What is Aripiprazole?

Introduction

Aripiprazole, sold under the brand names Abilify and Aristada among others, is an atypical antipsychotic. It is primarily used in the treatment of schizophrenia and bipolar disorder. Other uses include as an add-on treatment in major depressive disorder (MDD), tic disorders and irritability associated with autism. It is taken by mouth or injection into a muscle. A Cochrane review found low-quality evidence of effectiveness in treating schizophrenia.

In adults, side effects with greater than 10% incidence include weight gain, headache, akathisia, insomnia, and gastro-intestinal effects like nausea and constipation, and lightheadedness. Side effects in children are similar, and include sleepiness, increased appetite, and stuffy nose. A strong desire to gamble, binge eat, shop, and engage in sexual activity may also occur.

Common side effects include vomiting, constipation, sleepiness, dizziness, weight gain and movement disorders. Serious side effects may include neuroleptic malignant syndrome, tardive dyskinesia and anaphylaxis. It is not recommended for older people with dementia-related psychosis due to an increased risk of death. In pregnancy, there is evidence of possible harm to the baby. It is not recommended in women who are breastfeeding. It has not been very well studied in people less than 18 years old. The exact mode of action is not entirely clear but may involve effects on dopamine and serotonin.

Aripiprazole was approved for medical use in the United States in 2002. It is available as a generic medication. In 2019, it was the 101st most commonly prescribed medication in the United States, with more than 6 million prescriptions. Aripiprazole was discovered in 1988 by scientists at the Japanese firm Otsuka Pharmaceutical.

Brief History

Aripiprazole was discovered by scientists at Otsuka Pharmaceutical and was called OPC-14597. It was first published in 1995. Otsuka initially developed the drug, and partnered with Bristol-Myers Squibb (BMS) in 1999 to complete development, obtain approvals, and market aripiprazole.

It was approved by the US Food and Drug Administration (FDA) for schizophrenia in November 2002, and the European Medicines Agency in June 2004; for acute manic and mixed episodes associated with bipolar disorder on 01 October 2004; as an adjunct for major depressive disorder on 20 November 2007; and to treat irritability in children with autism on 20 November 2009. Likewise it was approved for use as a treatment for schizophrenia by the TGA of Australia in May 2003.

Aripiprazole has been approved by the FDA for the treatment of both acute manic and mixed episodes, in people older than ten years.

In 2006, the FDA required manufacturers to add a black box warning to the label, warning that older people who were given the drug for dementia-related psychosis were at greater risk of death.

In 2007, aripiprazole was approved by the FDA for the treatment of unipolar depression when used adjunctively with an antidepressant medication. That same year, BMS settled a case with the US government in which it paid $515 million; the case covered several drugs but the focus was on BMS’s off-label marketing of aripiprazole for children and older people with dementia.

In 2011 Otsuka and Lundbeck signed a collaboration to develop a depot formulation of apripiprazole.

As of 2013, Abilify had annual sales of US$7 billion. In 2013 BMS returned marketing rights to Otsuka, but kept manufacturing the drug. Also in 2013, Otsuka and Lundbeck received US and European marketing approval for an injectable depot formulation of aripiprazole.

Otsuka’s US patent on aripiprazole expired on 20 October 2014, but due to a paediatric extension, a generic did not become available until 20 April 2015. Barr Laboratories (now Teva Pharmaceuticals) initiated a patent challenge under the Hatch-Waxman Act in March 2007. On 15 November 2010, this challenge was rejected by the US District Court in New Jersey.

Otsuka’s European patent EP0367141 which would have expired on 26 October 2009, was extended by a Supplementary Protection Certificate (SPC) to 26 October 2014. The UK Intellectual Property Office decided on 04 March 2015 that the SPC could not be further extended by six months under Regulation (EC) No 1901/2006. Even if the decision is successfully appealed, protection in Europe will not extend beyond 26 April 2015.

From April 2013 to March 2014, sales of Abilify amounted to almost $6.9 billion.

In April 2015, the FDA announced the first generic versions. In October 2015, aripiprazole lauroxil, a prodrug of aripiprazole that is administered via intramuscular injection once every four to six weeks for the treatment of schizophrenia, was approved by the FDA.

In 2016, BMS settled cases with 42 US states that had charged BMS with off-label marketing to older people with dementia; BMS agreed to pay $19.5 million.

In November 2017, the FDA approved Abilify MyCite, a digital pill containing a sensor intended to record when its consumer takes their medication.

Medical Uses

Aripiprazole is primarily used for the treatment of schizophrenia or bipolar disorder.

Schizophrenia

The 2016 NICE guidance for treating psychosis and schizophrenia in children and young people recommended aripiprazole as a second line treatment after risperidone for people between 15 and 17 who are having an acute exacerbation or recurrence of psychosis or schizophrenia. A 2014 NICE review of the depot formulation of the drug found that it might have a role in treatment as an alternative to other depot formulations of second generation antipsychotics for people who have trouble taking medication as directed or who prefer it.

A 2014 Cochrane review comparing aripiprazole and other atypical antipsychotics found that it is difficult to determine differences as data quality is poor. A 2011 Cochrane review comparing aripiprazole with placebo concluded that high dropout rates in clinical trials, and a lack of outcome data regarding general functioning, behaviour, mortality, economic outcomes, or cognitive functioning make it difficult to definitively conclude that aripiprazole is useful for the prevention of relapse. A Cochrane review found only low quality evidence of effectiveness in treating schizophrenia. Accordingly, part of its methodology on quality of evidence is based on quantity of qualified studies.

A 2013 review found that it is in the middle range of 15 antipsychotics for effectiveness, approximately as effective as haloperidol and quetiapine and slightly more effective than ziprasidone, chlorpromazine, and asenapine, with better tolerability compared to the other antipsychotic drugs (4th best for weight gain, 5th best for extrapyramidal symptoms, best for prolactin elevation, 2nd best for QTc prolongation, and 5th best for sedation). The authors concluded that for acute psychotic episodes aripiprazole results in benefits in some aspects of the condition.

In 2013 the World Federation of Societies for Biological Psychiatry recommended aripiprazole for the treatment of acute exacerbations of schizophrenia as a Grade 1 recommendation and evidence level A.

The British Association for Psychopharmacology similarly recommends that all persons presenting with psychosis receive treatment with an antipsychotic, and that such treatment should continue for at least 1-2 years, as “There is no doubt that antipsychotic discontinuation is strongly associated with relapse during this period”. The guideline further notes that “Established schizophrenia requires continued maintenance with doses of antipsychotic medication within the recommended range (Evidence level A)”.

The British Association for Psychopharmacology and the World Federation of Societies for Biological Psychiatry suggest that there is little difference in effectiveness between antipsychotics in prevention of relapse, and recommend that the specific choice of antipsychotic be chosen based on each person’s preference and side effect profile. The latter group recommends switching to aripiprazole when excessive weight gain is encountered during treatment with other antipsychotics

Bipolar Disorder

Aripiprazole is effective for the treatment of acute manic episodes of bipolar disorder in adults, children, and adolescents. Used as maintenance therapy, it is useful for the prevention of manic episodes, but is not useful for bipolar depression. Thus, it is often used in combination with an additional mood stabiliser; however, co-administration with a mood stabiliser increases the risk of extrapyramidal side effects.

Major Depression

Aripiprazole is an effective add-on treatment for major depressive disorder; however, there is a greater rate of side effects such as weight gain and movement disorders. The overall benefit is small to moderate and its use appears to neither improve quality of life nor functioning. Aripiprazole may interact with some antidepressants, especially selective serotonin reuptake inhibitors (SSRIs). There are interactions with fluoxetine and paroxetine and lesser interactions with sertraline, escitalopram, citalopram, and fluvoxamine, which inhibit CYP2D6, for which aripiprazole is a substrate. CYP2D6 inhibitors increase aripiprazole concentrations to 2-3 times their normal level.

Autism

Short-term data (8 weeks) shows reduced irritability, hyperactivity, inappropriate speech, and stereotypy, but no change in lethargic behaviours. Adverse effects include weight gain, sleepiness, drooling and tremors. It is suggested that children and adolescents need to be monitored regularly while taking this medication, to evaluate if this treatment option is still effective after long-term use and note if side effects are worsening. Further studies are needed to understand if this drug is helpful for children after long term use.

