In psychiatry, stilted speech or pedantic speech is communication characterised by situationally-inappropriate formality (refer to Communication Deviance). This formality can be expressed both through abnormal prosody as well as speech content that is “inappropriately pompous, legalistic, philosophical, or quaint”. Often, such speech can act as evidence for autism spectrum disorder (ASD) or a thought disorder, a common symptom in schizophrenia or schizotypal personality disorder.
To diagnose stilted speech, researchers have previously looked for the following characteristics:
Speech conveying more information than necessary.
Vocabulary and grammar expected from formal writing rather than conversational speech.
Unneeded repetition or corrections.
While literal and long-winded word content is often the most identifiable feature of stilted speech, such speech often displays irregular prosody, especially in resonance. Often, the loudness, pitch, rate, and nasality of pedantic speech vary from normal speech, resulting in the perception of pedantic or stilted speaking. For example, overly loud or high-pitched speech can come across to listeners as overly forceful while slow or nasal speech creates an impression of condescension.
These attributions, which are commonly found in patients with ASD, partially account for why stilted speech has been considered a diagnostic criterion for the disorder. Stilted speech, along with atypical intonation, semantic drift, terseness, and perseveration, are all qualities known to be commonly impaired during conversation with adolescents on the autistic spectrum. Often, stilted speech found in children with ASD will also be especially stereotypic or rehearsed.
Patients with schizophrenia are also known to experience stilted speech. This symptom is attributed to both an inability to access more commonly used words and a difficulty understanding pragmatics – the relationship between language and context. However, stilted speech appears as a less common symptom compared to a certain number of other symptoms of the psychosis. This element of cognitive disorder is also exhibited as a symptom in the narcissistic personality disorder.
There is disagreement on the definition of psychophenomenology within the discipline of psychiatry, e.g. published sources provide definitions that are “various and sometimes conflicting (Rule 2005)”.
Communication deviance (CD) occurs when a speaker fails to effectively communicate meaning to their listener with confusing speech patterns or illogical patterns.
These disturbances can range from vague linguistic references, contradictory statements to more encompassing non-verbal problems at the level of turn-taking.
The term was originally introduced by Lyman Wynne and Margaret Singer in 1963 to describe a communication style found among parents who had children with schizophrenia. According to Wynne, people are able to focus their attention and identify meaning from external stimuli beginning with their interactions, particularly with their parents, during their early years of life. In family communication, deviance is present in the way members acknowledge or affirm one another as well as in task performance.
A recent meta-analysis reported that communication deviance is highly prevalent in parents of patients diagnosed with schizophrenia and adoption studies have reported significant associations between CD in the parent and thought disorder in the offspring, however, the mechanisms by which CD impacts on the offspring’s cognition are still unknown. Some researchers theorize that, in the case of a high degree of egocentric communication in parents where the sender and the receiver do not speak and listen according to each other’s premises, the child develops uncertainty.
The research of psychiatrists and psychoanalysts Lyman Wynne and Theodore Lidz on communication deviance and roles (e.g. pseudo-mutuality, pseudo-hostility, schism and skew) in families of people with schizophrenia also became influential with systems-communications-oriented theorists and therapists.
Diclazepam (Ro5-3448), also known as chlorodiazepam and 2′-chloro-diazepam, is a benzodiazepine and functional analogue of diazepam.
It was first synthesized by Leo Sternbach and his team at Hoffman-La Roche in 1960. It is not currently approved for use as a medication, but rather sold as an unscheduled substance. Efficacy and safety have not been tested in humans.
In animal models, its effects are similar to diazepam, possessing long-acting anxiolytic, anticonvulsant, hypnotic, sedative, skeletal muscle relaxant, and amnestic properties.
Metabolism
Metabolism of this compound has been assessed, revealing diclazepam has an approximate elimination half-life of 42 hours and undergoes N-demethylation to delorazepam, which can be detected in urine for 6 days following administration of the parent compound. Other metabolites detected were lorazepam and lormetazepam which were detectable in urine for 19 and 11 days, respectively, indicating hydroxylation by cytochrome P450 enzymes occurring concurrently with N-demethylation.
Legal Status
United Kingdom
In the UK, diclazepam has been classified as a Class C drug by the May 2017 amendment to The Misuse of Drugs Act 1971 along with several other benzodiazepine drugs.
