In psychology, logorrhea or logorrhoea (from Ancient Greek λόγος logos “word” and ῥέω rheo “to flow”), is a communication disorder that causes excessive wordiness and repetitiveness, which can cause incoherency.
Logorrhoea is sometimes classified as a mental illness, though it is more commonly classified as a symptom of mental illness or brain injury. This ailment is often reported as a symptom of Wernicke’s aphasia, where damage to the language processing centre of the brain creates difficulty in self-centred speech.
Logorrhoea is characterised by the constant need to talk. Occasionally, patients suffering from logorrhoea may produce speech with normal prosody and a slightly fast speech rate. Other related symptoms include the use of neologisms (new words without clear derivation, e.g. hipidomateous for hippopotamus), words that bear no apparent meaning, and, in some extreme cases, the creation of new words and morphosyntactic constructions. From the “stream of unchecked nonsense often under pressure and the lack of self-correction” that the patient may exhibit, and their circumlocution (the ability to talk around missing words) we may conclude that they are unaware of the grammatical errors they are making.
Examples of Logorrhoea
When a clinician said, “Tell me what you do with a comb”, to a patient suffering from mild Wernicke’s aphasia (which produces the symptom of logorrhoea), the patient responded:
“What do I do with a comb … what I do with a comb. Well a comb is a utensil or some such thing that can be used for arranging and rearranging the hair on the head both by men and by women. One could also make music with it by putting a piece of paper behind and blowing through it. Sometimes it could be used in art – in sculpture, for example, to make a series of lines in soft clay. It’s usually made of plastic and usually black, although it comes in other colors. It is carried in the pocket or until it’s needed, when it is taken out and used, then put back in the pocket. Is that what you had in mind?”
In this case, the patient maintained proper grammar and did not exhibit any signs of neologisms. However, the patient did use an overabundance of speech in responding to the clinician, as most people would simply respond, “I use a comb to comb my hair.”
In a more extreme version of logorrhoea aphasia, a clinician asked a male patient, also with Wernicke’s aphasia, what brought him to the hospital. The patient responded:
“Is this some of the work that we work as we did before? … All right … From when wine [why] I’m here. What’s wrong with me because I … was myself until the taenz took something about the time between me and my regular time in that time and they took the time in that time here and that’s when the time took around here and saw me around in it’s started with me no time and I bekan [began] work of nothing else that’s the way the doctor find me that way…”
In this example, the patient’s aphasia was much more severe. Not only was this a case of logorrhoea, but this included neologisms (such as “taenz” for “stroke” and “regular time” for “regular bath”) and a loss of proper sentence structure.
Logorrhoea has been shown to be associated with traumatic brain injuries in the frontal lobe as well as with lesions in the thalamus] and the ascending reticular inhibitory system and has been associated with aphasia. Logorrhoea can also result from a variety of psychiatric and neurological disorders including tachypsychia, mania, hyperactivity, catatonia, ADHD and schizophrenia.
Wernicke’s Aphasia, amongst other aphasias, are often associated with logorrhoea. Aphasia refers to the neurological disruption of language that occurs as a consequence of brain dysfunction. For a patient to truly have an aphasia, they cannot have been diagnosed with any other medical condition that may affect their cognition. Logorrhoea is a common symptom of Wernicke’s Aphasia, along with circumlocution, paraphasias, and neologisms. Often a patient with aphasia may present all of these symptoms at one time.
Excessive talking may be a symptom of an underlying illness and should be addressed by a medical provider if combined with hyperactivity or symptoms of mental illness, such as hallucinations. Treatment of logorrhoea depends on its underlying disorder, if any. Antipsychotics are often used, and lithium is a common supplement given to manic patients. For patients with lesions of the brain, attempting to correct their errors may upset and anger the patients, since the language centre of their brain may not be able to process that what they are saying is incorrect and wordy.
The concept has its origins as far back as the year 1889, when the German psychiatrist Emil Kraepelin first used the term of “periodic mania” to refer to people with recurrent manic episodes and no depression. One year later, Carl Wernicke proposed that mania and depression should be viewed as separate disorders. As the time went on, unipolar mania became an invalid diagnosis due to its variations across different patients. Currently patients with symptoms of mania, even in the absence of any depressive symptoms, would get the bipolar 1 diagnosis.
