to the research question, the disease that prompted a particular episode of care, or of the specialty of the attending physician. A related notion is that of complication, a condition that coexists or ensues, as defined in the Medical Subject Headings (MeSH)-controlled vocabulary maintained by the National Library of Medicine (NLM).

Causes

Scientists are studying the possible causes of bipolar disorder and most agree that there is no single cause. There have been very few studies conducted to examine the possible causes of Bipolar II. Those that have been done have not considered Bipolar I and Bipolar II separately and have had inconclusive results. Researchers have found that patients with either Bipolar I or II may have increased levels of blood calcium concentrations, but the results are inconclusive. The studies that have been conducted did not find a significant difference between those with Bipolar I or Bipolar II. There has been a study looking at genetics of Bipolar II disorder and the results are inconclusive; however, scientists did find that relatives of people with Bipolar II are more likely to develop the same bipolar disorder or major depression rather than developing Bipolar I disorder. 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

A person diagnosed with bipolar II disorder will have experienced at least one hypomanic episode, no manic episode, and one or more major depressive episodes. Although bipolar II is thought to be less severe than bipolar I in regards to symptom intensity, it is actually more severe and distressing with respect to episode frequency and overall course. Those with bipolar II often experience more frequent bouts of depressive episodes. Specific criteria defined by the DSM-5 for a bipolar II diagnosis:

  • Criteria have been met for at least one hypomanic episode and at least one major depressive episode.
  • There has never been a manic episode.
  • The occurrence of the hypomanic episode(s) and major depressive episode(s) is not better explained by schizoaffective disorder, schizophrenia, delusional disorder, or other specified or unspecified schizophrenia spectrum and other psychotic disorder.
  • Causes significant stress or impairment in social, occupational, or other important areas of functioning.

Studies have identified major differences between bipolar I and bipolar II in regards to their clinical features, comorbidity rates and family histories. According to Baek et al. (2011), during depressive episodes, bipolar II patients tend to show higher rates of psychomotor agitation, guilt, shame, suicidal ideation, and suicide attempts. Bipolar II patients have shown higher lifetime comorbidity rates of DSM axis I diagnoses such as phobias, anxiety disorders, substance & alcohol use, and eating disorders and there is a higher correlation between bipolar II patients and family history of psychiatric illness, including major depression and substance-related disorders. The occurrence rate of psychiatric illness in first degree relatives of bipolar II patients was 26.5%, versus 15.4% in bipolar I patients.

Screening instruments like the Mood Disorders Questionnaire (MDQ) are helpful tools in determining a patient’s status on the bipolar spectrum, and getting families involved can also improve chances of an accurate diagnosis and acknowledgment of hypomanic episodes. In addition, there are certain features that have been shown to increase the chances that depressed patients are suffering from 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.

Specifiers

  • Chronic.
  • With Anxious Distress (DSM-5).
  • With catatonic features.
  • With melancholic features.
  • With psychotic features.
  • With atypical features.
  • With postpartum onset.
  • Longitudinal course specifiers (with and without inter-episode recovery).
  • With seasonal pattern (applies only to the pattern of major depressive episodes).
  • With rapid cycling.

Treatments

Treatment typically includes three things: the treatment of acute hypomania, the treatment of acute depression, and the prevention of the relapse of either hypomania or depression. The main goal is to make sure that patients do not harm themselves.

Medications

The most common treatment for reducing bipolar II disorder symptoms is medication, usually in the form of mood stabilisers. However, treatment with mood stabilisers may produce a flat affect in the patient, which is dose-dependent. Concurrent use of SSRI antidepressants may help some with bipolar II disorder, though these medications should be used with caution because it is believed that they may cause a hypomanic switch.

The pharmaceutical management of bipolar II disorder is not generally supported by strong evidence, with limited randomised controlled trials (RCTs) published in the literature. Some medications used are:

  • Lithium: There is strong evidence that lithium is effective in treating both the depressive and hypomanic symptoms in bipolar II. In addition, its action as a mood stabiliser can be used to decrease the risk of hypomanic switch in patients treated with antidepressants.
  • Anticonvulsants: There is evidence that lamotrigine decreases the risk of relapse in rapid-cycling bipolar II. It appears to be more effective in bipolar II than bipolar I, suggesting that lamotrigine is more effective for the treatment of depressive rather than manic episodes. Doses ranging from 100-200 mg have been reported to have the most efficacy, while experimental doses of 400 mg have rendered little response. A large, multicentre trial comparing carbamazepine and lithium over two and a half years found that carbamazepine was superior in terms of preventing future episodes of bipolar II, although lithium was superior in individuals with bipolar I. There is also some evidence for the use of valproate and topiramate, although the results for the use of gabapentin have been disappointing.
  • Antidepressants: There is evidence to support the use of SSRI and SNRI antidepressants in bipolar II. Some sources consider them to be one of the first-line treatments. However, antidepressants also pose significant risks, including a switch to mania, rapid cycling, and dysphoria, so many psychiatrists advise against their use for bipolar. When used, antidepressants are typically combined with a mood stabiliser.
  • Antipsychotics: There is good evidence for the use of quetiapine, which has been shown to help to prevent recurrence in mania and depression, and it has been approved by the US Food and Drug Administration (FDA) for this indication. There is also some evidence for the use of risperidone, although the relevant trial was not placebo-controlled and was complicated by the use of other medications in some of the patients.
  • Dopamine agonists: There is evidence for the efficacy of pramipexole from one RCT.

Non-Pharmaceutical Therapies

Non-pharmaceutical therapies can also help those with the illness. These include:

Relapse can still occur, despite continued medication and therapy.

Prognosis

There is evidence to suggest that bipolar II has a more chronic course of illness than bipolar I disorder. 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 bipolar I patients experience. The natural course of bipolar II disorder, when left untreated, leads to patients spending the majority of their lives unwell with much of their suffering stemming from depression. Their recurrent depression results in personal suffering and disability.