Tic Disorders

Aripiprazole is approved for the treatment of Tourette’s syndrome. It is effective, safe, and well-tolerated for this use per systematic reviews and meta-analyses

Obsessive-Compulsive Disorder

A 2014 systematic review and meta-analysis concluded that add-on therapy with low dose aripiprazole is an effective treatment for obsessive-compulsive disorder (OCD) that does not improve with selective serotonin reuptake inhibitors (SSRIs) alone. The conclusion was based on the results of two relatively small, short-term trials, each of which demonstrated improvements in symptoms. Risperidone, another second-generation antipsychotic, appears to be superior to aripiprazole for this indication, and is recommended by the 2007 American Psychiatric Association guidelines. However, aripiprazole is cautiously recommended by a 2017 review on antipsychotics for OCD. Aripiprazole is not currently approved for the treatment of OCD and is instead used off-label for this indication.

Adverse Effects

In adults, side effects with greater than 10% incidence include weight gain, headache, akathisia, insomnia, and gastro-intestinal effects like nausea and constipation, and lightheadedness. Side effects in children are similar, and include sleepiness, increased appetite, and stuffy nose. A strong desire to gamble, binge eat, shop, and engage in sexual activity may also occur.

Uncontrolled movement such as restlessness, tremors, and muscle stiffness may occur.

Discontinuation

The British National Formulary recommends a gradual withdrawal when discontinuing antipsychotics to avoid acute withdrawal syndrome or rapid relapse. Symptoms of withdrawal commonly include nausea, vomiting, and loss of appetite. Other symptoms may include restlessness, increased sweating, and trouble sleeping. Less commonly there may be a feeling of the world spinning, numbness, or muscle pains. Symptoms generally resolve after a short period of time.

There is tentative evidence that discontinuation of antipsychotics can result in psychosis. It may also result in reoccurrence of the condition that is being treated. Rarely tardive dyskinesia can occur when the medication is stopped.

Overdose

Children or adults who ingested acute overdoses have usually manifested central nervous system depression ranging from mild sedation to coma; serum concentrations of aripiprazole and dehydroaripiprazole in these people were elevated by up to 3-4 fold over normal therapeutic levels; as of 2008 no deaths had been recorded.

Interactions

Aripiprazole is a substrate of CYP2D6 and CYP3A4. Coadministration with medications that inhibit (e.g. paroxetine, fluoxetine) or induce (e.g. carbamazepine) these metabolic enzymes are known to increase and decrease, respectively, plasma levels of aripiprazole.

Precautions should be taken in people with an established diagnosis of diabetes mellitus who are started on atypical antipsychotics along with other medications that affect blood sugar levels and should be monitored regularly for worsening of glucose control. The liquid form (oral solution) of this medication may contain up to 15 grams of sugar per dose.

Antipsychotics like aripiprazole and stimulant medications, such as amphetamine, are traditionally thought to have opposing effects to their effects on dopamine receptors: stimulants are thought to increase dopamine in the synaptic cleft, whereas antipsychotics are thought to decrease dopamine. However, it is an oversimplification to state the interaction as such, due to the differing actions of antipsychotics and stimulants in different parts of the brain, as well as the effects of antipsychotics on non-dopaminergic receptors. This interaction frequently occurs in the setting of comorbid attention-deficit hyperactivity disorder (ADHD) (for which stimulants are commonly prescribed) and off-label treatment of aggression with antipsychotics. Aripiprazole has been reported to provide some benefit in improving cognitive functioning in people with ADHD without other psychiatric comorbidities, though the results have been disputed. The combination of antipsychotics like aripiprazole with stimulants should not be considered an absolute contraindication.

Pharmacology

Pharmacodynamics

Aripiprazole’s mechanism of action is different from those of the other FDA-approved atypical antipsychotics (e.g., clozapine, olanzapine, quetiapine, ziprasidone, and risperidone). It shows differential engagement at the dopamine receptor (D2). It appears to show predominantly antagonist activity on postsynaptic D2 receptors and partial agonist activity on presynaptic D2 receptors, D3, and partially D4 and is a partial activator of serotonin (5-HT1A, 5-HT2A, 5-HT2B, 5-HT6, and 5-HT7). It also shows lower and likely insignificant effect on histamine (H1), epinephrine/norepinephrine (α), and otherwise dopamine (D4), as well as the serotonin transporter. Aripiprazole acts by modulating neurotransmission overactivity of dopamine, which is thought to mitigate schizophrenia symptoms.

As a pharmacologically unique antipsychotic with pronounced functional selectivity, characterization of this dopamine D2 partial agonist (with an intrinsic activity of ~25%) as being similar to a full agonist but at a reduced level of activity presents a misleading oversimplification of its actions; for example, among other effects, aripiprazole has been shown, in vitro, to bind to and/or induce receptor conformations (i.e. facilitate receptor shapes) in such a way as to not only prevent receptor internalisation (and, thus, lower receptor density) but even to lower the rate of receptor internalisation below that of neurons not in the presence of agonists (including dopamine) or antagonists. It is often the nature of partial agonists, including aripiprazole, to display a stabilising effect (such as on mood in this case) with agonistic activity when there are low levels of endogenous neurotransmitters (such as dopamine) and antagonistic activity in the presence of high levels of agonists associated with events such as mania, psychosis, and drug use. In addition to aripiprazole’s partial agonism and functional selectivity characteristics, its effectiveness may be mediated by its very high dopamine D2 receptor occupancy (approximately 32%, 53%, 72%, 80%, and 97% at daily dosages of 0.5 mg, 1 mg, 2 mg, 10 mg, and 40 mg respectively) as well as balanced selectivity for pre- and postsynaptic receptors (as suggested by its equal affinity for both D2S and D2L receptor forms). Aripiprazole has been characterised as possessing predominantly antagonistic activity on postsynaptic D2 receptors and partial agonist activity on presynaptic D2 receptors; however, while this explanation intuitively explains the drug’s efficacy as an antipsychotic, as degree of agonism is a function of more than a drug’s inherent properties as well as in vitro demonstration of aripiprazole’s partial agonism in cells expressing postsynaptic (D2L) receptors, it was noted that “It is unlikely that the differential actions of aripiprazole as an agonist, antagonist, or partial agonist were entirely due to differences in relative D2 receptor expression since aripiprazole was an antagonist in cells with the highest level of expression (4.6 pmol/mg) and a partial agonist in cells with an intermediate level of expression (0.5-1 pmol/mg). Instead, the current data are most parsimoniously explained by the ‘functional selectivity’ hypothesis of Lawler et al (1999)”. Aripiprazole is also a partial agonist of the D3 receptor. In healthy human volunteers, D2 and D3 receptor occupancy levels are high, with average levels ranging between approximately 71% at 2 mg/day to approximately 96% at 40 mg/day. Most atypical antipsychotics bind preferentially to extrastriatal receptors, but aripiprazole appears to be less preferential in this regard, as binding rates are high throughout the brain.

Aripiprazole is also a partial agonist of the serotonin 5-HT1A receptor (intrinsic activity = 68%). Casting doubt on the significance of aripiprazole’s agonism of 5-HT1A receptors, a PET scan study of 12 patients receiving doses ranging from 10 to 30 mg found 5-HT1A receptor occupancy to be only 16% compared to ~90% for D2. It is a very weak partial agonist of the 5-HT2A receptor (intrinsic activity = 12.7%), and like other atypical antipsychotics, displays a functional antagonist profile at this receptor. The drug differs from other atypical antipsychotics in having higher affinity for the D2 receptor than for the 5-HT2A receptor. At the 5-HT2B receptor, aripiprazole has both great binding affinity and acts as a potent inverse agonist, “Aripiprazole decreased PI hydrolysis from a basal level of 61% down to a low of 30% at 1000 nM, with an EC50 of 11 nM”. Unlike other antipsychotics, aripiprazole is a high-efficacy partial agonist of the 5-HT2C receptor (intrinsic activity = 82%) and with relatively weak affinity; this property may underlie the minimal weight gain seen in the course of therapy. At the 5-HT7 receptor, aripiprazole is a very weak partial agonist with barely measurable intrinsic activity, and hence is a functional antagonist of this receptor. Aripiprazole also shows lower but likely clinically insignificant affinity for a number of other sites, such as the histamine H1, α-adrenergic, and dopamine D4 receptors as well as the serotonin transporter, while it has negligible affinity for the muscarinic acetylcholine receptors.