Symptoms of unipolar mania are similar to those of bipolar mania. They can include:
Secondary mania, also known as organic mania, is a variation of bipolar disorder that is caused by physical trauma or illness.
Bipolar disorder has a 1% prevalence rate in the United States and secondary mania is likely a small subset of that percentage. Secondary mania exhibits symptoms similar to that of mania in bipolar I and bipolar II disorders. This includes an elevated mood or affect, psychotic state, accelerated speech, increased motor activity, irritability, and flight ideas. A unique criterion for secondary mania is the lack of history of mental illness that causes mania, such as bipolar disorder. Unlike bipolar disorder, which has an average age of onset at 25 years, secondary mania has an average age of onset at 45 years. Little is known about secondary mania, as much of the research on it is case studies and retrospective accounts. However, it has been connected to several causes such as traumatic brain injury, HIV/AIDS, and stroke.
One of the primary documented causes of secondary mania is traumatic brain injury, also called closed-head injury. For example, Jorge and colleagues examined the effects of traumatic brain injury and its correlation with secondary mania. They collected participants that in the previous year had had traumatic brain injuries. They did 3, 6, and 12-month follow-ups with the patients where they took psychiatric interviews to measure impairment of daily life, intellectual, and social function. Within the 9% of patients that met the criteria for secondary mania, a correlation between secondary mania and temporal basal polar lesion was found. On average, the duration of secondary mania was 2 months. A second study found that out of 66 patients with a closed head injury, 9% experienced mania during the 12-month period after their injury.
In a case study a 24-year-old man complained of symptoms of mania. He had no prior mental health issues, no family history for mental health disorders, and no history of substance abuse. After a medical examination, he was diagnosed with mania and psychotic symptoms. Soon after he reported having a severe headache and after examination it was found he had a heterogeneous lesion covering most of his left thalamus. After the lesion was discovered, his diagnosis was revised to be “organic mood disorder (left cerebral AVM, Arteriovenous malformation, with secondary mania)”. Another study by Jorge and colleagues looked at the effects of traumatic brain injury and its correlation with secondary mania.
Secondary mania has been associated with HIV/AIDS in a number of cases. According to Ellen and colleagues, secondary mania is reported in 1.2% of HIV-positive patients and 4.3% positive in those with AIDS. In one case study by Chou and colleagues, a 78-year-old man was admitted to the hospital for manic symptoms. “The symptoms included decreased sleep, elevated mood, increased energy, hyperactivity, racing thoughts, and eccentric behaviour”. The patient had no prior history of mental health problems in his family or his own medical records. He was temporarily diagnosed with bipolar one. It was later discovered that he suffered from HIV/AIDS and his diagnosis was altered to secondary mania.
Many drugs have direct or indirect effects on neurotransmitters. Steroids are especially proficient at causing changes to the chemistry of neurotransmitters. In a study, 40 women were given steroids to help with their rheumatoid arthritis. Three subjects developed manic symptoms within the first week of taking the steroid. Two had never had a diagnosis of a mental illness, and one of the three women was noted to be “emotionally labile” and had had a suicide attempt but no hospitalisation. It was noted that the mania was not caused by an electrolyte imbalance, but the exact cause was uncertain.
According to Ogawa and Ueki, secondary mania has also been associated with caffeine consumption. A 43-year-old man, with no prior history of mental illness, reportedly switched to drinking 10 cups of coffee a day. After consuming this amount, he was reported to have manic symptoms such as elevated mood, talkativeness, hyperactivity, grandiosity, flight of ideas, and insomnia. This led to his admission into a hospital. After examination, they removed caffeine from the man’s diet, resulting in the cessation of manic symptoms. The doctors then concluded that either the caffeine had acted as a catalyst for bipolar disorder or that he had secondary mania. Unfortunately, little research is done on studying the interaction between mood disorders and caffeine.