This disability can present itself in the form of psychosocial impairment, which has been suggested to be worse in bipolar II patients than in bipolar I patients. 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. Rapid cycling is quite common in those with Bipolar 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. Women are more prone to rapid cycling between hypomanic episodes and depressive episodes. To improve a patient’s prognosis, long-term therapy is most favourably 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.

Functioning

The deficits in functioning associated with Bipolar II disorder stem mostly from the recurrent depression that Bipolar II patients suffer from. Depressive symptoms are much more disabling than hypomanic symptoms and are potentially as, or more disabling than mania symptoms. 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 Bipolar II disorder, they have been implicated heavily as a major cause of psychosocial disability. 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 Bipolar II. It has been suggested that symptom interference in relation to social and interpersonal relationships in Bipolar II Disorder is worse than symptom interference in other chronic medical illnesses such as cancer. This social impairment can last for years, even after treatment that has resulted in a resolution of mood symptoms.

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

The impact on a patient’s psychosocial functioning stems from the depressive symptoms (more common in Bipolar II than Bipolar I). An increase in these symptoms’ severity seems to correlate with a significant increase in psychosocial disability. 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.

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. Bipolar II patients have also been shown to present worse cognitive functioning than those patients with Bipolar I, though they demonstrate about the same disability when it comes to occupational functioning, interpersonal relationships, and autonomy. 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 Bipolar II patient populations. After treatment and while in remission, Bipolar II patients tend to report a good psychosocial functioning but they still score less than patients without the disorder. These lasting impacts further suggest that a prolonged exposure to an untreated Bipolar II disorder can lead to permanent adverse effects on functioning.

Recovery and Recurrence

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

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. Even with treatment, patients do not always regain full functioning, especially in the social realm. There is a very clear gap between symptomatic recovery and full functional recovery for both Bipolar I and Bipolar II patients. As such, and because those with Bipolar 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. 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.

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

Along with medication, other forms of therapy have been shown to be beneficial for Bipolar 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. The plan has to aim high. Otherwise, patients will relapse into depression. 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.

Mortality

Several studies have shown that the risk of suicide is higher in patients who suffer from Bipolar II than those who suffer from Bipolar I, and especially higher than patients who suffer from major depressive disorder.

In results of a summary of several lifetime study experiments, it was found that 24% of Bipolar II patients experienced suicidal ideation or suicide attempts compared to 17% in Bipolar I patients and 12% in major depressive patients. Bipolar disorders, in general, are the third leading cause of death in 15 to 24 year olds. Bipolar II patients were also found to employ more lethal means and have more complete suicides overall.

Bipolar 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 Bipolar II, are also associated with an increased risk of suicide. The tendency for Bipolar II to be misdiagnosed and treated ineffectively, or not at all in some cases, leads to an increased risk.

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.

Suicide, which is both a stereotypic yet highly individualised act, is a common endpoint for many patients with severe psychiatric illness. The mood disorders (depression and bipolar manic-depression) 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. With the exception of lithium – which is the most demonstrably effective treatment against suicide – remarkably little is known about specific contributions of mood-altering treatments to minimising mortality rates in persons with major mood disorders in general and bipolar depression in particular. 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.

Society and Culture

Select list of people with bipolar disorder:

  • Heath Black revealed in his autobiography, Black, that he has been diagnosed with Bipolar II.
  • Maria Bamford has been diagnosed with Bipolar II.
  • Geoff Bullock, singer-songwriter, was diagnosed with Bipolar II.
  • Mariah Carey was diagnosed with Bipolar 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 Bipolar II.
  • Joe Gilgun has been diagnosed with Bipolar II.
  • Shane Hmiel has been diagnosed with Bipolar II.
  • Jesse Jackson Jr. has been diagnosed with Bipolar II.
  • Thomas Eagleton received a diagnosis of Bipolar II from Dr. Frederick K. Goodwin.
  • Carrie Fisher had been diagnosed with Bipolar II.
  • Albert Lasker is speculated to have had Bipolar II.
  • Demi Lovato has been diagnosed with Bipolar II.
  • Evan Perry, subject of the documentary Boy Interrupted, was diagnosed with Bipolar II.
  • Sylvia Plath is speculated to have had Bipolar II.
  • Richard Rossi, filmmaker, musician, and maverick minister was diagnosed with Bipolar II.
  • Rumer has been diagnosed with Bipolar II.
  • Robert Schumann is speculated to have had Bipolar II.
  • Catherine Zeta-Jones received treatment for Bipolar II disorder 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.

What is Bipolar I Disorder?

Introduction

Bipolar I disorder (BD-I; pronounced “type one bipolar disorder”) is a type of bipolar spectrum disorder characterised by the occurrence of at least one manic episode, with or without mixed or psychotic features.

Most people also, at other times, have one or more depressive episodes, and all experience a hypomanic stage before progressing to full mania.

It is a type of bipolar disorder, and conforms to the classic concept of manic-depressive illness, which can include psychosis during mood episodes.

Refer to Bipolar II Disorder and Mixed Affective State.

Bipolar mood shifts.

Diagnosis

The essential feature of bipolar I disorder is a clinical course characterised by the occurrence of one or more manic episodes or mixed episodes. Often, individuals have had one or more major depressive episodes. One episode of mania is sufficient to make the diagnosis of bipolar disorder; the person may or may not have a history of major depressive disorder. Episodes of substance-induced mood disorder due to the direct effects of a medication, or other somatic treatments for depression, drug abuse, or toxin exposure, or of mood disorder due to a general medical condition need to be excluded before a diagnosis of bipolar I disorder can be made. Bipolar I disorder requires confirmation of only 1 full manic episode for diagnosis, but may be associated with hypomanic and depressive episodes as well. Diagnosis for bipolar II disorder does not include a full manic episode; instead, it requires the occurrence of both a hypomanic episode and a major depressive episode. Serious aggression has been reported to occur in one of every ten first-major episode BD-I patients with psychotic features, its prevalence in this group being particularly high in association with a recent suicide attempt, alcohol-abuse, learning disability, or manic polarity in the first episode.