Since the actions of aripiprazole differ markedly across receptor systems aripiprazole was sometimes an antagonist (e.g. at 5-HT6 and D2L), sometimes an inverse agonist (e.g. 5-HT2B), sometimes a partial agonist (e.g. D2L), and sometimes a full agonist (D3, D4). Aripiprazole was frequently found to be a partial agonist, with an intrinsic activity that could be low (D2L, 5-HT2A, 5-HT7), intermediate (5-HT1A), or high (D4, 5-HT2C). This mixture of agonist actions at D2-dopamine receptors is consistent with the hypothesis that aripiprazole has ‘functionally selective’ actions. The ‘functional-selectivity’ hypothesis proposes that a mixture of agonist/partial agonist/antagonist actions are likely. According to this hypothesis, agonists may induce structural changes in receptor conformations that are differentially ‘sensed’ by the local complement of G proteins to induce a variety of functional actions depending upon the precise cellular milieu. The diverse actions of aripiprazole at D2-dopamine receptors are clearly cell-type specific (e.g. agonism, antagonism, partial agonism), and are most parsimoniously explained by the ‘functional selectivity’ hypothesis.

Since 5-HT2C receptors have been implicated in the control of depression, OCD, and appetite, agonism at the 5-HT2C receptor might be associated with therapeutic potential in obsessive compulsive disorder, obesity, and depression. 5-HT2C agonism has been demonstrated to induce anorexia via enhancement of serotonergic neurotransmission via activation of 5-HT2C receptors; it is conceivable that the 5-HT2C agonist actions of aripiprazole may, thus, be partly responsible for the minimal weight gain associated with this compound in clinical trials. In terms of potential action as an anti-obsessional agent, it is worthwhile noting that a variety of 5-HT2A/5-HT2C agonists have shown promise as anti-obsessional agents, yet many of these compounds are hallucinogenic, presumably due to 5-HT2A activation. Aripiprazole has a favourable pharmacological profile in being a 5-HT2A antagonist and a 5-HT2C partial agonist. Based on this profile, one can predict that aripiprazole may have anti-obsessional and anorectic actions in humans.

Wood and Reavill’s (2007) review of published and unpublished data proposed that, at therapeutically relevant doses, aripiprazole may act essentially as a selective partial agonist of the D2 receptor without significantly affecting the majority of serotonin receptors. A positron emission tomography imaging study found that 10 to 30 mg/day aripiprazole resulted in 85 to 95% occupancy of the D2 receptor in various brain areas (putamen, caudate, ventral striatum) versus 54 to 60% occupancy of the 5-HT2A receptor and only 16% occupancy of the 5-HT1A receptor. It has been suggested that the low occupancy of the 5-HT1A receptor by aripiprazole may have been an erroneous measurement however.

Aripiprazole acts by modulating neurotransmission overactivity on the dopaminergic mesolimbic pathway, which is thought to be a cause of positive schizophrenia symptoms. Due to its agonist activity on D2 receptors, aripiprazole may also increase dopaminergic activity to optimal levels in the mesocortical pathways where it is reduce.

Pharmacokinetics

Aripiprazole displays linear kinetics and has an elimination half-life of approximately 75 hours. Steady-state plasma concentrations are achieved in about 14 days. Cmax (maximum plasma concentration) is achieved 3-5 hours after oral dosing. Bioavailability of the oral tablets is about 90% and the drug undergoes extensive hepatic metabolization (dehydrogenation, hydroxylation, and N-dealkylation), principally by the enzymes CYP2D6 and CYP3A4. Its only known active metabolite is dehydro-aripiprazole, which typically accumulates to approximately 40% of the aripiprazole concentration. The parenteral drug is excreted only in traces, and its metabolites, active or not, are excreted via faeces and urine.

Chemistry

Aripiprazole is a phenylpiperazine and is chemically related to nefazodone, etoperidone, and trazodone. It is unusual in having twelve known crystalline polymorphs.

Society and Culture

Classification

Aripiprazole has been described as the prototypical third-generation antipsychotic, as opposed to first-generation (typical) antipsychotics like haloperidol and second-generation (atypical) antipsychotics like clozapine. It has received this classification due to its partial agonism of dopamine receptors, and is the first of its kind in this regard among antipsychotics, which before aripiprazole acted only as dopamine receptor antagonists. The introduction of aripiprazole has led to a paradigm shift from a dopamine antagonist-based approach to a dopamine agonist-based approach for antipsychotic drug development.

Research

Attention Deficit Hyperactivity Disorder

Aripiprazole was under development for the treatment of attention-deficit hyperactivity disorder (ADHD), but development for this indication was discontinued. A 2017 meta review found only preliminary evidence (studies with small sample sizes and methodological problems) for aripiprazole in the treatment of ADHD. A 2013 systematic review of aripiprazole for ADHD similarly reported that there is insufficient evidence of effectiveness to support aripiprazole as a treatment for the condition. Although all 6 non-controlled open-label studies in the review reported effectiveness, two small randomised controlled trials found that aripiprazole did not significantly decrease ADHD symptoms. A high rate of adverse effects with aripiprazole such as weight gain, sedation, and headache was noted. Most research on aripiprazole for ADHD is in children and adolescents. Evidence on aripiprazole specifically for adult ADHD appears to be limited to a single case report.

Substance Dependence

Aripiprazole has been studied for the treatment of amphetamine dependence and other substance use disorders, but more research is needed to support aripiprazole for these potential uses. Available evidence of aripiprazole for amphetamine dependence is mixed. Some studies have reported attenuation of the effects of amphetamines by aripiprazole, whereas other studies have reported both enhancement of the effects of amphetamines and increased use of amphetamines by aripiprazole. As such, aripiprazole may not only be ineffective but potentially harmful for treatment of amphetamine dependence, and caution is warranted with regard to its use for such purposes.

Other Uses

Aripiprazole is under development for the treatment of agitation and pervasive child development disorders. As of May 2021, it is in phase 3 clinical trials for these indications.

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What is Disruptive Mood Dysregulation Disorder?

Introduction

Disruptive mood dysregulation disorder (DMDD) is a mental disorder in children and adolescents characterised by a persistently irritable or angry mood and frequent temper outbursts that are disproportionate to the situation and significantly more severe than the typical reaction of same-aged peers.

DMDD was added to the DSM-5 as a type of depressive disorder diagnosis for youths. The symptoms of DMDD resemble those of attention deficit hyperactivity disorder (ADHD), oppositional defiant disorder (ODD), anxiety disorders, and childhood bipolar disorder.

DMDD first appeared as a disorder in the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) in 2013 and is classified as a mood disorder. Treatments include medication to manage mood symptoms as well as individual and family therapy to address emotion-regulation skills. Children with DMDD are at risk for developing depression and anxiety later in life.

Brief History

Beginning in the 1990s, some clinicians began observing children with hyperactivity, irritability, and severe temper outbursts. These symptoms greatly interfered with their lives at home, school, and with friends. Because other diagnoses, like ADHD and ODD, did not capture the severity of children’s irritability and anger, many of these children were diagnosed with bipolar disorder. Longitudinal studies showed that children with chronic irritability and temper outbursts often developed later problems with anxiety and depression, and rarely developed bipolar disorder in adolescence or adulthood. Consequently, the developers of DSM-5 created a new diagnostic label, DMDD, to describe children with persistent irritability and angry outbursts. In 2013, the American Psychiatric Association (APA) added DMDD to the DSM-5 and classified it as a depressive disorder.

Signs and Symptoms

Children with DMDD show severe and recurrent temper outbursts three or more times per week. These outbursts can be verbal or behavioural. Verbal outbursts often are described by observers as “rages”, “fits”, or “tantrums”. Children may scream, yell, and cry for excessively long periods of time, sometimes with little provocation. Physical outbursts may be directed toward people or property. Children may throw objects; hit, slap, or bite others; destroy toys or furniture; or otherwise act in a harmful or destructive manner.