A case study by Liang and Yang was of a 75-year-old woman who was admitted to the hospital with fever, chills, headache, and vomiting. Upon doing a mental test, they discovered she had symptoms of mania. However, she had no prior history of mental illness. When speaking with the family they discovered that the symptoms had manifested two weeks prior. Eventually, she was diagnosed with enterococcal meningitis for her physical symptoms and secondary mania for her psychological symptoms. The study stated that the exact link between the secondary mania and the enterococcal meningitis is unknown.
Since its first discovery over 30 years ago, secondary mania has been difficult to conceptualise. The primary arguments regarding its aetiology are:
Secondary mania is a form of toxic psychosis rather than actual mania; and
Secondary mania is really latent bipolar disorder that happened to coincide with an injury.
Toxic psychosis is a state which is caused by substance abuse; this could mean being in a confused state from the substance. The main argument against this theory is that mania in general has toxic origins and secondary mania is no different in this regard. However, analyses of secondary mania tend to exclude cases in which the person experienced high levels of confusion. Therefore, stating that it is a toxic state does not take away from the validity of its existence as long as the cases of secondary mania are narrowed to those without the confused state. The second argument is harder to dispute, as it is possible that secondary mania is late-onset bipolar disorder. The way this claim is disputed is through looking at the history of the patient. They check to see if there is a negative pre-morbid history, a lack of history of mental illness, age of onset, and the close proximity of the organic trauma to the mania.
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.
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.
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.
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.
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 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 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.
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.
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.
Bipolar disorder in children, or paediatric bipolar disorder (PBD), is a controversial mental disorder in children and adolescents that is mainly diagnosed in the United States, and is hypothesized to be like bipolar disorder (BD) in adults, thus is proposed as an explanation for extreme changes in mood and behaviour accompanying periods of depressed or irritable moods and periods of elevated moods so called manic or hypomanic episodes.
These shifts are sometimes quick, but usually are gradual. The average age of onset of paediatric bipolar disorder is unclear, but the risk increases with the onset of puberty. Bipolar disorder is rare in childhood. Paediatric bipolar disorder is typically more severe and has a poorer prognosis than bipolar disorder with onset in late-adolescence or adulthood.
The DSM has specified that the criteria for bipolar disorder can be applied to children since 1980. However, the exact criteria for diagnosing paediatric bipolar disorder remains controversial and heavily debated. There are big differences in how commonly it is diagnosed across clinics and in different countries. There has been a rapid increase in research on the topic, but training and clinical practice lag behind.
Identifying bipolar disorder in youth is challenging. Children often exhibit chronic rather than episodic mania periods. Almost always, these chronic problems have causes other than bipolar disorder. The criteria for paediatric bipolar disorder can also often be masked by developmental differences. Comorbid disorders make determining what symptoms are signs of bipolar disorder and which are due to other disorders (e.g. OCD, ADHD, disruptive behaviour problems) difficult, leading to complications in treatment. For example, a common treatment for OCD are serotonin re-uptake inhibitors (SRIs), however, SRIs can lead to mood instability and worsening bipolar disorder. The most common misdiagnosis for ADHD in the USA is paediatric bipolar disorder due to hyperactivity being described as prolonged periods of mania. Empirical research conducted in 2004 found that “bipolar disorder (in preadolescence) was initially misdiagnosed in 12 out of 24 youths” (Mahoney, 2004). This is a dangerous misdiagnosis due to the vastly different treatment forms. Firstly, ADHD does not require mood stabilisers like paediatric bipolar disorder. Secondly, the stimulants given to treat ADHD have been shown to cause psychosis and exacerbate mania in paediatric bipolar disorder (Wendling, 2009). This misuse of medication can lead to mood episodes, suicidality, and hospitalisation.
Descriptions of children with symptoms similar to contemporary concepts of mania date back to the 18th century. In 1898, a detailed psychiatric case history was published about a 13-year-old that met Jean-Pierre Falret and Jules Baillarger’s criteria for folie circulaire, which is congruent to the modern conception of bipolar I disorder.
In Emil Kraepelin’s descriptions of bipolar disorder in the 1920s, which he called “manic depressive insanity”, he noted the rare possibility that it could occur in children. In addition to Kraepelin, Adolf Meyer, Karl Abraham, and Melanie Klein were some of the first to document bipolar disorder symptoms in children in the first half of the 20th century. It was not mentioned much in English literature until the 1970s when interest in researching the subject increased. It became more accepted as a diagnosis in children in the 1980s after the DSM-III (1980) specified that the same criteria for diagnosing bipolar disorder in adults could also be applied to children.