Bipolar I disorder (and bipolar II disorder) is often comorbid with other disorders including PTSD, substance use disorders and a variety of mood disorders. Up to 40% of people with bipolar disorder also present with PTSD, with higher rates occurring in women and individuals with bipolar I disorder. In addition, the episodes must not be better accounted for by schizoaffective disorder or superimposed on schizophrenia, schizophreniform disorder, delusional disorder, or a psychotic disorder not otherwise specified.

Medical Assessment

Regular medical assessments are performed to rule-out secondary causes of mania and depression. These tests include complete blood count, glucose, serum chemistry/electrolyte panel, thyroid function test, liver function test, renal function test, urinalysis, vitamin B12 and folate levels, HIV screening, syphilis screening, and pregnancy test, and when clinically indicated, an electrocardiogram (ECG), an electroencephalogram (EEG), a computed tomography (CT scan), and/or a magnetic resonance imagining (MRI) may be ordered. Drug screening includes recreational drugs, particularly synthetic cannabinoids, and exposure to toxins.

Diagnostic and Statistical Manual of Mental Disorders, 4th Edition (DSM-IV-TR)

Dx Code #DisorderDescription
296.0xBipolar ISingle manic episode
296.40Bipolar IMost recent episode hypomanic
296.4xBipolar IMost recent episode manic
296.5xBipolar IMost recent episode depressed
296.6xBipolar IMost recent episode mixed
296.7Bipolar IMost recent episode unspecified

Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5)

In May 2013, American Psychiatric Association released the fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-5). There are several proposed revisions to occur in the diagnostic criteria of Bipolar I Disorder and its subtypes. For Bipolar I Disorder 296.40 (most recent episode hypomanic) and 296.4x (most recent episode manic), the proposed revision includes the following specifiers: with psychotic features, with mixed features, with catatonic features, with rapid cycling, with anxiety (mild to severe), with suicide risk severity, with seasonal pattern, and with postpartum onset. Bipolar I Disorder 296.5x (most recent episode depressed) will include all of the above specifiers plus the following: with melancholic features and with atypical features. The categories for specifiers will be removed in DSM-5 and criterion A will add or there are at least 3 symptoms of major depression of which one of the symptoms is depressed mood or anhedonia. For Bipolar I Disorder 296.7 (most recent episode unspecified), the listed specifiers will be removed.

The criteria for manic and hypomanic episodes in criteria A & B will be edited. Criterion A will include “and present most of the day, nearly every day”, and criterion B will include “and represent a noticeable change from usual behaviour”. These criteria as defined in the DSM-IV-TR have created confusion for clinicians and need to be more clearly defined.

There have also been proposed revisions to criterion B of the diagnostic criteria for a Hypomanic Episode, which is used to diagnose For Bipolar I Disorder 296.40, Most Recent Episode Hypomanic. Criterion B lists “inflated self-esteem, flight of ideas, distractibility, and decreased need for sleep” as symptoms of a Hypomanic Episode. This has been confusing in the field of child psychiatry because these symptoms closely overlap with symptoms of attention deficit hyperactivity disorder (ADHD).

Note that many of the above changes are still under active consideration and are not definite. For more information regarding proposed revisions to the DSM-5, please visit their website at dsm5.org.

ICD-10

  • F31 Bipolar Affective Disorder.
  • F31.6 Bipolar Affective Disorder, Current Episode Mixed.
  • F30 Manic Episode.
  • F30.0 Hypomania.
  • F30.1 Mania Without Psychotic Symptoms.
  • F30.2 Mania With Psychotic Symptoms.
  • F32 Depressive Episode.
  • F32.0 Mild Depressive Episode.
  • F32.1 Moderate Depressive Episode.
  • F32.2 Severe Depressive Episode Without Psychotic Symptoms.
  • F32.3 Severe Depressive Episode With Psychotic Symptoms.

Treatment

Medication

Mood stabilisers are often used as part of the treatment process.

  • Lithium is the mainstay in the management of bipolar disorder but it has a narrow therapeutic range and typically requires monitoring.
  • Anticonvulsants, such as valproate, carbamazepine, or lamotrigine.
  • Atypical antipsychotics, such as quetiapine, risperidone, olanzapine, or aripiprazole.
  • Electroconvulsive therapy, a psychiatric treatment in which seizures are electrically induced in anesthetised patients for therapeutic effect.

Antidepressant-induced mania occurs in 20-40% of people with bipolar disorder. Mood stabilisers, especially lithium, may protect against this effect, but some research contradicts this.

A frequent problem in these individuals is nonadherence to pharmacological treatment; long-acting injectable antipsychotics may contribute to solving this issue in some patients.

A review of validated treatment guidelines for bipolar disorder by international bodies was published in 2020.

Education

Psychosocial interventions can be used for managing acute depressive episodes and for maintenance treatment to aid in relapse prevention. This includes psycho education, cognitive behavioural therapy (CBT), family-focused therapy (FFT), interpersonal and social-rhythm therapy (IPSRT), and peer support.

Information on the condition, importance of regular sleep patterns, routines and eating habits and the importance of compliance with medication as prescribed. Behaviour modification through counselling can have positive influence to help reduce the effects of risky behaviour during the manic phase. Additionally, the lifetime prevalence for bipolar I disorder is estimated to be 1%.

What is the Altman Self-Rating Mania Scale?

Introduction

The Altman Self-Rating Mania Scale (ASRM) is a 5-item self-reported diagnostic scale which can be used to assess the presence and severity manic and hypomanic symptoms, most commonly in patients diagnosed with bipolar disorder.

Effectiveness

The ASRM scale has been shown to be an effective self-reported questionnaire for screening patients with acute mania as well as measuring anti-manic treatment effects. Though only a 5-question instrument, the scale’s compatibility with the clinician administered Young Mania Rating Scale and the DSM-IV criteria give substantial diagnostic power for such a brief instrument.