Children with DMDD also display persistently irritable or angry mood that is observable by others. Parents, teachers, and classmates describe these children as habitually angry, touchy, grouchy, or easily “set off”. Unlike the irritability that can be a symptom of other childhood disorders, such as ODD, anxiety disorders, and major depressive disorder (MDD), the irritability displayed by children with DMDD is not episodic or situation-dependent. In DMDD, the irritability or anger is severe and is shown most of the day, nearly every day in multiple settings, lasting for one or more years.

The DSM-5 includes several additional diagnostic criteria which describe the duration, setting, and onset of the disorder: the outbursts must be present for at least 12 months and occur in at least two settings (e.g. home and school), and it must be severe in at least one setting. Symptoms appear before the age of 10, and diagnosis must be made between ages 6 and 18.

Comorbidity

The core features of DMDD – temper outbursts and chronic irritability – are sometimes seen in children and adolescents with other psychiatric conditions. Differentiating DMDD from these other conditions can be difficult. Three disorders that most closely resemble DMDD are ADHD, oppositional defiant disorder (ODD), and bipolar disorder in children.

ADHD

ADHD is a neurodevelopmental disorder characterised by problems with inattention and/or hyperactivity-impulsivity.

ODD

ODD is a disruptive behaviour disorder characterised by oppositional, defiant, and sometimes hostile actions directed towards others.

Bipolar Disorder

One of the main differences between DMDD and bipolar disorder is that the irritability and anger outbursts associated with DMDD are not episodic; symptoms of DMDD are chronic and displayed constantly on an almost daily basis. On the other hand, bipolar disorder is characterised by distinct manic or hypomanic episodes usually lasting a few days, or a few weeks at most, that parents should be able to differentiate from their child’s typical mood and behaviour in between episodes. The DSM precludes a dual diagnosis of DMDD and bipolar disorder. Bipolar disorder alone should be used for youths who show classic symptoms of episodic mania or hypomania.

Prior to adolescence, DMDD is much more common than bipolar disorder. Most children with DMDD see a decrease in symptoms as they enter adulthood, whereas individuals with bipolar disorder typically display symptoms for the first time as teenagers and young adults. Children with DMDD are more at risk for developing MDD or generalised anxiety disorder when they are older rather than bipolar disorder.

Causes

Youth with DMDD have difficulty attending, processing, and responding to negative emotional stimuli and social experiences in their everyday lives. For example, some studies have shown youths with DMDD to have problems interpreting the social cues and emotional expressions of others. These youths may be especially bad at judging others’ negative emotional displays, such as feelings of sadness, fearfulness, and anger. Functional MRI studies suggest that under-activity of the amygdala, the brain area that plays a role in the interpretation and expression of emotions and novel stimuli, is associated with these deficits. Deficits in interpreting social cues may predispose children to instances of anger and aggression in social settings with little provocation. For examples, youths with DMDD may selectively attend to negative social cues (e.g. others scowling, teasing) and minimize all other information about the social events. They may also misinterpret the emotional displays of others, believing others’ benign actions to be hostile or threatening. Consequently, they may be more likely than their peers to act in impulsive and angry ways.

Children with DMDD may also have difficulty regulating negative emotions once they are elicited. To study these problems with emotion regulation, researchers asked children with DMDD to play computer games that are rigged so that children will lose. While playing these games, children with DMDD report more agitation and negative emotional arousal than their typically-developing peers. Furthermore, youths with DMDD showed markedly greater activity in the medial frontal gyrus and anterior cingulate cortex compared to other youths. These brain regions are important because they are involved in evaluating and processing negative emotions, monitoring one’s own emotional state, and selecting an effective response when upset, angry, or frustrated. Altogether, these findings suggest that youths with DMDD are more strongly influenced by negative events than other youths. They may become more upset and select less effective and socially acceptable ways to deal with negative emotions when they arise.

Treatment

Medication

Evidence for treatment is weak, and treatment is determined based on the physician’s response to the symptoms that people with DMDD present. Because the mood stabilizing medication, lithium, is effective in treating adults with bipolar disorder, some physicians have used it to treat DMDD although it has not been shown to be better than placebo in alleviating the signs and symptoms of DMDD.[7] DMDD is treated with a combination of medications that target the child’s symptom presentation. For youths with DMDD alone, antidepressant medication is sometimes used to treat underlying problems with irritability or sadness. For youths with unusually strong temper outbursts, an atypical antipsychotic medication, such as risperidone, may be warranted. Both medications, however, are associated with significant side effects in children. Finally, for children with both DMDD and ADHD, stimulant medication is sometimes used to reduce symptoms of impulsivity.

Psychosocial

Several cognitive-behavioural interventions have been developed to help youths with chronic irritability and temper outbursts. Because many youths with DMDD show problems with ADHD and oppositional-defiant behaviour, experts initially tried to treat these children using contingency management. This type of intervention involves teaching parents to reinforce children’s appropriate behaviour and extinguish (usually through systematic ignoring or time out) inappropriate behaviour. Although contingency management can be helpful for ADHD and ODD symptoms, it does not seem to reduce the most salient features of DMDD, namely, irritability and anger.

Epidemiology

There are not good estimates of the prevalence of DMDD, but primary studies have found a rate of 0.8 to 3.3%. Epidemiological studies show that approximately 3.2% of children in the community have chronic problems with irritability and temper, the essential features of DMDD. These problems are probably more common among clinic-referred youths. Parents report that approximately 30% of children hospitalised for psychiatric problems meet diagnostic criteria for DMDD; 15% meet criteria based on the observations of hospital staff.

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What is Anosognosia?

Introduction

Anosognosia is a condition in which a person with a disability is cognitively unaware of having it due to an underlying physical or psychological (e.g. PTSD, Stockholm syndrome, schizophrenia, bipolar disorder, dementia) condition.

Anosognosia can result from physiological damage to brain structures, typically to the parietal lobe or a diffuse lesion on the fronto-temporal-parietal area in the right hemisphere, and is thus a neuropsychiatric disorder. A deficit of self-awareness, it was first named by the neurologist Joseph Babinski in 1914. Phenomenologically, anosognosia has similarities to denial, which is a psychological defence mechanism; attempts have been made at a unified explanation. Anosognosia is sometimes accompanied by asomatognosia, a form of neglect in which patients deny ownership of body parts such as their limbs. The term is from Ancient Greek ἀ- a-, ‘without’, νόσος nosos, ‘disease’ and γνῶσις gnōsis, ‘knowledge’. It is also considered a disorder that makes the treatment of the patient more difficult, since it may affect negatively the therapeutic relationship.

Causes

Relatively little has been discovered about the cause of the condition since its initial identification. Recent empirical studies tend to consider anosognosia a multi-componential syndrome or multi-faceted phenomenon. That is it can be manifested by failure to be aware of a number of specific deficits, including motor (hemiplegia), sensory (hemianaesthesia, hemianopia), spatial (unilateral neglect), memory (dementia), and language (receptive aphasia) due to impairment of anatomo-functionally discrete monitoring systems.

Anosognosia is relatively common following different causes of brain injury, such as stroke and traumatic brain injury; for example, anosognosia for hemiparesis (weakness of one side of the body) with onset of acute stroke is estimated at between 10% and 18%. However, it can appear to occur in conjunction with virtually any neurological impairment. It is more frequent in the acute than in the chronic phase and more prominent for assessment in the cases with right hemispheric lesions than with the left. Anosognosia is not related to global mental confusion, cognitive flexibility, other major intellectual disturbances, or mere sensory/perceptual deficits.

The condition does not seem to be directly related to sensory loss but is thought to be caused by damage to higher level neurocognitive processes that are involved in integrating sensory information with processes that support spatial or bodily representations (including the somatosensory system). Anosognosia is thought to be related to unilateral neglect, a condition often found after damage to the non-dominant (usually the right) hemisphere of the cerebral cortex in which people seem unable to attend to, or sometimes comprehend, anything on a certain side of their body (usually the left).