Recognition came twenty years after, with epidemiological studies showing that approximately 20% of adults with bipolar disorder already had symptoms in childhood or adolescence. Nevertheless, onset before age 10 was thought to be rare, below 0.5% of the cases. During the second half of the century misdiagnosis with schizophrenia was not rare in the non-adult population due to common co-occurrence of psychosis and mania, this issue diminishing with an increased following of the DSM criteria in the last part of the 20th century.
The prevalence of bipolar in youth is estimated at 2%.
Diagnosis is made based on a clinical interview by a psychiatrist or other licensed mental health practitioner. There are no blood tests or brain scans to diagnose bipolar disorder. Obtaining information on family history and the use of questionnaires and checklists are helpful in making an accurate diagnosis. Commonly used assessment tools include the:
In both the American Psychiatric Association’s DSM-5 and the World Health Organisation’s ICD-10, the same criteria used to diagnose bipolar disorder in adults are used to make the diagnosis in children with some adjustments to account for differences in age and developmental stage. For example, the DSM-5 specifies that in children, depressive episodes can manifest as persistently irritable moods.
In diagnosing manic episodes, it is important to compare the changes in mood and behaviour to the child’s normal mood and behaviours at baseline instead of to other children or adults. For example, grandiosity (i.e. unrealistic overestimation of one’s intelligence, talent, or abilities) is normal at varying degrees during childhood and adolescence. Therefore, grandiosity is only considered symptomatic of mania in children when the beliefs are held despite being presented with concrete evidence otherwise or when they lead to a child attempting activities that are clearly dangerous, and most importantly, when the grandiose beliefs are an obvious change from that particular child’s normal self-view in between episodes.
The diagnosis of childhood bipolar disorder is controversial, although it is recognised that bipolar disorder typical symptoms are dysfunctional and have negative consequences for minors suffering them. Main discussion is centred on whether what is called bipolar disorder in children refers to the same disorder than when diagnosing adults, and the related question on whether adults’ criteria for diagnosis are useful and accurate when applied to children. More specifically, main discussion over diagnosis in children circles around mania symptomatology and its differences between children and adults.
Diagnostic criteria may not correctly separate children with bipolar disorder from other problems such as ADHD, and emphasize fast mood cycles.
Medications can produce important side effects, so interventions have been recommended to be closely monitored and families of patients to be informed of the different possible problems that can arise. Atypical antipsychotics are more effective than mood stabilizers, but have more side effects. Typical antipsychotics may produce weight gains as well as other metabolic problems, including diabetes mellitus type 2 and hyperlipidaemia. Extrapyramidal secondary effects may appear with these medications. These include tardive dyskinesia, a difficult-to-treat movement disorder (dyskinesia) that can appear after long-term use of antipsychotics. Liver and kidney damage are a possibility with mood stabilisers.
Psychological treatment usually includes some combination of education on the disease, group therapy and cognitive behavioural therapy (CBT). Children with bipolar disorder and their families are informed, in ways accordingly to their age and family role, about the different aspects of bipolar disorder and its management including causes, signs and symptoms and treatments. Group therapy aims to improve social skills and manage group conflicts, with role-playing as a critical tool. Finally, cognitive-behavioural training is directed towards the participants having a better understanding and control over their emotions and behaviours.
Lithium or Divalproex is recommended for first-line treatment.
Partial (minimal to moderate) improvement with monotherapy, augment with another of the first-line recommendations.
Stage 2: Monotherapy with an alternative drug, then augmentation.
Stage 3: Possible medication combinations – lithium plus Divalproex, lithium plus atypical, or Divalproex plus atypical.
Stage 4: Combination of 2-3 mood stabilisers.
Stage 5: Alternate monotherapy with oxcarbazepine, ziprasidone, or aripiprazole (all Level D).
Stage 6: For nonresponse or intolerable side effects – clozapine for children or adolescents, or electroconvulsive therapy (ECT) for adolescents only.