Format

The Altman Self-Rating Mania Scale assess differences in “normal” or baseline levels in five subjective and behavioural areas:

  • Positive mood.
  • Self-confidence.
  • Sleep patterns.
  • Speech patterns and amount.
  • Motor activity.

Each of these areas has five statements which correspond to scores 0 through 4; with 0 being unchanged from “normal” or baseline, to 4 being overtly manic thoughts or behaviour. The subject is asked to choose one statement from each of the five areas that best describes the way they have been feeling over the past week.

Scoring

Scores above a 5 are indicative of mania, or hypomania, with the severity of symptoms increasing with higher scores. Examining score changes over time is also used to determine the efficacy of a particular treatment in a clinical setting and to qualify whether the severity a manic episode is increasing or decreasing.

What is Mania?

Introduction

Mania, also known as manic syndrome, is a mental and behavioural disorder defined as a state of abnormally elevated arousal, affect, and energy level, or “a state of heightened overall activation with enhanced affective expression together with lability of affect.”

During a manic episode, an individual will experience rapidly changing emotions and moods, highly influenced by surrounding stimuli. Although mania is often conceived as a “mirror image” to depression, the heightened mood can be either euphoric or dysphoric. As the mania intensifies, irritability can be more pronounced and result in anxiety or anger.

The symptoms of mania include elevated mood (either euphoric or irritable), flight of ideas and pressure of speech, increased energy, decreased need and desire for sleep, and hyperactivity. They are most plainly evident in fully developed hypomanic states. However, in full-blown mania, they undergo progressively severe exacerbations and become more and more obscured by other signs and symptoms, such as delusions and fragmentation of behaviour.

Refer to Bipolar I Disorder, Bipolar II Disorder, and Mixed Affective State.

Etymology

The nosology of the various stages of a manic episode has changed over the decades. The word derives from the Ancient Greek μανία (manía), “madness, frenzy” and the verb μαίνομαι (maínomai), “to be mad, to rage, to be furious”.

Causes and Diagnosis

Mania is a syndrome with multiple causes. Although the vast majority of cases occur in the context of bipolar disorder, it is a key component of other psychiatric disorders (such as schizoaffective disorder, bipolar type) and may also occur secondary to various general medical conditions, such as multiple sclerosis; certain medications may perpetuate a manic state, for example prednisone; or substances prone to abuse, especially stimulants, such as caffeine and cocaine. In the current DSM-5, hypomanic episodes are separated from the more severe full manic episodes, which, in turn, are characterised as either mild, moderate, or severe, with certain diagnostic criteria (e.g. catatonia, psychosis). Mania is divided into three stages:

  • Hypomania, or stage I;
  • Acute mania, or stage II; and
  • Delirious mania (delirium), or stage III.

This “staging” of a manic episode is useful from a descriptive and differential diagnostic point of view.

Mania varies in intensity, from mild mania (hypomania) to delirious mania, marked by such symptoms as disorientation, florid psychosis, incoherence, and catatonia. Standardised tools such as Altman Self-Rating Mania Scale and Young Mania Rating Scale can be used to measure severity of manic episodes. Because mania and hypomania have also long been associated with creativity and artistic talent, it is not always the case that the clearly manic/hypomanic bipolar patient needs or wants medical help; such persons often either retain sufficient self-control to function normally or are unaware that they have “gone manic” severely enough to be committed or to commit themselves. Manic persons often can be mistaken for being under the influence of drugs.

Classification

Mixed States

Refer to Mixed Affective State.

In a mixed affective state, the individual, though meeting the general criteria for a hypomanic (discussed below) or manic episode, experiences three or more concurrent depressive symptoms. This has caused some speculation, among clinicians, that mania and depression, rather than constituting “true” polar opposites, are, rather, two independent axes in a unipolar – bipolar spectrum.

A mixed affective state, especially with prominent manic symptoms, places the patient at a greater risk for suicide. Depression on its own is a risk factor but, when coupled with an increase in energy and goal-directed activity, the patient is far more likely to act with violence on suicidal impulses.

Hypomania

Refer to Hypomania.

Hypomania, which means “less than mania”, is a lowered state of mania that does little to impair function or decrease quality of life. It may, in fact, increase productivity and creativity. In hypomania, there is less need for sleep and both goal-motivated behaviour and metabolism increase. Some studies exploring brain metabolism in subjects with hypomania, however, did not find any conclusive link; while there are studies that reported abnormalities, some failed to detect differences. Though the elevated mood and energy level typical of hypomania could be seen as a benefit, true mania itself generally has many undesirable consequences including suicidal tendencies, and hypomania can, if the prominent mood is irritable as opposed to euphoric, be a rather unpleasant experience. In addition, the exaggerated case of hypomania can lead to problems. For instance, trait-based positivity for a person could make them more engaging and outgoing, and cause them to have a positive outlook in life. When exaggerated in hypomania, however, such a person can display excessive optimism, grandiosity, and poor decision making, often with little regard to the consequences.

Associated Disorders

A single manic episode, in the absence of secondary causes, (i.e. substance use disorders, pharmacologics, or general medical conditions) is often sufficient to diagnose bipolar I disorder. Hypomania may be indicative of bipolar II disorder. Manic episodes are often complicated by delusions and/or hallucinations; and if the psychotic features persist for a duration significantly longer than the episode of typical mania (two weeks or more), a diagnosis of schizoaffective disorder is more appropriate. Certain obsessive-compulsive spectrum disorders as well as impulse control disorders share the suffix “-mania,” namely, kleptomania, pyromania, and trichotillomania. Despite the unfortunate association implied by the name, however, no connection exists between mania or bipolar disorder and these disorders. Furthermore, evidence indicates a B12 deficiency can also cause symptoms characteristic of mania and psychosis.

Hyperthyroidism can produce similar symptoms to those of mania, such as agitation, elevated mood, increased energy, hyperactivity, sleep disturbances and sometimes, especially in severe cases, psychosis.