Anosognosia can be selective in that an affected person with multiple impairments may seem unaware of only one handicap, while appearing to be fully aware of any others. This is consistent with the idea that the source of the problem relates to spatial representation of the body. For example, anosognosia for hemiplegia may occur with or without intact awareness of visuo-spatial unilateral neglect. This phenomenon of double dissociation can be an indicator of domain-specific disorders of awareness modules, meaning that in anosognosia, brain damage can selectively impact the self-monitoring process of one specific physical or cognitive function rather than a spatial location of the body.

There are also studies showing that the manoeuvre of vestibular stimulation could temporarily improve both the syndrome of spatial unilateral neglect and of anosognosia for left hemiplegia. Combining the findings of hemispheric asymmetry to the right, association with spatial unilateral neglect, and the temporal improvement on both syndromes, it is suggested there can be a spatial component underlying the mechanism of anosognosia for motor weakness and that neural processes could be modulated similarly. There were some cases of anosognosia for right hemiplegia after left hemisphere damage, but the frequency of this type of anosognosia has not been estimated.

Anosognosia may occur as part of receptive aphasia, a language disorder that causes poor comprehension of speech and the production of fluent but incomprehensible sentences. A patient with receptive aphasia cannot correct his own phonetics errors and shows “anger and disappointment with the person with whom s/he is speaking because that person fails to understand her/him”. This may be a result of brain damage to the posterior portion of the superior temporal gyrus, believed to contain representations of word sounds. With those representations significantly distorted, patients with receptive aphasia are unable to monitor their mistakes. Other patients with receptive aphasia are fully aware of their condition and speech inhibitions, but cannot monitor their condition, which is not the same as anosognosia and therefore cannot explain the occurrence of neologistic jargon.

Psychiatry

Although largely used to describe unawareness of impairment after brain injury or stroke, the term “anosognosia” is occasionally used to describe the lack of insight shown by some people with anorexia nervosa. They do not seem to recognise that they have a mental illness. There is evidence that anosognosia related to schizophrenia may be the result of frontal lobe damage. E. Fuller Torrey, a psychiatrist and schizophrenia researcher, has stated that among those with schizophrenia and bipolar disorder, anosognosia is the most prevalent reason for not taking medications.

Diagnosis

Clinically, anosognosia is often assessed by giving patients an anosognosia questionnaire in order to assess their metacognitive knowledge of deficits. However, neither of the existing questionnaires applied in the clinics are designed thoroughly for evaluating the multidimensional nature of this clinical phenomenon; nor are the responses obtained via offline questionnaire capable of revealing the discrepancy of awareness observed from their online task performance. The discrepancy is noticed when patients showed no awareness of their deficits from the offline responses to the questionnaire but demonstrated reluctance or verbal circumlocution when asked to perform an online task. For example, patients with anosognosia for hemiplegia may find excuses not to perform a bimanual task even though they do not admit it is because of their paralysed arms.

A similar situation can happen to patients with anosognosia for cognitive deficits after traumatic brain injury when monitoring their errors during the tasks regarding their memory and attention (online emergent awareness) and when predicting their performance right before the same tasks (online anticipatory awareness). It can also occur among patients with dementia and anosognosia for memory deficit when prompted with dementia-related words, showing possible pre-attentive processing and implicit knowledge of their memory problems. Patients with anosognosia may also overestimate their performance when asked in first-person formed questions but not from a third-person perspective when the questions referring to others.

When assessing the causes of anosognosia within stroke patients, CT scans have been used to assess where the greatest amount of damage is found within the various areas of the brain. Stroke patients with mild and severe levels of anosognosia (determined by response to an anosognosia questionnaire) have been linked to lesions within the temporoparietal and thalamic regions, when compared to those who experience moderate anosognosia, or none at all. In contrast, after a stroke, people with moderate anosognosia have a higher frequency of lesions involving the basal ganglia, compared to those with mild or severe anosognosia.

Treatment

In regard to anosognosia for neurological patients, no long-term treatments exist. As with unilateral neglect, caloric reflex testing (squirting ice cold water into the left ear) is known to temporarily ameliorate unawareness of impairment. It is not entirely clear how this works, although it is thought that the unconscious shift of attention or focus caused by the intense stimulation of the vestibular system temporarily influences awareness. Most cases of anosognosia appear to simply disappear over time, while other cases can last indefinitely. Normally, long-term cases are treated with cognitive therapy to train patients to adjust for their inoperable limbs (though it is believed that these patients still are not “aware” of their disability). Another commonly used method is the use of feedback – comparing clients’ self-predicted performance with their actual performance on a task in an attempt to improve insight.

Neurorehabilitation is difficult because, as anosognosia impairs the patient’s desire to seek medical aid, it may also impair their ability to seek rehabilitation. A lack of awareness of the deficit makes cooperative, mindful work with a therapist difficult. In the acute phase, very little can be done to improve their awareness, but during this time, it is important for the therapist to build a therapeutic alliance with patients by entering their phenomenological field and reducing their frustration and confusion. Since severity changes over time, no single method of treatment or rehabilitation has emerged or will likely emerge.

In regard to psychiatric patients, empirical studies verify that, for individuals with severe mental illnesses, lack of awareness of illness is significantly associated with both medication non-compliance and re-hospitalisation. Fifteen percent of individuals with severe mental illnesses who refuse to take medication voluntarily under any circumstances may require some form of coercion to remain compliant because of anosognosia. Coercive psychiatric treatment is a delicate and complex legal and ethical issue.

One study of voluntary and involuntary inpatients confirmed that committed patients require coercive treatment because they fail to recognise their need for care. The patients committed to the hospital had significantly lower measures of insight than the voluntary patients.

Anosognosia is also closely related to other cognitive dysfunctions that may impair the capacity of an individual to continuously participate in treatment. Other research has suggested that attitudes toward treatment can improve after involuntary treatment and that previously committed patients tend later to seek voluntary treatment.

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What is Schizophrenics Anonymous?

Introduction

Schizophrenics Anonymous is a peer support group to help people who are affected by schizophrenia and related disorders including bipolar disorder, schizoaffective disorder, psychotic depression and psychosis.

Brief History

The programme was established in Detroit in 1985. The founder was Joanne Verbanic, who was diagnosed with schizophrenia in 1970. Shortly before forming SA, Verbanic publicly disclosed her diagnosis and discussed her illness on national television in an effort to challenge the stigma associated with the condition. She was a 2006 recipient of a Lilly Reintegration Award in recognition of her lifetime contributions to the mental health community, and she continued to be active as a spokesperson for persons with schizophrenia and other mental illness until her death on 07 May 2015.

By 2007, more than 150 local SA groups operated in 31 of the 50 United States, and in Australia, Brazil, Canada, Mexico, France, India and Venezuela.

Technical support for Schizophrenics Anonymous was provided by the National Schizophrenia Foundation (NSF) until 2007 when NSF ceased operations. In response to the loss of a national sponsor, a group of consumers, family members, and mental health providers came together to form a not-for-profit organisation, Schizophrenia and Related Disorders Alliance of America (SARDAA).

SARDAA promotes recovery for persons with schizophrenia and related brain disorders including bipolar disorder, schizoaffective disorder, depression with psychosis, and experience with psychosis. They envision a future in which every person with a schizophrenia-related brain disorder has the opportunity to recover from their disorders. The name Schizophrenics Anonymous was changed to Schizophrenia Alliance in 2015 and added Psychosis Support and Acceptance in 2018. They provide an online directory of SA groups, sponsor five weekly SA conference calls, and one Family and Friends conference call. At their annual conference, the group trains individuals and groups who have started or would like to start an SA group.

Although some SA groups are organised by mental health professionals, research has suggested that peer-led SA groups are more sustainable and longer lasting. Some groups are organised in psychiatric hospitals or jails and are not open to the public.

Programme Principles

The SA programme is based on the twelve-step model, but includes just six steps. The organisation describes the programme’s purpose of helping participants to learn about schizophrenia, “restore dignity and sense of purpose,” obtain “fellowship, positive support, and companionship,” improve their attitudes about their lives and their illnesses, and take “positive steps towards recovery.”