BPD I, manic or mixed, with psychosis:
Stage 1: Same as BPD I without psychosis except for first-line treatment warrants a combination of mood stabiliser and an atypical antipsychotic.
Stages 2-4: Varying combinations and augmentations.
Stage 5: Alternate monotherapy (oxcarbazepine) plus an atypical antipsychotic.
Chronic medication is often needed, with relapses of individuals reaching rates over 90% in those not following medication indications and almost to 40% in those complying with medication regimens in some studies. Compared to adults, a juvenile onset has in general a similar or worse course, although age of onset predicts the duration of the episodes more than the prognosis. A risk factor for a worse outcome is the existence of additional (comorbid) pathologies.
Children with bipolar disorder are more likely to suicide than other children.
The Child Mania Rating Scales (CMRS) is a 21-item diagnostic screening measure designed to identify symptoms of mania in children and adolescents aged 9-17 using diagnostic criteria from the DSM-IV, developed by Pavuluri and colleagues.
There is also a 10-item short form. The measure assesses the child’s mood and behaviour symptoms, asking parents or teachers to rate how often the symptoms have caused a problem for the youth in the past month. Clinical studies have found the CMRS to be reliable and valid when completed by parents in the assessment of children’s bipolar symptoms. The CMRS also can differentiate cases of paediatric bipolar disorder from those with ADHD or no disorder, as well as delineating bipolar subtypes. A meta-analysis comparing the different rating scales available found that the CMRS was one of the best performing scales in terms of telling cases with bipolar disorder apart from other clinical diagnoses. The CMRS has also been found to provide a reliable and valid assessment of symptoms longitudinally over the course of treatment. The combination of showing good reliability and validity across multiple samples and clinical settings, along with being free and brief to score, make the CMRS a promising tool, especially since most other checklists available for youths do not assess manic symptoms.
The Child Mania Rating Scale (CMRS) was created as a complement already existing measures like the Altman Self-Rating Mania Scale and the Young Mania Rating Scale, which were formulated for adults. The purpose of the CMRS is to both assess the symptoms of mania in paediatric bipolar disorder, and to accurately discriminate the symptoms of mania from symptoms of ADHD. It is important that the CMRS accurately discriminate from symptoms of ADHD because core symptoms of adolescent Bipolar Disorder and ADHD are shared between the two disorders: hyperactivity, impulsivity, and distractibility. The CMRS was designed specifically for younger children who may or may not have the ability to accurately answer questions about their behaviour. As a result, the questionnaire is filled out by parents are/or caregivers who work with the children on a daily basis. Previous mania scales were designed for use by either the clinician or the patient. Therefore, the CMRS is unique in that it allows parents and caregivers to contribute information about their child’s symptoms. This is especially important in cases where the child may be too young to fill out the questionnaires themselves.
Historically, effective rating and diagnosis of mania has been limited. Though many mania scales have been tested on adult populations, the Young Mania Rating Scale (YMRS) – which was tested against the child version (CMRS) as standard measure for screening mania- is the only adult scale that has also been studied for validity and reliability in prepubertal children. Previous attempts include the Beigel Scale/Manic State Rating Scale (MSRS) and the Patterson Scale, which used nurse and clinician reports to rate levels of mania. Neither scale effectively and consistently captured levels of mania in patients. Other measures of paediatric mania are generally limited because they are completed by the clinician, introducing potential for bias, and because they lack the depth necessary to differentiate between patient-specific ways in which symptoms are presented. The CMRS Parent and Teacher versions attempt to address some of the limitations by including a checklist that can gather information about behaviour at home, school, and other settings, rather than focusing only on what a clinician could directly observe. One study examined the accuracy of a shortened version of the CMRS-P, which included only 10 items, and found that its accuracy was similar to the full scale.
Typically, the CMRS takes only 10-15 minutes to administer. The questions ask about behaviour-specific actions and tendencies the child may have exhibited within the past month. The parent rates the behaviour on a scale from 1 to 4, where 1=never/rarely, 2=sometimes, 3=often, and 4=very often. A clinician examines the total score and determines if the child has ADHD or Bipolar Disorder. If a diagnosis Bipolar Disorder is deemed to be appropriate, the clinician will also determine the sub-type.