Signs and Symptoms

A manic episode is defined in the American Psychiatric Association’s diagnostic manual as a “distinct period of abnormally and persistently elevated, expansive, or irritable mood and abnormally and persistently increased activity or energy, lasting at least 1 week and present most of the day, nearly every day (or any duration, if hospitalisation is necessary),” where the mood is not caused by drugs/medication or a non-mental medical illness (e.g. hyperthyroidism), and: (a) is causing obvious difficulties at work or in social relationships and activities, or (b) requires admission to hospital to protect the person or others, or (c) the person is suffering psychosis.

To be classified as a manic episode, while the disturbed mood and an increase in goal-directed activity or energy is present, at least three (or four, if only irritability is present) of the following must have been consistently present:

  • Inflated self-esteem or grandiosity.
  • Decreased need for sleep (e.g. feels rested after 3 hours of sleep).
  • More talkative than usual, or acts pressured to keep talking.
  • Flights of ideas or subjective experience that thoughts are racing.
  • Increase in goal-directed activity, or psychomotor acceleration.
  • Distractibility (too easily drawn to unimportant or irrelevant external stimuli).
  • Excessive involvement in activities with a high likelihood of painful consequences.(e.g. extravagant shopping, improbable commercial schemes, hypersexuality).

Though the activities one participates in while in a manic state are not always negative, those with the potential to have negative outcomes are far more likely.

If the person is concurrently depressed, they are said to be having a mixed episode.

The World Health Organisation’s classification system defines a manic episode as one where mood is higher than the person’s situation warrants and may vary from relaxed high spirits to barely controllable exuberance, is accompanied by hyperactivity, a compulsion to speak, a reduced sleep requirement, difficulty sustaining attention, and/or often increased distractibility. Frequently, confidence and self-esteem are excessively enlarged, and grand, extravagant ideas are expressed. Behaviour that is out-of-character and risky, foolish or inappropriate may result from a loss of normal social restraint.

Some people also have physical symptoms, such as sweating, pacing, and weight loss. In full-blown mania, often the manic person will feel as though their goal(s) are of paramount importance, that there are no consequences, or that negative consequences would be minimal, and that they need not exercise restraint in the pursuit of what they are after. Hypomania is different, as it may cause little or no impairment in function. The hypomanic person’s connection with the external world, and its standards of interaction, remain intact, although intensity of moods is heightened. But those who suffer from prolonged unresolved hypomania do run the risk of developing full mania, and may cross that “line” without even realising they have done so.

One of the signature symptoms of mania (and to a lesser extent, hypomania) is what many have described as racing thoughts. These are usually instances in which the manic person is excessively distracted by objectively unimportant stimuli. This experience creates an absent-mindedness where the manic individual’s thoughts totally preoccupy them, making them unable to keep track of time, or be aware of anything besides the flow of thoughts. Racing thoughts also interfere with the ability to fall asleep.

Manic states are always relative to the normal state of intensity of the afflicted individual; thus, already irritable patients may find themselves losing their tempers even more quickly, and an academically gifted person may, during the hypomanic stage, adopt seemingly “genius” characteristics and an ability to perform and articulate at a level far beyond that which they would be capable of during euthymia. A very simple indicator of a manic state would be if a heretofore clinically depressed patient suddenly becomes inordinately energetic, enthusiastic, cheerful, aggressive, or “over-happy”. Other, often less obvious, elements of mania include delusions (generally of either grandeur or persecution, according to whether the predominant mood is euphoric or irritable), hypersensitivity, hypervigilance, hypersexuality, hyper-religiosity, hyperactivity and impulsivity, a compulsion to over explain (typically accompanied by pressure of speech), grandiose schemes and ideas, and a decreased need for sleep (for example, feeling rested after only 3 or 4 hours of sleep). In the case of the latter, the eyes of such patients may both look and seem abnormally “wide open”, rarely blinking, and may contribute to some clinicians’ erroneous belief that these patients are under the influence of a stimulant drug, when the patient, in fact, is either not on any mind-altering substances or is actually on a depressant drug. Individuals may also engage in out-of-character behaviour during the episode, such as questionable business transactions, wasteful expenditures of money (e.g. spending sprees), risky sexual activity, abuse of recreational substances, excessive gambling, reckless behaviour (such as extreme speeding or other daredevil activity), abnormal social interaction (e.g. over-familiarity and conversing with strangers), or highly vocal arguments. These behaviours may increase stress in personal relationships, lead to problems at work, and increase the risk of altercations with law enforcement. There is a high risk of impulsively taking part in activities potentially harmful to the self and others.

Although “severely elevated mood” sounds somewhat desirable and enjoyable, the experience of mania is ultimately often quite unpleasant and sometimes disturbing, if not frightening, for the person involved and for those close to them, and it may lead to impulsive behaviour that may later be regretted. It can also often be complicated by the sufferer’s lack of judgment and insight regarding periods of exacerbation of characteristic states. Manic patients are frequently grandiose, obsessive, impulsive, irritable, belligerent, and frequently deny anything is wrong with them. Because mania frequently encourages high energy and decreased perception of need or ability to sleep, within a few days of a manic cycle, sleep-deprived psychosis may appear, further complicating the ability to think clearly. Racing thoughts and misperceptions lead to frustration and decreased ability to communicate with others.

Mania may also, as earlier mentioned, be divided into three “stages”. Stage I corresponds with hypomania and may feature typical hypomanic characteristics, such as gregariousness and euphoria. In stages II and III mania, however, the patient may be extraordinarily irritable, psychotic or even delirious. These latter two stages are referred to as acute and delirious (or Bell’s), respectively.

Cause

Various triggers have been associated with switching from euthymic or depressed states into mania. One common trigger of mania is antidepressant therapy. Studies show that the risk of switching while on an antidepressant is between 6-69%. Dopaminergic drugs such as reuptake inhibitors and dopamine agonists may also increase risk of switch. Other medication possibly include glutaminergic agents and drugs that alter the hypothalamic-pituitary-adrenal (HPA) axis. Lifestyle triggers include irregular sleep-wake schedules and sleep deprivation, as well as extremely emotional or stressful stimuli.