Joanne Verbanic wrote the original “Schizophrenics Anonymous” book, better known as “The Blue Book,” which describes the six steps to recovery. The steps require members to admit they need help, take responsibility for their choices and consequences, believe they have the inner strength to help themselves and others, forgive themselves and others, understand that false beliefs contribute to their problems and change those beliefs, and decide to turn their lives over to a higher power.

Research

One study about the risks of professional partnerships centres on the partnership between Schizophrenics Anonymous (SA) and the Mental Health Association of Michigan (MHAM) over a 14-year period. The study shows that the professional partnership resulted in increased access to SA Groups across Michigan and organisation expansion and development within SA. The professional influence also lead more SA Groups to be held in more traditional mental health treatment settings and led to more professional-led SA groups.

Self-help groups are more available to people who live independently. Researchers at Michigan State University studied whether SA would be successful in group homes. The results were positive: the groups had high attendance and participation and were well liked. However, staff members controlled who could lead and who could attend the meetings, and how the meetings should be run. The programs fell apart. The same obstacle occurred in SA groups started in prisons and monitored by employees.

This page is based on the copyrighted Wikipedia article <https://en.wikipedia.org/wiki/Schizophrenics_Anonymous&gt;; it is used under the Creative Commons Attribution-ShareAlike 3.0 Unported License (CC-BY-SA). You may redistribute it, verbatim or modified, providing that you comply with the terms of the CC-BY-SA.

What is the Depression and Bipolar Support Alliance?

Introduction

The Depression and Bipolar Support Alliance (DBSA), formerly the National Depressive and Manic Depressive Association (NDMDA), is a non-profit organisation providing support groups for people who live with depression or bipolar disorder as well as their friends and family.

Refer to Depression and Bipolar Support Alliance (Greater Houston).

Background

DBSA’s scope, also includes outreach, education and advocacy regarding depression and bipolar disorder. DBSA employs a small staff and operates with the guidance of a Scientific Advisory Board.

DBSA sponsors online and “face to face” support groups. A nonrandomized study found participants in such groups reported their coping skills, medication compliance, and acceptance of their illness correlated with participation. Member hospitalization decreased by 49% (from 82% to 33%). Following an initial meeting, members were found to be 6.8 times more likely to attend subsequent meetings if accompanied by a member the first time.

DBSA is a not-for-profit 501(c)(3) organisation and receives over 21 million hits per year on their combined websites. Each month, DBSA distributes nearly 20,000 educational materials free of charge to anyone requesting information about mood disorders. DBSA reaches nearly five million people through their educational materials and programs, exhibit materials, and media activities.

What is the Depression and Bipolar Support Alliance (Greater Houston)?

Introduction

The Depression and Bipolar Support Alliance (DBSA) Greater Houston is a 501(c)(3) non-profit organisation located in Houston, Texas.

DBSA provides free and confidential support groups for individuals living with, or family and friends affected by, depression or bipolar disorder. Each support group is led by a facilitator trained by the organisation. Select groups target specific populations including veterans, adolescents, and parents of adolescents, young adults, senior citizens, LGBT Community, homeless individuals and Spanish-speaking individuals.

Refer to Depression and Bipolar Support Alliance (DBSA).

Brief History

Established in 1979, the Depressive and Manic Disorder Association (DMDA) of Greater Houston sponsored up to five weekly support groups for those with depressive or manic depressive disorders. In 2003, DMDA Greater Houston changed its name to DBSA Greater Houston and formed its own 501(c) (3) corporation. Currently, DBSA Greater Houston sponsors nearly 70 weekly support groups at 50 different locations throughout the Houston metropolitan area. The Houston organisation is the largest of the nation’s DBSA chapters, serving over 1,000 support group participants annually.

Affiliation

The Depression and Bipolar Support Alliance of Greater Houston is a chapter member of the National Depression and Bipolar Support Alliance organisation based in Chicago, Illinois. Additionally, the organisation has developed collaborations with a number of Houston area mental health and social service providers including the Texas Department of Corrections, the Harris County judicial system, the Michael DeBakey VA Hospital, Mental Health of America, National Alliance on Mental Illness and the AIDS Foundation of Houston. Every group provided by DBSA Greater Houston is a collaboration with another organisation in the community. For a list of collaborations, visit the organisations website.

Statistics

DBSA Greater Houston utilises 75 trained volunteer and professional facilitators to provide nearly 70 weekly support groups. According to an independently conducted demographics study in 2008, 64% of DBSA Greater Houston participants were female, 36% were male; 77% were diagnosed individuals while 23% were family members; 66% reported a diagnosis and/or symptoms of depression, 69% were diagnosed with bipolar disorder; 88% were prescribed psychotropic medications and 65% were in professional therapy.

The Depression and Bipolar Support Alliance of Greater Houston conducts an annual satisfaction survey for participants. In 2013, the results continued to show a high rating of satisfaction with a score of 4.28 out of a possible 5, which represents excellence. Also, it was found that the longer a person attends group, the more satisfied they are with the experience and the more skills they learn to manage their disorder.

In 2006 DBSA Greater received the Chapter of the Year award from the national Depression and Bipolar Support Alliance.

Recent Developments

On 24 September 2013, the Depression and Bipolar Support Alliance of Greater Houston hosted its second annual Help, Hope, and Healing Luncheon with speakers Jessie Close and actress, Glenn Close. Jessie lives with Bipolar Disorder and Glenn talked about the perspective of the family and gave 2 monologues.

The Depression and Bipolar Support Alliance of Greater Houston hosted its first annual Help, Hope, and Healing luncheon at the River Oaks Country Club on 24 September 2012 featuring Jane Pauley as the speaker. Jane Pauley is known for her work on Dateline NBC and the Today Show. Ms. Pauley lives with Bipolar Disorder.

In the fall of 2008, DBSA Greater Houston published an outcome study independently conducted by Dr. Ralph Culler, former Associate Dean of Research at the Hogg Foundation for Mental Health. The outcome study was designed to analyse the effectiveness of the DBSA Greater Houston support group model. The study provided tools for DBSA Greater Houston to:

  • Provide quantitative and qualitative evidence that its support group model is effective;
  • Prove DBSA Greater Houston’s accountability to individuals utilising its services; and
  • Learn how the benefits of DBSA occur.

This study provided evidenced-based results that the DBSA Greater Houston support group model was effective in a number of areas. The study used an outcome questionnaire which asked a broad range of questions regarding demographics, medical data, outcome assessments and satisfaction with the support group experience. On average 89% of group participants experienced an improvement in their quality of life as a direct benefit of their participation in the DBSA groups. 93% of participants reported high or very high satisfaction with their DBSA support group experience.

What are Grandiose Delusions?

Introduction

Grandiose delusions (GD) – also known as delusions of grandeur or expansive delusions – are a subtype of delusion that occur in patients suffering from a wide range of psychiatric diseases, including two-thirds of patients in manic state of bipolar disorder, half of those with schizophrenia, patients with the grandiose subtype of delusional disorder, and a substantial portion of those with substance abuse disorders.

GDs are characterised by fantastical beliefs that one is famous, omnipotent, wealthy, or otherwise very powerful. The delusions are generally fantastic and typically have a religious, science fictional, or supernatural theme. There is a relative lack of research into GD, in contrast to persecutory delusions and auditory hallucinations. About 10% of healthy people experience grandiose thoughts but do not meet full criteria for a diagnosis of GD.

Signs and Symptoms

According to the DSM-IV-TR diagnostic criteria for delusional disorders, grandiose-type symptoms include exaggerated beliefs of:

  • Self-worth.
  • Power.
  • Knowledge.
  • Identity.
  • Exceptional relationship to a deity or famous person.

For example, a patient who has fictitious beliefs about his or her power or authority may believe himself or herself to be a ruling monarch who deserves to be treated like royalty. There are substantial differences in the degree of grandiosity linked with grandiose delusions in different patients. Some patients believe they are God, the Queen of the United Kingdom, a president’s son, a famous rock star, and some other examples. Others are not as expansive and think they are skilled athletes or great inventors.

Expansive delusions may be maintained by auditory hallucinations, which advise the patient that they are significant, or confabulations, when, for example, the patient gives a thorough description of their coronation or marriage to the king. Grandiose and expansive delusions may also be part of fantastic hallucinosis in which all forms of hallucinations occur.