Disorganised schizophrenia, or hebephrenia, was a subtype of schizophrenia prior to 2013. Subtypes of schizophrenia were no longer recognised as separate conditions in DSM 5 published in 2013. The disorder is no longer listed in the 11th revision of the International Classification of Diseases (ICD-11).
Disorganised schizophrenia is classified within ICD-10 the existing classification, in practice, until the 01 January 2022, as a mental and behavioural disorder, because the classification was thought to be an extreme expression of the disorganisation syndrome that has been hypothesized to be one aspect of a three-factor model of symptoms in schizophrenia, the other factors being reality distortion (involving delusions and hallucinations) and psychomotor poverty (lack of speech, lack of spontaneous movement and various aspects of blunting of emotion).
Presentation
The condition is also known as hebephrenia, named after the Greek term for “adolescence” – ἥβη (hḗbē) – and possibly the ancient-Greek goddess of youth, Hebe, daughter of Hera. The term refers to the ostensibly more prominent appearance of the disorder in persons around puberty.
The prominent characteristics of this form are disorganised behaviour and speech (see formal thought disorder), including loosened associations and schizophasia (“word salad”), and flat or inappropriate affect. In addition, psychiatrists must rule out any possible sign of catatonic schizophrenia.
The most prominent features of disorganised schizophrenia are not delusions and hallucinations, as in paranoid schizophrenia, although fragmentary delusions (unsystemised and often hypochondriacal) and hallucinations may be present. A person with disorganised schizophrenia may also experience behavioural disorganisation, which may impair his or her ability to carry out daily activities such as showering or eating.
The emotional responses of such people often seem strange or inappropriate. Inappropriate facial responses may be common, and behaviour is sometimes described as “silly”, such as inappropriate laughter. Sometimes, there is a complete lack of emotion, including anhedonia (lack of pleasure), and avolition (lack of motivation). Some of these features are also present in other types of schizophrenia, but they are most prominent in disorganised schizophrenia.
Treatment
This form of schizophrenia is typically associated with early onset (often between the ages of 15 and 25 years) and is thought to have a poor prognosis because of the rapid development of negative symptoms and decline in social functioning.
Use of electroconvulsive therapy has been proposed; however, the effectiveness after treatment is in question.
1946 – Michele Elliott, author, psychologist and founder of child protection charity Kidscape.
Michele Elliott
Michele Irmiter Elliott OBE is an author, psychologist, teacher and the founder and director of child protection charity Kidscape. She has chaired World Health Organisation and Home Office working groups and is a Winston Churchill fellow.
Early Life
Elliott was born on 07 January 1946 to James Irmiter and Ivy (née Dashwood). She graduated from Dixie Hollins High School in 1964. She attended the University of South Florida and the University of Florida, gaining a BA in Science and Education and a Masters’ degree in Psychology. She began working with families and children in 1968 in London.
Work
Elliott worked as a child psychologist at The American School in London, where her husband was a social studies teacher.
Kidscape
Elliott founded Kidscape in 1984 to help children stay safe from sexual abuse and from bullying.
Elliott has been a high-profile figure and Kidscape was named Charity of the Year in 2000. Writing in The Guardian, David Brindle suggested the award was “an undoubted reflection of the vibrancy of Michele Elliott”.
Female Child Sexual Abuse Offenders
Elliott, who had previously written books about male abuse of children, has undertaken pioneering work in investigating and raising awareness of the problem and extent of child sexual abuse committed by women, and the topic of female paedophilia, publishing the book Female Sexual Abuse of Children The Last Taboo in 1992. The book was well received by professionals and survivors’ organisations. Mike Lew described it as “an important and challenging work”, helping “to forge a new understanding of the issues”. Doody’s annual stated it was “an extremely valuable book for all professionals, and it greatly increases the current state of knowledge, or lack of that knowledge, that can have a profound influence on the survivor’s development and recovery”.
Elliott’s work in exposing the issue of child sexual abuse committed by women has also resulted in hostility from feminists. While compiling Female Sexual Abuse of Children, Elliott organised a conference in London concerning sexual abuse by women. After publishing the book, Elliott was subject to a “deluge” of hate mail from feminists.
Awards
In 2008 Elliot was honoured with an OBE by the Queen for services to children. The following year she was named Children and Young People’s Champion. She was awarded an honorary doctorate by Post University in 1998 and another honorary doctorate by the University of Birmingham in 2003. She was awarded a Winston Churchill Fellowship in 1996. Her book, “Bullies, Cyberbullies and Frenemies” received the Literary Classics Gold Award in 2013.