Various genes that have been implicated in genetic studies of bipolar have been manipulated in preclinical animal models to produce syndromes reflecting different aspects of mania. CLOCK and DBP polymorphisms have been linked to bipolar in population studies, and behavioural changes induced by knockout are reversed by lithium treatment. Metabotropic glutamate receptor 6 has been genetically linked to bipolar, and found to be under-expressed in the cortex. Pituitary adenylate cyclase-activating peptide has been associated with bipolar in gene linkage studies, and knockout in mice produces mania like-behaviour. Targets of various treatments such as GSK-3, and ERK1 have also demonstrated mania like behaviour in preclinical models.

Mania may be associated with strokes, especially cerebral lesions in the right hemisphere.

Deep brain stimulation of the subthalamic nucleus in Parkinson’s disease has been associated with mania, especially with electrodes placed in the ventromedial STN. A proposed mechanism involves increased excitatory input from the STN to dopaminergic nuclei.

Mania can also be caused by physical trauma or illness. When the causes are physical, it is called secondary mania.

Mechanism

Refer to Biology of Bipolar Disorder.

The mechanism underlying mania is unknown, but the neurocognitive profile of mania is highly consistent with dysfunction in the right prefrontal cortex, a common finding in neuroimaging studies. Various lines of evidence from post-mortem studies and the putative mechanisms of anti-manic agents point to abnormalities in GSK-3, dopamine, Protein kinase C and Inositol monophosphatase.

Meta analysis of neuroimaging studies demonstrate increased thalamic activity, and bilaterally reduced inferior frontal gyrus activation. Activity in the amygdala and other subcortical structures such as the ventral striatum tend to be increased, although results are inconsistent and likely dependent upon task characteristics such as valence. Reduced functional connectivity between the ventral prefrontal cortex and amygdala along with variable findings supports a hypothesis of general dysregulation of subcortical structures by the prefrontal cortex. A bias towards positively valenced stimuli, and increased responsiveness in reward circuitry may predispose towards mania. Mania tends to be associated with right hemisphere lesions, while depression tends to be associated with left hemisphere lesions.

Post-mortem examinations of bipolar disorder demonstrate increased expression of Protein Kinase C (PKC). While limited, some studies demonstrate manipulation of PKC in animals produces behavioural changes mirroring mania, and treatment with PKC inhibitor tamoxifen (also an anti-oestrogen drug) demonstrates antimanic effects. Traditional antimanic drugs also demonstrate PKC inhibiting properties, among other effects such as GSK3 inhibition.

Manic episodes may be triggered by dopamine receptor agonists, and this combined with tentative reports of increased VMAT2 activity, measured via PET scans of radioligand binding, suggests a role of dopamine in mania. Decreased cerebrospinal fluid levels of the serotonin metabolite 5-HIAA have been found in manic patients too, which may be explained by a failure of serotonergic regulation and dopaminergic hyperactivity.

Limited evidence suggests that mania is associated with behavioural reward hypersensitivity, as well as with neural reward hypersensitivity. Electrophysiological evidence supporting this comes from studies associating left frontal EEG activity with mania. As left frontal EEG activity is generally thought to be a reflection of behavioural activation system activity, this is thought to support a role for reward hypersensitivity in mania. Tentative evidence also comes from one study that reported an association between manic traits and feedback negativity during receipt of monetary reward or loss. Neuroimaging evidence during acute mania is sparse, but one study reported elevated orbitofrontal cortex activity to monetary reward, and another study reported elevated striatal activity to reward omission. The latter finding was interpreted in the context of either elevated baseline activity (resulting in a null finding of reward hypersensitivity), or reduced ability to discriminate between reward and punishment, still supporting reward hyperactivity in mania. Punishment hyposensitivity, as reflected in a number of neuroimaging studies as reduced lateral orbitofrontal response to punishment, has been proposed as a mechanism of reward hypersensitivity in mania.

Diagnosis

In the ICD-10 there are several disorders with the manic syndrome:

  • Organic manic disorder (F06.30).
  • Mania without psychotic symptoms (F30.1).
  • Mania with psychotic symptoms (F30.2).
  • Other manic episodes (F30.8).
  • Unspecified manic episode (F30.9).
  • Manic type of schizoaffective disorder (F25.0).
  • Bipolar affective disorder, current episode manic without psychotic symptoms (F31.1).
  • Bipolar affective disorder, current episode manic with psychotic symptoms (F31.2).

Treatment

Before beginning treatment for mania, careful differential diagnosis must be performed to rule out secondary causes.

The acute treatment of a manic episode of bipolar disorder involves the utilisation of either a mood stabiliser (Carbamazepine, valproate, lithium, or lamotrigine) or an atypical antipsychotic (olanzapine, quetiapine, risperidone, or aripiprazole). The use of antipsychotic agents in the treatment of acute mania was reviewed by Tohen and Vieta in 2009.

When the manic behaviours have gone, long-term treatment then focuses on prophylactic treatment to try to stabilise the patient’s mood, typically through a combination of pharmacotherapy and psychotherapy. The likelihood of having a relapse is very high for those who have experienced two or more episodes of mania or depression. While medication for bipolar disorder is important to manage symptoms of mania and depression, studies show relying on medications alone is not the most effective method of treatment. Medication is most effective when used in combination with other bipolar disorder treatments, including psychotherapy, self-help coping strategies, and healthy lifestyle choices.

Lithium is the classic mood stabiliser to prevent further manic and depressive episodes. A systematic review found that long term lithium treatment substantially reduces the risk of bipolar manic relapse, by 42%. Anticonvulsants such as valproate, oxcarbazepine and carbamazepine are also used for prophylaxis. More recent drug solutions include lamotrigine and topiramate, both anticonvulsants as well.