There is a short version (10 items) of the CMRS called the Brief CMRS/Brief CMRS-P. The shorter version was created because a shorter version is preferred to longer assessments if the shorter gives similar accuracy, which it does. Additionally, there is a teacher’s version of the CMRS called the CMRS-Teacher (CMRS-T).
Reliability and Validity
Table 1: Rubric for evaluating norms and reliability for the Child Mania Rating Scale.
Designed originally as a self-report scale; parent and youth report correlate about the same as cross-informant scores correlate in general.
r = .96 over 1 week. Data on test-retest reliability over longer periods are needed.
No published studies formally checking repeatability.
Construct validity analyses (Exploratory Factor Analysis and Confirmatory Factor Analysis) for the CMRS-P indicated that the scale is unidimensional. Internal consistency measured by Cronbach’s alpha was .96 in a sample consisting of ADHD, Bipolar, and healthy control participants. In a sample of participants with bipolar disorder, the cronbach’s alpha was 91. Additionally, it has the ability to accurately differentiate paediatric bipolar disorder from ADHD and healthy controls greater than 90% of the time.
The teacher version (CMRS-T) also has 21 items. The internal consistency, measured by Cronbach’s alpha, was .86. Correlations between the parent and teacher versions of the CMRS range from .23 to .27. The CMRS teacher version has not been shown to discriminate bipolar from nonbipolar cases at better than chance levels and is not recommended for use in clinical practice for diagnosing bipolar disorder in children.
Table 2: Evaluation of validity and utility for the Child Mania Rating Scale
Rating (Adequate, Good, Excellent, Too Good)
Covers both DSM diagnostic symptoms and a range of associated features. Consistently distinguishes between PBP sub-types and comorbid disorders.
Construct Validity (e.g. Predictive, Concurrent, Convergent, and Discriminant Validity)
Shows convergent validity with other symptom scales. Correlations between CMRS-P and other several clinician-rating scales intended to measure manic symptoms (e.g. Washington University Schedule for Affective Disorder and Schizophrenia mania module, the Schedule for Affective Disorders and Schizophrenia Mania Rating Scale, and the Young Mania Rating Scales) were excellent (.78 to .98).
Preliminary studies show that CMRS scores discriminate cases with unipolar and bipolar mood disorders from other clinical disorders. AUCs of >.90 are quite high. Comparison to healthy controls might imply unrealistic performance when compared to realities of clinical practice.
Shown to be effective for ethnically representative samples. More research and multiple settings are needed to sufficiently determine generalization.
The CMRS-P has also been found to be sensitive in detecting symptom change over the course of treatment in multiple studies.
Free (public domain), designed to be completed in 10-15 minutes, preliminary data are promising. Less research than some of the other contenders, but easier reading level than General Behaviour Inventory and more sensitive to treatment effects than Mood Disorder Questionnaire.
Development and History
The CMRS was developed as a shorter, reliable, and valid parent-report screening instrument for mania. The short form was derived from the CMRS 21 item scale which is the first original mania rating scale developed for children and adolescents. It was not developed from the Young Mania Rating Scale (YMRS) that was originally designed for adults, ‘Young’ being the name of the author than the fact that it was a scale for ‘young’ population. The YMRS was derived from the Parent-Young Mania Rating Scale (P-YMRS). This scale, developed from the YMRS, was created for use with adult inpatients. The items of the P-YMRS did not include the updated DSM-IV criteria for adolescent Bipolar Disorder, and it includes several items with poor factor loadings. Furthermore, the content is not developmentally appropriate for children, as many of the items require insight or appearance, which are irrelevant to young children. Another promising measure is the GBI as it has good psychometric properties. However, the GBI is lengthy and complicated and requires the child to have at least a 7th-grade reading ability. One of the most widely used measures of mania symptoms is the Kiddie Schedule for Affective Disorders and Schizophrenia mania section. However, this measure is extremely extensive and requires much clinical training to administer.
During the development of the CMRS, researchers found that reliable and more accurate diagnostic accuracy is found in parent reports in comparison to teacher reports or self-reports and that these other reports rarely added new information to the parent report. Furthermore, the areas under the curve (AUC) of parent-rated instruments reported modest to excellent validity. Based on the evidence, the developers of the CMRS chose to create a measure that relied mainly on parent report.