Chlorpromazine (CPZ), marketed under the brand names Thorazine and Largactil among others, is an antipsychotic medication.
It is primarily used to treat psychotic disorders such as schizophrenia. Other uses include the treatment of bipolar disorder, severe behavioural problems in children including those with attention deficit hyperactivity disorder, nausea and vomiting, anxiety before surgery, and hiccups that do not improve following other measures. It can be given by mouth, by injection into a muscle, or into a vein.
Chlorpromazine is in the typical antipsychotic class, and, chemically, is one of the phenothiazines. Its mechanism of action is not entirely clear but believed to be related to its ability as a dopamine antagonist. It also has anti-serotonergic and antihistaminergic properties.
Common side effects include movement problems, sleepiness, dry mouth, low blood pressure upon standing, and increased weight. Serious side effects may include the potentially permanent movement disorder tardive dyskinesia, neuroleptic malignant syndrome, severe lowering of the seizure threshold, and low white blood cell levels. In older people with psychosis as a result of dementia it may increase the risk of death. It is unclear if it is safe for use in pregnancy.
Chlorpromazine was developed in 1950 and was the first antipsychotic. It is on the World Health Organisation’s List of Essential Medicines. Its introduction has been labelled as one of the great advances in the history of psychiatry. It is available as a generic medication.
Brief History
In 1933, the French pharmaceutical company Laboratoires Rhône-Poulenc began to search for new anti-histamines. In 1947, it synthesized promethazine, a phenothiazine derivative, which was found to have more pronounced sedative and antihistaminic effects than earlier drugs. A year later, the French surgeon Pierre Huguenard used promethazine together with pethidine as part of a cocktail to induce relaxation and indifference in surgical patients. Another surgeon, Henri Laborit, believed the compound stabilized the central nervous system by causing “artificial hibernation”, and described this state as “sedation without narcosis”. He suggested to Rhône-Poulenc that they develop a compound with better stabilising properties. In December 1950, the chemist Paul Charpentier produced a series of compounds that included RP4560 or chlorpromazine.[5] Simone Courvoisier conducted behavioural tests and found chlorpromazine produced indifference to aversive stimuli in rats.
Chlorpromazine was distributed for testing to physicians between April and August 1951. Laborit trialled the medicine on at the Val-de-Grâce military hospital in Paris, using it as an anaesthetic booster in intravenous doses of 50 to 100 mg on surgery patients and confirming it as the best drug to date in calming and reducing shock, with patients reporting improved well being afterwards. He also noted its hypothermic effect and suggested it may induce artificial hibernation. Laborit thought this would allow the body to better tolerate major surgery by reducing shock, a novel idea at the time. Known colloquially as “Laborit’s drug”, chlorpromazine was released onto the market in 1953 by Rhône-Poulenc and given the trade name Largactil, derived from large “broad” and acti* “activity.
Following on, Laborit considered whether chlorpromazine may have a role in managing patients with severe burns, Raynaud’s phenomenon, or psychiatric disorders. At the Villejuif Mental Hospital in November 1951, he and Montassut administered an intravenous dose to psychiatrist Cornelia Quarti who was acting as a volunteer. Quarti noted the indifference, but fainted upon getting up to go to the toilet, and so further testing was discontinued (orthostatic hypotension is a known side effect of chlorpromazine). Despite this, Laborit continued to push for testing in psychiatric patients during early 1952. Psychiatrists were reluctant initially, but on 19 January 1952, it was administered (alongside pethidine, pentothal and ECT) to Jacques Lh. a 24-year-old manic patient, who responded dramatically, and was discharged after three weeks having received 855 mg of the drug in total.
Pierre Deniker had heard about Laborit’s work from his brother-in-law, who was a surgeon, and ordered chlorpromazine for a clinical trial at the Sainte-Anne Hospital Centre in Paris where he was Men’s Service Chief. Together with the Director of the hospital, Professor Jean Delay, they published their first clinical trial in 1952, in which they treated 38 psychotic patients with daily injections of chlorpromazine without the use of other sedating agents. The response was dramatic; treatment with chlorpromazine went beyond simple sedation with patients showing improvements in thinking and emotional behaviour. They also found that doses higher than those used by Laborit were required, giving patients 75-100 mg daily.