In some cases, long-acting benzodiazepines, particularly clonazepam, are used after other options are exhausted. In more urgent circumstances, such as in emergency rooms, lorazepam, combined with haloperidol, is used to promptly alleviate symptoms of agitation, aggression, and psychosis.

Antidepressant monotherapy is not recommended for the treatment of depression in patients with bipolar disorders I or II, and no benefit has been demonstrated by combining antidepressants with mood stabilisers in these patients. Some atypical antidepressants, however, such as mirtazepine and trazodone have been occasionally used after other options have failed.

Society and Culture

In Electroboy: A Memoir of Mania by Andy Behrman, he describes his experience of mania as “the most perfect prescription glasses with which to see the world… life appears in front of you like an oversized movie screen”. Behrman indicates early in his memoir that he sees himself not as a person suffering from an uncontrollable disabling illness, but as a director of the movie that is his vivid and emotionally alive life. There is some evidence that people in the creative industries suffer from bipolar disorder more often than those in other occupations. Winston Churchill had periods of manic symptoms that may have been both an asset and a liability.

English actor Stephen Fry, who suffers from bipolar disorder, recounts manic behaviour during his adolescence: “When I was about 17 … going around London on two stolen credit cards, it was a sort of fantastic reinvention of myself, an attempt to. I bought ridiculous suits with stiff collars and silk ties from the 1920s, and would go to the Savoy and Ritz and drink cocktails.” While he has experienced suicidal thoughts, he says the manic side of his condition has had positive contributions on his life.

What is Hypomania?

Introduction

Hypomania (literally “under mania” or “less than mania”) is a mental and behavioural disorder, characterised essentially by an apparently non-contextual elevation of mood (euphoria) which contributes to persistently disinhibited behaviour.

The individual afflicted may suffer with irritability, not necessarily less severe than full mania; in fact, the presence of marked irritability is a documented feature of hypomanic and mixed episodes in Bipolar type II. According to DSM-5 criteria, hypomania is distinct from mania in that there is no significant functional impairment; mania, by DSM-5 definition, does include significant functional impairment and may have psychotic features.

Characteristic behaviours of persons experiencing hypomania are a notable decrease in the need for sleep, an overall increase in energy, unusual behaviours and actions, and a markedly distinctive increase in talkativeness and confidence, commonly exhibited with a flight of creative ideas. Other symptoms related to this may include feelings of grandiosity, distractibility, and hypersexuality. While hypomanic behaviour often generates productivity and excitement, it can become troublesome if the subject engages in risky or otherwise inadvisable behaviours, and/or the symptoms manifest themselves in trouble with everyday life events. When manic episodes are separated into stages of a progression according to symptomatic severity and associated features, hypomania constitutes the first stage of the syndrome, wherein the cardinal features (euphoria or heightened irritability, pressure of speech and activity, increased energy, decreased need for sleep, and flight of ideas) are most plainly evident.

Refer to Bipolar I Disorder, Bipolar II Disorder, and Mixed Affective State.

Etymology

The Ancient Greek physician Hippocrates called one personality type ‘hypomanic’ (Greek: ὑπομαινόμενοι, hypomainómenoi). In 19th century psychiatry, when mania had a broad meaning of insanity, 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 into consideration the word used by Hippocrates, to name those types of mania that show a less severe phenomenological picture, ‘hypomania'”. Narrower operational definitions of hypomania were developed in the 1960s and 1970s.

Signs and Symptoms

Individuals in a hypomanic state have a decreased need for sleep, are extremely gregarious and competitive, and have a great deal of energy. They are, otherwise, often fully functioning (unlike individuals suffering from a full manic episode).

Distinctive Markers

Specifically, hypomania is distinguished from mania by the absence of psychotic symptoms, and by its lesser degree of impact on functioning.

Hypomania is a feature of bipolar II disorder and cyclothymia, but can also occur in schizoaffective disorder. Hypomania is also a feature of bipolar I disorder; it arises in sequential procession as the mood disorder fluctuates between normal mood (euthymia) and mania. Some individuals with bipolar I disorder have hypomanic as well as manic episodes. Hypomania can also occur when moods progress downwards from a manic mood state to a normal mood. Hypomania is sometimes credited with increasing creativity and productive energy. Numerous people with bipolar disorder have credited hypomania with giving them an edge in their theatre of work.

People who experience hyperthymia, or “chronic hypomania”, encounter the same symptoms as hypomania but on a longer-term basis.

Associated Disorders

Cyclothymia, a condition of continuous mood fluctuations, is characterised by oscillating experiences of hypomania and depression that fail to meet the diagnostic criteria for either manic or major depressive episodes. These periods are often interspersed with periods of relatively normal (euthymic) functioning.

When a patient presents with a history of at least one episode of both hypomania and major depression, each of which meet the diagnostic criteria, bipolar II disorder is diagnosed. In some cases, depressive episodes routinely occur during the fall or winter and hypomanic ones in the spring or summer. In such cases, one speaks of a “seasonal pattern”.

If left untreated, and in those so predisposed, hypomania may transition into mania, which may be psychotic, in which case bipolar I disorder is the correct diagnosis.

Causes

Often in those who have experienced their first episode of hypomania – generally without psychotic features – there may be a long or recent history of depression or a mix of hypomania combined with depression (known as mixed-state) prior to the emergence of manic symptoms. This commonly surfaces in the mid to late teens. Because the teenage years are typically an emotionally charged time of life, it is not unusual for mood swings to be passed off as normal hormonal teen behaviour and for a diagnosis of bipolar disorder to be missed until there is evidence of an obvious manic or hypomanic phase.

In cases of drug-induced hypomanic episodes in unipolar depressives, the hypomania can almost invariably be eliminated by lowering medication dosage, withdrawing the drug entirely, or changing to a different medication if discontinuation of treatment is not possible.

Hypomania can be associated with narcissistic personality disorder.