Other parent report measures have been used to screen for Paediatric Bipolar Disorder, but these measures were not developed to look specifically for mania. One such measure is the Child Behaviour Checklist (CBCL). The CBCL, in addition to providing markers of psychopathology, has been used to detect mania in children. However, on the CBCL, researchers saw a consistent pattern of elevated scores, especially on the following symptoms: aggressive behaviour, attention problems, delinquency, anxiety, and depression. This pattern may be due to the high comorbidity of ADHD, oppositional defiant disorder, conduct disorder, and anxiety disorders in children with paediatric Bipolar Disorder. And although the CBCL is a reliable and validated measure, low scores on the CBCL may only rule out mania – conversely, it would be erroneous to rule in mania using CBCL scores alone.
For these reasons, the CMRS was developed to accurately and reliably assess mania in paediatric Bipolar Disorder, and differentiate its symptoms from other disorders with high comorbidity with paediatric Bipolar Disorder.
Though there is no gold-standard screening tool for Paediatric Bipolar Disorder, the CMRS has been described as a promising and useful tool for such a purpose. For example, institutional protocols for diagnosing and evaluating Bipolar Disorder in children may use the CMRS as an initial screening tool to establish the need to further evaluation of mania symptoms. In addition, the parent version of the CMRS (the CMRS-P) has been used in research studies to detect changes in children’s mania symptoms due to pharmacotherapy or psychotherapy. The CMRS is the first measure specifically developed for the purpose of screening for Bipolar Disorder in children. As such, it offers an alternative to broadband rating scales like the Child Behaviour Checklist, which has been used as a screening tool for Bipolar Disorder in children with mixed findings regarding its reliability.
Furthermore, the CMRS-P (both the brief and full versions) have shown to be effective in distinguishing between mania and ADHD. The brief version effectively retains characteristics of the original CMRS, allowing for wider application and longitudinal use. Psychometric studies of the CMRS has demonstrated that the measure has excellent reliability and validity. Internal consistency is excellent and the measure correlates with clinician-administered interview measures for diagnosing paediatric mania. The measure is also accurately able to differentiate symptoms of paediatric Bipolar Disorder from ADHD and healthy control groups more than 90% of the time. Furthermore, the use of the CMRS in pharmacological research suggests that this measure is sensitive to treatment over time, which means that you can use this measure to assess treatment effectiveness.
The CMRS suffers from the same problems as other self-report inventories, in that scores can be easily exaggerated or minimised by the person completing them – in this case, the parent or teacher – in a phenomenon called the social desirability bias. Like all questionnaires, the way the instrument is administered can also influence the final score. If a person is asked to fill out the form in front of other people in a clinical environment, for instance, social expectations have been shown to elicit a different response compared to administration via a postal survey. The age of the youth also may matter. Although the Child Mania Rating Scale has been shown to be a valid and reliable measure of mania in children, one concern is that its validity might change as the youth becomes an adolescent, and parents or teachers have less influence and awareness about the youth’s behaviour outside of the home or school. Additionally, it is also unclear of the CMRS’s ability to assess the change in mania systems as a child cycles out of mania and into depression.
Use in Other Populations
While the CMRS has not been validated in other languages, the CBCL, YMRS, GBI, and KSADS all have. However, the CMRS has been tested and translated into Spanish. The CMRS is available in fourteen languages with back translation through native/bilingual speakers, though not tested in all languages.
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.
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 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.
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.
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.
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
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.
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.
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:
Mixed states are associated with greater levels of suicidality than non-mixed depression. Antidepressants may increase this risk.
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.
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.
Disrupted circadian rhythm.
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).
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.
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.
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.
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.
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.
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 can also help those with the illness. These include:
Relapse can still occur, despite continued medication and therapy.
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.
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.
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.
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.
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.
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 #
Single manic episode
Most recent episode hypomanic
Most recent episode manic
Most recent episode depressed
Most recent episode mixed
Most 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.
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.
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%.
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.
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.
The Altman Self-Rating Mania Scale assess differences in “normal” or baseline levels in five subjective and behavioural areas:
Speech patterns and amount.
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.
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.