Deniker then visited America, where the publication of their work alerted the American psychiatric community that the new treatment might represent a real breakthrough. Heinz Lehmann of the Verdun Protestant Hospital in Montreal trialled it in 70 patients and also noted its striking effects, with patients’ symptoms resolving after many years of unrelenting psychosis. By 1954, chlorpromazine was being used in the United States to treat schizophrenia, mania, psychomotor excitement, and other psychotic disorders. Rhône-Poulenc licensed chlorpromazine to Smith Kline & French (today’s GlaxoSmithKline) in 1953. In 1955 it was approved in the United States for the treatment of emesis (vomiting). The effect of this drug in emptying psychiatric hospitals has been compared to that of penicillin and infectious diseases. But the popularity of the drug fell from the late 1960s as newer drugs came on the scene. From chlorpromazine a number of other similar antipsychotics were developed. It also led to the discovery of antidepressants.
Chlorpromazine largely replaced electroconvulsive therapy, hydrotherapy, psychosurgery, and insulin shock therapy. By 1964, about 50 million people worldwide had taken it. Chlorpromazine, in widespread use for 50 years, remains a “benchmark” drug in the treatment of schizophrenia, an effective drug although not a perfect one. The relative strengths or potencies of other antipsychotics are often ranked or measured against chlorpromazine in aliquots of 100 mg, termed chlorpromazine equivalents or CPZE.
In the movie: “Shutter Island”, chlorpromazine is presented as being the new medicament for psychosis treatment however with adverse effects like tremors or abstinence syndrome.
Brand Names
Brand names include Thorazine, Largactil, Hibernal, and Megaphen (sold by Bayer in West-Germany since July 1953).
Medical Uses
Chlorpromazine is used in the treatment of both acute and chronic psychoses, including schizophrenia and the manic phase of bipolar disorder, as well as amphetamine-induced psychosis.
In a 2013 comparison of 15 antipsychotics in schizophrenia, chlorpromazine demonstrated mild-standard effectiveness. It was 13% more effective than lurasidone and iloperidone, approximately as effective as ziprasidone and asenapine, and 12–16% less effective than haloperidol, quetiapine, and aripiprazole.
A 2014 systematic review carried out by Cochrane included 55 trials that compared the effectiveness of chlorpromazine versus placebo for the treatment of schizophrenia. Compared to the placebo group, patients under chlorpromazine experienced less relapse during 6 months to 2 years follow-up. No difference was found between the two groups beyond two years of follow-up. Patients under chlorpromazine showed a global improvement in symptoms and functioning. The systematic review also highlighted the fact that the side effects of the drug were ‘severe and debilitating’, including sedation, considerable weight gain, a lowering of blood pressure, and an increased risk of suffering from acute movement disorders. They also noted that the quality of evidence of the 55 included trials was very low and that 315 trials could not be included in the systematic review due to their poor quality. They called for further research on the subject, as chlorpromazine is a cheap benchmark drug and one of the most used treatments for schizophrenia worldwide.
Chlorpromazine has also been used in porphyria and as part of tetanus treatment. It still is recommended for short-term management of severe anxiety and psychotic aggression. Resistant and severe hiccups, severe nausea/emesis, and preanesthetic conditioning are other uses. Symptoms of delirium in hospitalised AIDS patients have been effectively treated with low doses of chlorpromazine.
Other
Chlorpromazine is occasionally used off-label for treatment of severe migraine. It is often, particularly as palliation, used in small doses to reduce nausea suffered by opioid-treated cancer patients and to intensify and prolong the analgesia of the opioids as well. Efficacy has been shown in treatment of symptomatic hypertensive emergency.
In Germany, chlorpromazine still carries label indications for insomnia, severe pruritus, and preanaesthesia.
Chlorpromazine and other phenothiazines have been demonstrated to possess antimicrobial properties, but are not currently used for this purpose except for a very small number of cases.
Adverse Effects
There appears to be a dose-dependent risk for seizures with chlorpromazine treatment. Tardive dyskinesia (involuntary, repetitive body movements) and akathisia (a feeling of inner restlessness and inability to stay still) are less commonly seen with chlorpromazine than they are with high potency typical antipsychotics such as haloperidol or trifluoperazine, and some evidence suggests that, with conservative dosing, the incidence of such effects for chlorpromazine may be comparable to that of newer agents such as risperidone or olanzapine.