Psychopathology

Mania and hypomania are usually studied together as components of bipolar disorders, and the pathophysiology is usually assumed to be the same. Given that norepinephrine and dopaminergic drugs are capable of triggering hypomania, theories relating to monoamine hyperactivity have been proposed. A theory unifying depression and mania in bipolar individuals proposes that decreased serotonergic regulation of other monoamines can result in either depressive or manic symptoms. Lesions on the right side frontal and temporal lobes have further been associated with mania.

Diagnosis

The DSM-IV-TR defines a hypomanic episode as including, over the course of at least four days, elevated mood plus three of the following symptoms OR irritable mood plus four of the following symptoms, when the behaviours are clearly different from how the person typically acts when not depressed:

  • Pressured speech.
  • Inflated self-esteem or grandiosity.
  • Decreased need for sleep.
  • Flight of ideas or the subjective experience that thoughts are racing.
  • Easily distracted.
  • Increase in goal-directed activity (e.g. social activity, at work, or hypersexuality), or psychomotor agitation.
  • Involvement in pleasurable activities that may have a high potential for negative psycho-social or physical consequences (e.g. the person engages in unrestrained buying sprees, sexual indiscretions, reckless driving, physical and verbal conflicts, foolish business investments, quitting a job to pursue some grandiose goal, etc.).

Treatment

Medications

Antimanic drugs are used to control acute attacks and prevent recurring episodes of hypomania combined with a range of psychological therapies. The recommended length of treatment ranges from 2 years to 5 years. Anti-depressants may also be required for existing treatments but are avoided in patients who have had a recent history with hypomania. Sertraline has often been debated to have side effects that can trigger hypomania.

A Quick Overview of Bipolar Disorder

Introduction

The following is a quick overview of and topical guide to bipolar disorder (you can find a detailed article on Bipolar Disorder here and an Overview of Bipolar Disorder in Children here).

Bipolar disorder is characterised by episodes of depression and mania.

Bipolar disorder is a mental disorder with periods of depression and periods of elevated mood. The elevated mood is significant and is known as mania or hypomania, depending on its severity, or whether symptoms of psychosis are present. During mania, an individual behaves or feels abnormally energetic, happy, or irritable. Individuals often make poorly thought out decisions with little regard to the consequences. The need for sleep is usually reduced during manic phases. During periods of depression, there may be crying, a negative outlook on life, and poor eye contact with others. The risk of suicide among those with the illness is high at greater than 6% over 20 years, while self-harm occurs in 30-40%. Other mental health issues such as anxiety disorders and substance use disorder are commonly associated. Also known as manic depression.

What is Bipolar Disorder?

Bipolar disorder can be described as all of the following:

  • Mental disorder.
  • Functional abnormality or disturbance characterised by a behavioural or mental pattern that may cause suffering or a poor ability to function in life.
  • Such features may be persistent, relapsing and remitting, or occur as a single episode.

You can find an overview of the Biology of Bipolar Disorder here.

Bipolar Spectrum

TypeDescription
Bipolar IBipolar disorder with at least one manic episode (with or without psychosis), possibly with hypomanic and/or depressive episodes as well.
Bipolar IIbipolar disorder with at least one depressive and at least one hypomanic episode, without any full mania.
Cyclothymia“Mild” bipolar disorder, with symptoms of hypomania and depression not severe enough to be classified as bipolar I or II.
DysthymiaAkin to depression, with symptoms that are long-lasting but less severe.
Major Depressive DisorderA mood disorder involving low mood, low energy, poor self-esteem, lack of interest in enjoyable activities, and/or aches and pains.
Schizoaffective DisorderMood swings combined with psychosis; has subtypes bipolar type and depressive type.
ManiaA state of hyperactivity, heightened mood (euphoric or irritable), low sleep, pressured speech, grandiosity, and/or racing thoughts; may include psychotic features like delusions or hallucinations.
Mixed Affective StateA state with traits of both mania and depression (e.g. irritability, low mood, suicidality, and racing thoughts at the same time).
HypomaniaA state of high mood similar to that of mania but less severe.
Major Depressive EpisodeAn episode with signs of major depressive disorder.

Symptoms of Bipolar Disorder

  • General:
    • Anxiety: A state of increased stress and worry.
    • Emotional dysregulation: Difficulty regulating one’s mood, resulting in mood swings.
    • Sleep disorder: Disordered sleeping habits.
  • Signs Typical of Mania:
    • Delusion: Fixed belief that cannot be changed despite reason or evidence, not explained by common cultural beliefs.
    • Hallucination: Perceiving something that is not actually present.
    • Insomnia: Difficulty falling and/or staying asleep.
    • Pressured speech: Rapid, erratic, and/or frenzied speech that can be difficult for others to understand and interrupt.
    • Psychosis: Inability to distinguish between reality and fantasy.
    • Racing thoughts: Rapid thinking, sometimes experienced as distracting or distressing.
  • Signs Typical of Depression:
    • Anhedonia: Reduced ability to experience pleasure.
    • Dysphoria: A state of profound unhappiness or discomfort.
    • Hypersomnia: Excessive sleeping and/or sleepiness.
    • Self harm: Causing intentional pain or injury to the body, often as self-punishment or emotional release.
    • Suicidal ideation: Considering committing suicide.

Treatment of Bipolar Disorder

Medication

  • Mood stabilisers: medication that reduces mood swings and allows the user to experience a more typical range of moods.
  • Anticonvulsants.
  • Carbamazepine.
  • Gabapentin.
  • Lamotrigine (Lamictal).
  • Oxcarbazepine.
  • Topiramate.
  • Valproic acid.
  • Sodium valproate.
  • Valproate semisodium.
  • Lithium pharmacology.
  • Lithium carbonate.
  • Lithium citrate.
  • Lithium sulfate.
  • Antipsychotics.
  • Alprazolam (Solanax and Xanax).
  • Benzodiazepines.

Non-Pharmaceutical Treatment of Bipolar Disorder

  • Clinical psychology.
  • Electroconvulsive therapy.
  • Involuntary commitment.
  • Light therapy.
  • Psychotherapy.
  • Transcranial magnetic stimulation.