Positive Functions

Grandiose delusions frequently serve a very positive function by sustaining or increasing their self-esteem. As a result, it is essential to consider the consequences of removing the grandiose delusion on self-esteem when trying to modify the grandiose delusion in therapy. In many instances of grandiosity, it is suitable to go for a fractional rather than a total modification, which permits those elements of the delusion that are central for self-esteem to be preserved. For example, a person who believes they are a senior secret service agent gains a great sense of self-esteem and purpose from this belief, thus until this sense of self-esteem can be provided from elsewhere, it is best not to attempt modification.

Comorbidity

Schizophrenia

Schizophrenia is a mental disorder distinguished by a loss of contact with reality and the occurrence of psychotic behaviours, including hallucinations and delusions (unreal beliefs which endure even when there is contrary evidence). Delusions may include the false and constant idea that the person is being followed or poisoned, or that the person’s thoughts are being broadcast for others to listen to. Delusions in schizophrenia often develop as a response to the individual attempting to explain their hallucinations. Patients who experience recurrent auditory hallucinations can develop the delusion that other people are scheming against them and are dishonest when they say they do not hear the voices that the delusional person believes that he or she hears.

Specifically, grandiose delusions are frequently found in paranoid schizophrenia, in which a person has an extremely exaggerated sense of his or her significance, personality, knowledge, or authority. For example, the person may declare to own a major corporation and kindly offer to write a hospital staff member a check for $5 million if only help them escape from the hospital. Other common grandiose delusions in schizophrenia include religious delusions such as the belief that one is Jesus Christ.

Bipolar Disorder

Refer to Bipolar Disorder.

Bipolar I disorder can lead to severe affective dysregulation, or mood states that sway from exceedingly low (depression) to exceptionally high (mania). In hypomania or mania, some bipolar patients can suffer grandiose delusions. In its most severe manifestation, days without sleep, auditory and other hallucinations, or uncontrollable racing thoughts can reinforce these delusions. In mania, this illness affects emotions and can also lead to impulsivity and disorganised thinking, which can be harnessed to increase their sense of grandiosity. Protecting this delusion can also lead to extreme irritability, paranoia, and fear. Sometimes their anxiety can be so over-blown that they believe others are jealous of them and, thus, undermine their “extraordinary abilities,” persecuting them or even scheming to seize what they already have.

The vast majority of bipolar patients rarely experience delusions. Typically, when experiencing or displaying a stage of heightened excitability called mania, they can experience joy, rage, and other intense emotions that can cycle out of control, along with thoughts or beliefs that are grandiose. Some of these grandiose thoughts can be expressed as strong beliefs that the patient is very rich or famous or has super-human abilities, or can even lead to severe suicidal ideations. In the most severe form, in what was formerly labelled as megalomania, the bipolar patient may hear voices that support these grandiose beliefs. In their delusions, they can believe that they are, for example, a king, a creative genius, or can even exterminate the world’s poverty because of their extreme generosity.

Cause(s)

There are two alternative causes for developing grandiose delusions:

  1. Delusion-as-defence: Defence of the mind against lower self-esteem and depression.
  2. Emotion-consistent: Result of exaggerated emotions.

Anatomical Aspects

Grandiose delusions may be related to lesions of the frontal lobe. Temporal lobe lesions have been mainly reported in patients with delusions of persecution and of guilt, while frontal and frontotemporal involvement have been described in patients with grandiose delusions, Cotard’s syndrome, and delusional misidentification syndrome.

Diagnosis

Patients with a wide range of mental disorders which disturb brain function experience different kinds of delusions, including grandiose delusions. Grandiose delusions usually occur in patients with syndromes associated with secondary mania, such as Huntington’s disease, Parkinson’s disease, and Wilson’s disease. Secondary mania has also been caused by substances such as L-DOPA and isoniazid which modify the monoaminergic neurotransmitter function. Vitamin B12 deficiency, uraemia, hyperthyroidism as well as the carcinoid syndrome have been found to cause secondary mania, and thus grandiose delusions.

In diagnosing delusions, the MacArthur-Maudsley Assessment of Delusions Schedule is used to assess the patient

Treatment

In patients suffering from schizophrenia, grandiose and religious delusions are found to be the least susceptible to cognitive behavioural interventions. Cognitive behavioural intervention is a form of psychological therapy, initially used for depression, but currently used for a variety of different mental disorders, in hope of providing relief from distress and disability. During therapy, grandiose delusions were linked to patients’ underlying beliefs by using inference chaining. Some examples of interventions performed to improve the patient’s state were focus on specific themes, clarification of patient’s neologisms, and thought linkage. During thought linkage, the patient is asked repeatedly by the therapist to explain their jumps in thought from one subject to a completely different one.

Patients suffering from mental disorders that experience grandiose delusions have been found to have a lower risk of having suicidal thoughts and attempts.

Epidemiology

In researching over 1000 individuals of a vast range of backgrounds, Stompe and colleagues (2006) found that grandiosity remains as the second most common delusion after persecutory delusions. A variation in the occurrence of grandiosity delusions in schizophrenic patients across cultures has also been observed. In research done by Appelbaum et al. it has been found that GDs appeared more commonly in patients with bipolar disorder (59%) than in patients with schizophrenia (49%), followed by presence in substance misuse disorder patients (30%) and depressed patients (21%).

A relationship has been claimed between the age of onset of bipolar disorder and the occurrence of GDs. According to Carlson et al. (2000), grandiose delusions appeared in 74% of the patients who were 21 or younger at the time of the onset, while they occurred only in 40% of individuals 30 years or older at the time of the onset.

Prevalence

Research suggests that the severity of the delusions of grandeur is directly related to a higher self-esteem in individuals and inversely related to any individual’s severity of depression and negative self-evaluations. Lucas et al. (1962) found that there is no significant gender difference in the establishment of grandiose delusion. However, there is a claim that ‘the particular content of Grandiose delusions’ may be variable across both genders. Also, it has been noted that the presence of GDs in people with at least grammar or high school education was greater than lesser educated persons. Similarly, the presence of grandiose delusions in individuals who are the eldest is greater than in individuals who are the youngest of their siblings.

What was the Icarus Project?

Introduction

The Icarus Project was a media and activist endeavour broadly aligned to the anti-psychiatry movement and recovery approach, arguing that mental illness should be understood as an issue of social justice and that a person’s mental state can improve through greater social support and collective liberation.

It shares similarities with the academic fields of Psychopolitics and Mad Studies. The name is derived from Icarus, a hero in Greek mythology, and is metaphorically used to convey that the experiences of mental distress and other extreme mental states can lead to “potential[ly] flying dangerously close to the sun.”

Brief History

In 2002, musician Sascha Altman DuBrul wrote “Bipolar World”, an article published in the San Francisco Bay Guardian. The article described his experiences being diagnosed with bipolar disorder. Among the dozens of e-mails and other correspondence that he received after this publication was a letter from Ashley McNamara, now known as Jacks, an artist and writer who identified strongly with DuBrul’s experiences. DuBrul and McNamara corresponded for a few weeks before finally meeting in person and deciding to start The Icarus Project. Years later, musician-activist Bonfire Madigan Shive and counsellor/activist Will Hall became a key leader in The Icarus Project’s administration and development.

In the Journal of Medical Humanities, co-founder DuBrul wrote of The Icarus Project:

Though we did not fully understand it in the early days, we were walking in the footsteps of a large body of knowledge and thought from the 1960s, grouped under the category of Anti-Psychiatry.

He also noted the group and its members were inspired by a range of social trends and schools of thought including anarchism, permaculture/sustainable ecology, LGBTQ rights, harm reduction, global justice movement, the Beat Generation, counterculture, and punk rock. He writes, “Our response to the label ‘bipolar’ was not a ‘normal’ response, which is why the Icarus Project brought a new perspective to psychic diversity. To create this perspective, we drew inspiration from many social movements and subcultural communities that came before us. So even though our response was unusual, it did not arise in a vacuum. In creating the Icarus Project, we wove together the ideas and practices in these movements to imagine a powerful new counter narrative to the dominant mental health narrative that went beyond a questioning of the language around ‘bipolar’ and critiqued the system itself.”