Chlorpromazine may deposit in ocular tissues when taken in high dosages for long periods of time.
Contraindications
Absolute contraindications include:
Circulatory depression.
CNS depression.
Coma.
Drug intoxication.
Bone marrow suppression.
Phaeochromocytoma.
Hepatic failure.
Active liver disease.
Previous hypersensitivity (including jaundice, agranulocytosis, etc.) to phenothiazines, especially chlorpromazine, or any of the excipients in the formulation being used.
Relative contraindications include:
Epilepsy.
Parkinson’s disease.
Myasthenia gravis.
Hypoparathyroidism.
Prostatic hypertrophy.
Very rarely, elongation of the QT interval may occur, increasing the risk of potentially fatal arrhythmias.
Interactions
Consuming food prior to taking chlorpromazine orally limits its absorption, likewise cotreatment with benztropine can also reduce chlorpromazine absorption. Alcohol can also reduce chlorpromazine absorption. Antacids slow chlorpromazine absorption. Lithium and chronic treatment with barbiturates can increase chlorpromazine clearance significantly. Tricyclic antidepressants (TCAs) can decrease chlorpromazine clearance and hence increase chlorpromazine exposure. Cotreatment with CYP1A2 inhibitors like ciprofloxacin, fluvoxamine or vemurafenib can reduce chlorpromazine clearance and hence increase exposure and potentially also adverse effects. Chlorpromazine can also potentiate the CNS depressant effects of drugs like barbiturates, benzodiazepines, opioids, lithium and anaesthetics and hence increase the potential for adverse effects such as respiratory depression and sedation.
It is also a moderate inhibitor of CYP2D6 and also a substrate for CYP2D6 and hence can inhibit its own metabolism. It can also inhibit the clearance of CYP2D6 substrates such as dextromethorphan and hence also potentiate their effects. Other drugs like codeine and tamoxifen which require CYP2D6-mediated activation into their respective active metabolites may have their therapeutic effects attenuated. Likewise CYP2D6 inhibitors such as paroxetine or fluoxetine can reduce chlorpromazine clearance and hence increase serum levels of chlorpromazine and hence potentially also its adverse effects. Chlorpromazine also reduces phenytoin levels and increases valproic acid levels. It also reduces propranolol clearance and antagonises the therapeutic effects of antidiabetic agents, levodopa (a Parkinson’s medication. This is likely due to the fact that chlorpromazine antagonises the D2 receptor which is one of the receptors dopamine, a levodopa metabolite, activates), amphetamines and anticoagulants. It may also interact with anticholinergic drugs such as orphenadrine to produce hypoglycaemia (low blood sugar).
Chlorpromazine may also interact with epinephrine (adrenaline) to produce a paradoxical fall in blood pressure. Monoamine oxidase inhibitors (MAOIs) and thiazide diuretics may also accentuate the orthostatic hypotension experienced by those receiving chlorpromazine treatment. Quinidine may interact with chlorpromazine to increase myocardialdepression. Likewise it may also antagonize the effects of clonidine and guanethidine. It also may reduce the seizure threshold and hence a corresponding titration of anticonvulsant treatments should be considered. Prochlorperazine and desferrioxamine may also interact with chlorpromazine to produce transient metabolic encephalopathy.
Other drugs that prolong the QT interval such as quinidine, verapamil, amiodarone, sotalol and methadone may also interact with chlorpromazine to produce additive QT interval prolongation.
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.
Pharmacology
Chlorpromazine is classified as a low-potency typical antipsychotic. Low-potency antipsychotics have more anticholinergic side effects, such as dry mouth, sedation, and constipation, and lower rates of extrapyramidal side effects, while high-potency antipsychotics (such as haloperidol) have the reverse profile.
Pharmacodynamics
Chlorpromazine is a very effective antagonist of D2 dopamine receptors and similar receptors, such as D3 and D5. Unlike most other drugs of this genre, it also has a high affinity for D1 receptors. Blocking these receptors causes diminished neurotransmitter binding in the forebrain, resulting in many different effects. Dopamine, unable to bind with a receptor, causes a feedback loop that causes dopaminergic neurons to release more dopamine. Therefore, upon first taking the drug, patients will experience an increase in dopaminergic neural activity. Eventually, dopamine production of the neurons will drop substantially and dopamine will be removed from the synaptic cleft. At this point, neural activity decreases greatly; the continual blockade of receptors only compounds this effect.
Chlorpromazine acts as an antagonist (blocking agent) on different postsynaptic and presynaptic receptors:
Dopamine receptors (subtypes D1, D2, D3 and D4), which account for its different antipsychotic properties on productive and unproductive symptoms, in the mesolimbic dopamine system accounts for the antipsychotic effect whereas the blockade in the nigrostriatal system produces the extrapyramidal effects.
Serotonin receptors (5-HT2, 5-HT6 and 5-HT7), with anxiolytic, antidepressant and anti-aggressive properties as well as an attenuation of extrapyramidal side effects, but also leading to weight gain and ejaculation difficulties.
Histamine receptors (H1 receptors, accounting for sedation, antiemetic effect, vertigo, and weight gain).
α1- and α2-adrenergic receptors (accounting for sympatholytic properties, lowering of blood pressure, reflex tachycardia, vertigo, sedation, hypersalivation and incontinence as well as sexual dysfunction, but may also attenuate pseudoparkinsonism – controversial. Also associated with weight gain as a result of blockage of the adrenergic alpha 1 receptor).
M1 and M2 muscarinic acetylcholine receptors (causing anticholinergic symptoms such as dry mouth, blurred vision, constipation, difficulty or inability to urinate, sinus tachycardia, electrocardiographic changes and loss of memory, but the anticholinergic action may attenuate extrapyramidal side effects).
The presumed effectiveness of the antipsychotic drugs relied on their ability to block dopamine receptors. This assumption arose from the dopamine hypothesis that maintains that both schizophrenia and bipolar disorder are a result of excessive dopamine activity. Furthermore, psychomotor stimulants like cocaine that increase dopamine levels can cause psychotic symptoms if taken in excess.
Chlorpromazine and other typical antipsychotics are primarily blockers of D2 receptors. In fact an almost perfect correlation exists between the therapeutic dose of a typical antipsychotic and the drug’s affinity for the D2 receptor. Therefore, a larger dose is required if the drug’s affinity for the D2 receptor is relatively weak. A correlation exists between average clinical potency and affinity of the antipsychotics for dopamine receptors. Chlorpromazine tends to have greater effect at serotonin receptors than at D2 receptors, which is notably the opposite effect of the other typical antipsychotics. Therefore, chlorpromazine with respect to its effects on dopamine and serotonin receptors is more similar to the atypical antipsychotics than to the typical antipsychotics.
Chlorpromazine and other antipsychotics with sedative properties such as promazine and thioridazine are among the most potent agents at α-adrenergic receptors. Furthermore, they are also among the most potent antipsychotics at histamine H1 receptors. This finding is in agreement with the pharmaceutical development of chlorpromazine and other antipsychotics as anti-histamine agents. Furthermore, the brain has a higher density of histamine H1 receptors than any body organ examined which may account for why chlorpromazine and other phenothiazine antipsychotics are as potent at these sites as the most potent classical antihistamines.
In addition to influencing the neurotransmitters dopamine, serotonin, epinephrine, norepinephrine, and acetylcholine it has been reported that antipsychotic drugs could achieve glutamatergic effects. This mechanism involves direct effects on antipsychotic drugs on glutamate receptors. By using the technique of functional neurochemical assay chlorpromazine and phenothiazine derivatives have been shown to have inhibitory effects on NMDA receptors that appeared to be mediated by action at the Zn site. It was found that there is an increase of NMDA activity at low concentrations and suppression at high concentrations of the drug. No significant difference in glutamate and glycine activity from the effects of chlorpromazine were reported. Further work will be necessary to determine if the influence in NMDA receptors by antipsychotic drugs contributes to their effectiveness.
Chlorpromazine does also act as a FIASMA (functional inhibitor of acid sphingomyelinase).
Peripheral Effects
Chlorpromazine is an antagonist to H1 receptors (provoking antiallergic effects), H2 receptors (reduction of forming of gastric juice), M1 and M2 receptors (dry mouth, reduction in forming of gastric juice) and some 5-HT receptors (different anti-allergic/gastrointestinal actions).
Because it acts on so many receptors, chlorpromazine is often referred to as a “dirty drug”.
Veterinary Use
The veterinary use of chlorpromazine has generally been superseded by use of acepromazine.