The first step, they decided, was creating a website where people who identified with “bipolar and other ‘mental illness’ [could] find real community and contribute to it.” DuBrul states that by 2003, “The Icarus Project website was up and running, and a virtual community began to evolve around the discussion forums.” He notes that user-generated content online enabled The Icarus Project’s growth: “We were attracting interesting people, creating discussion forums with names like ‘Alternate Dimensions or Psychotic Delusions’ and ‘Experiencing Madness and Extreme States.’ There was no place else where people who used psych meds and people who did not, people who identified with diagnostic categories and people who did not, could all talk with each other and share stories. Because of the outreach in the anarchist and activist community, there was a high percentage of creative people with a radical political analysis. And with the (seeming) anonymity of the Internet, people felt comfortable being honest and sharing intimate stories about their lives. Our website served as a refuge for a diverse group of people who were learning the ways in which new narratives could be woven about their lives.”

Mission

The Icarus Project’s stated aims are to provide a “support network and education project by and for people who experience the world in ways that are often diagnosed as mental illness.” The national Icarus Collective staff is set up to support local groups instead of creating the smaller organisations themselves. The responsibilities of the local group are to gather people locally for support, education, activism, and access to alternatives to mainstream medical diagnosis and treatment. The Project advocates self-determination and caution when approaching psychiatric care. It encourages harm reduction, alternatives to the prevailing medical model that is accepted by the vast majority of mental health professionals, and self-determination in treatment and diagnosis. Key members of The Icarus Project state that they “envision a world with more options to navigate mental health issues: options that support self-determination, centre people who are most impacted by mental health-based oppression, and most critically, uplift social transformation as central to individual wellbeing.”

In 2005, Journalist Jennifer Itzenson noted that the Icarus Project accepts those with a wide range of perspectives on mental health issues, but also describes “an edge of militancy within the group,” particularly among those who reject medication. Itzenson also writes that while medical professionals applaud groups like the Icarus Project for providing a sense of support and community, and combating social stigmas related to bipolar and other mental health issues, the group’s questioning of the medical paradigm is “misguided” and that rejecting medication is a “potentially fatal choice” for those with bipolar disorder. A Newsweek article provides the following perspective on The Icarus Project’s stance towards medication: “While some critics might view Icaristas as irresponsible, their skepticism about drugs isn’t entirely unfounded. Lately, a number of antipsychotic drugs have been found to cause some troubling side effects.”

Writer Mark Lukach describes in an article for Pacific Standard his experience asking co-founder Sascha Altman DuBrul about the role of psychiatric medication as a part of his wife’s recovery from a bipolar diagnosis. Lukach articulates The Icarus Project’s approach to self-determination in psychiatric treatment. Lukach wrote:

“As for medication, DuBrul said that he believed that the answer to the question of whether or not to use pharmaceuticals needed to be far more nuanced than yes or no. The best response might be maybe, sometimes, or only certain medications. For instance, DuBrul shared that he takes lithium every night because he’s confident that, after four hospitalizations and over a decade with the label bipolar, the medication is a positive part of his care. Not the whole solution, but a piece.”

Anthropologist Erica Hua Fletcher describes Icarus Project member’s diverse ways of discussing altered mental states in the Journal of Medical Humanities. Fletcher writes:

While many Icarus contributors have found relief through the use of psycho-pharmaceutical interventions and other bio-psychiatric technologies, they also have experienced the limitations of medical paradigms and language to recognize the fullness of their lives. Because of this, they frequently adopt alternative words and phrases beyond bio-psychiatric terms to describe their mental states such as “neurodivergent processing,” “diasporas of distressing symptoms,” “sensory/cognitive/emotional trauma,” or “cognitive-emotional terror.” “Bipolar disorder” is interchangeable with highs and lows; “psychosis” can be seen as a reckoning; and nonconsensus realities can describe extreme experiences, which psychiatrists could label as symptoms of “schizophrenia” (such as hearing voices others do not hear or seeing objects others do not see). Such alternative words and phrases do not diminish the utility of bio- psychiatric terminology nor do they directly undermine medical treatment options, yet they allow for a range of descriptors and call for attention to individual needs and desires. They call us to listen to personal stories, to forces at work within communities, and to reevaluate the languages that enframe mental illness as such.” She goes on to state, “Alternative language beyond the biomedical paradigm of mental illness fosters a diversity of paradigms. Moreover, it can create a reflective space for those with mental suffering (and for their healthcare providers) to see themselves outside of a medical identity, reevaluate their self-care regimens, advocate for the care they would like to receive, and connect to others who may have similar concerns about ascribing to solely psycho-pharmaceutical interventions.”

As of early 2018, Icarus Project staff describe their expertise in social activism, herbalism, and labour organising; none is a licensed medical or mental health professional. Icarus Project advisory board members describe themselves as educators, artists, activists, writers, healers, community organisers, and other creative types and some identify as Latinx, queer, trans, people of colour or mixed race, and trauma survivors; none is a licensed medical or mental health professional. Leadership currently offers publications on self-care and community care, workshops and training for peers, training and talks for providers, peer support spaces, webinars, and other events.

Structure/Funding

The Icarus Project is currently under the fiscal sponsorship of FJC, a non-profit 501(c)3 umbrella organization arm of an investment firm, based in New York City. The Icarus Project currently gets the bulk of its money from foundation grants, including the Ittleson Foundation, but it also has many individual donors.

The Icarus Project Network

Places where local chapters met included Anchorage, Alaska; Asheville, North Carolina; Atlanta, Georgia; Boston, Massachusetts; Conway, Arkansas; Chicago, Illinois; Los Angeles, California (Wildflowers’ Movement); Minneapolis, Minnesota; Madison, Wisconsin; New York City, New York; Northampton, Massachusetts (Freedom Centre); Philadelphia, Pennsylvania; Portland, Oregon; San Francisco (Bay Area), California; Columbus, Ohio; Gainesville, Florida.

Media Mentions

The Icarus Project has been mentioned in passing in The New York Times as a resource for those who “don’t want to ‘get better'”, by Frontline 20/20, and many local media outlets.

Publications

Educational materials published by The Icarus Project have been published in Spanish, German, French, Italian, Japanese, Greek, and Bosnian/Croatian. Some of these publications are listed below:

  • In March 2004, The Icarus Project released Navigating the Space Between Brilliance and Madness; A Reader and Roadmap of Bipolar Worlds. The book is currently in its 6th printing.
  • In July 2006, The Icarus Project released the first draft of Friends Make the Best Medicine: A Guide to Creating Community Mental Health Support Networks.
  • In 2008, The Icarus Project released Through the Labyrinth; A Harm Reduction Guide to Coming Off Psychiatric Drugs, and in 2009 this publication was translated into Spanish and German and made available for free download on the Icarus Project website.
  • In 2012, The Icarus Project released Mindful Occupation: Rising Up without Burning Out.
  • In 2015, The Icarus Project released Madness and Oppression: Personal Paths to Transformation and Collective Liberation.

Filmography

Films about Icarus Project members are listed below:

  • Ken Paul Rosenthal (2010). Crooked Beauty. 30 min. Poetic documentary featuring Jacks McNamara. In Mad Dance Mental Health Film Trilogy.
  • Ken Paul Rosenthal (2018). Whisper Rapture. 36 min. A doc-opera featuring Bonfire Madigan Shive.

What is Unipolar Mania?

Introduction

Unipolar mania is an unrecognised mental illness characterised by episodes of mania and normal mood, with the absence of depressive symptoms.

Refer to Bipolar Disorder.

Background

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

Symptoms of unipolar mania are similar to those of bipolar mania. They can include:

  • Elevated self-esteem or grandiosity.
  • Increased motivation or psychomotor agitation.
  • Decreased need for sleep.
  • Unusually talkative.
  • Difficulty maintaining attention.
  • Racing thoughts.
  • Excessive involvement in activities with a high likelihood of painful consequences.(e.g. extravagant shopping, improbable commercial schemes, hypersexuality).

The episode generally have a stronger tendency to present with psychosis or/and need psychiatric assistance.

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.