Chlorpromazine may be used as an antiemetic in dogs and cats, or, less often, as sedative before anaesthesia. In horses, it often causes ataxia and lethargy, and is therefore seldom used.
It is commonly used to decrease nausea in animals that are too young for other common anti-emetics. It is also sometimes used as a preanesthetic and muscle relaxant in cattle, swine, sheep, and goats.
The use of chlorpromazine in food-producing animals is not permitted in the EU, as a maximum residue limit could not be determined following assessment by the European Medicines Agency.
Research
Chlorpromazine has tentative benefit in animals infected with Naegleria fowleri. and shows antifungal and antibacterial activity in vitro.
The emphasis of the treatment of bipolar disorder is on effective management of the long-term course of the illness, which can involve treatment of emergent symptoms.
Treatment methods include pharmacological and psychological techniques.
Principles
The primary treatment for bipolar disorder consists of medications called mood stabilisers, which are used to prevent or control episodes of mania or depression. Medications from several classes have mood stabilising activity. Many individuals may require a combination of medication to achieve full remission of symptoms. As it is impossible to predict which medication will work best for a particular individual, it may take some trial and error to find the best medication or combination for a specific patient. Psychotherapy also has a role in the treatment of bipolar disorder. The goal of treatment is not to cure the disorder but rather to control the symptoms and the course of the disorder. Generally speaking, maintenance treatment of bipolar disorder continues long after symptom control has been achieved.
Following diagnostic evaluation, the treating clinician must determine the optimal treatment setting in order to ensure the patient’s safety. Assessment of suicide risk is key, as the rate of suicide completion among those with bipolar disorder may be as high as 10-15%. Hospitalisation should be considered in patients whose judgement is significantly impaired by their illness, and those who have not responded to outpatient treatment; this may need to be done on an involuntary basis. Treatment setting should regularly be re-evaluated to ensure that it is optimal for the patient’s needs.
Mood Stabilisers
Lithium Salts
Lithium salts have been used for centuries as a first-line treatment for bipolar disorder. In ancient times, doctors would send their mentally ill patients to drink from “alkali springs” as a treatment. Although they were not aware of it, they were actually prescribing lithium, which was present in high concentration within the waters. The therapeutic effect of lithium salts appears to be entirely due to the lithium ion, Li+.
Its exact mechanism of action is uncertain, although there are several possibilities such as inhibition of inositol monophosphatase, modulation of G proteins or regulation of gene expression for growth factors and neuronal plasticity. There is strong evidence for its effectiveness in acute treatment and prevention of recurrence of mania. It can also be effective in bipolar depression, although the evidence is not as strong. It is also effective in reducing the risk of suicide in patients with mood disorders.
Potential side effects from lithium include gastrointestinal upset, tremor, sedation, excessive thirst, frequent urination, cognitive problems, impaired motor coordination, hair loss, and acne. Excessive levels of lithium can be harmful to the kidneys, and increase the risk of side effects in general. As a result, kidney function and blood levels of lithium are monitored in patients being treated with lithium. Therapeutic plasma levels of lithium range from 0.5 to 1.5 mEq/L, with levels of 0.8 or higher being desirable in acute mania.
Lithium levels should be above 0.6 mEq/L to reduce both manic and depressive episodes in patients. A recent review concludes that the standard lithium serum level should be 0.60-0.80 mmol/L with optional reduction to 0.40-0.60 mmol/L in case of good response but poor tolerance or an increase to 0.80-1.00 mmol/L in case of insufficient response and good tolerance.
Monitoring is generally more frequent when lithium is being initiated, and the frequency can be decreased once a patient is stabilised on a given dose. Thyroid hormones should also be monitored periodically, as lithium can increase the risk of hypothyroidism.
Anticonvulsants
A number of anti-convulsant drugs are used as mood stabilisers, and the suspected mechanism is related to the theory that mania can “kindle” further mania, similar to the kindling model of seizures. Valproic acid, or valproate, was one of the first anti-convulsants tested for use in bipolar disorder. It has proven to be effective for treating acute mania. The mania prevention and antidepressant effects of valproic acid have not been well demonstrated. Valproic acid is less effective than lithium at preventing and treating depressive episodes.
Carbamazepine was the first anti-convulsant shown to be effective for treating bipolar mania. It has not been extensively studied in bipolar depression. It is generally considered a second-line agent due to its side effect profile. Lamotrigine is considered a first-line agent for the treatment of bipolar depression. It is effective in preventing the recurrence of both mania and depression, but it has not proved useful in treating acute mania.
Zonisamide (trade name Zonegran), another anti-convulsant, also may show promise in treating bipolar depression. Various other anti-convulsants have been tested in bipolar disorder, but there is little evidence of their effectiveness. Other anti-convulsants effective in some cases and being studied closer include phenytoin, levetiracetam, pregabalin and valnoctamide.
Each anti-convulsant agent has a unique side-effect profile. Valproic acid can frequently cause sedation or gastrointestinal upset, which can be minimised by giving the related drug divalproex, which is available in an enteric-coated tablet. These side effects tend to disappear over time. According to studies conducted in Finland in patients with epilepsy, valproate may increase testosterone levels in teenage girls and produce polycystic ovary syndrome in women who began taking the medication before age 20. Increased testosterone can lead to polycystic ovary syndrome with irregular or absent menses, obesity, and abnormal growth of hair. Therefore, young female patients taking valproate should be monitored carefully by a physician. Excessive levels of valproate can lead to impaired liver function, and liver enzymes and serum valproate level, with a target of 50–125 µg/L, should be monitored periodically.
Side effects of carbamazepine include blurred vision, double vision, ataxia, weight gain, nausea, and fatigue, as well as some rare but serious side effects such as blood dyscrasias, pancreatitis, exfoliative dermatitis, and hepatic failure. Monitoring of liver enzymes, platelets, and blood cell counts are recommended.
Lamotrigine generally has minimal side effects, but the dose must be increased slowly to avoid rashes, including exfoliative dermatitis.
Atypical Antipsychotic Drugs
Antipsychotics work best in the manic phase of bipolar disorder. Second-generation or atypical antipsychotics (including aripiprazole, olanzapine, quetiapine, paliperidone, risperidone, and ziprasidone) have emerged as effective mood stabilisers. The evidence for this is fairly recent, as in 2003 the American Psychiatric Press noted that atypical anti-psychotics should be used as adjuncts to other anti-manic drugs because their mood stabilising properties had not been well established. The mechanism is not well known, but may be related to effects on glutamate activity. Several studies have shown atypical antipsychotics to be effective both as single-agent and adjunctive treatments. Antidepressant effectiveness varies, which may be related to different serotonergic and dopaminergic receptor binding profiles. Quetiapine and the combination of olanzapine and fluoxetine have both demonstrated effectiveness in bipolar depression.
In light of recent evidence, olanzapine (Zyprexa) has been US Food and Drug Administration (FDA) approved as an effective monotherapy for the maintenance of bipolar disorder. A head-to-head randomised control trial (RCT) in 2005 has also shown olanzapine monotherapy to be just as effective and safe as lithium in prophylaxis.
The atypical antipsychotics differ somewhat in side effect profiles, but most have some risk of sedation, weight gain, and extrapyramidal symptoms (including tremor, stiffness, and restlessness). They may also increase the risk of metabolic syndrome, so metabolic monitoring should be performed regularly, including checks of serum cholesterol, triglycerides, and glucose, weight, blood pressure, and waist circumference. Taking antipsychotics for long periods or at high doses can also cause tardive dyskinesia – a sometimes incurable neurological disorder resulting in involuntary, repetitive body movements. The risk of tardive dyskinesia appears to be lower in second-generation antipsychotics than in first-generation antipsychotics but as with first-generation drugs, increases with time spent on medications and in older patients.
New Treatments
A variety of other agents have been tried in bipolar disorder, including benzodiazepines, calcium channel blockers, L-methylfolate, and thyroid hormone. Modafinil (Provigil) and Pramipexole (Mirapex) have been suggested for treating cognitive dysfunction associated with bipolar depression, but evidence supporting their use is quite limited. In addition riluzole, a glutamatergic drug used in ALS has been studied as an adjunct or monotherapy treatment in bipolar depression, with mixed and inconsistent results. The selective oestrogen receptor modulator medication tamoxifen has shown rapid and robust efficacy treating acute mania in bipolar patients. This action is likely due not to tamoxifen’s oestrogen-modulating properties, but due to its secondary action as an inhibitor of protein Kinase C.
Cognitive Effects of Mood Stabilisers
Bipolar patients taking antipsychotics have lower scores on tests of memory and full-scale IQ than patients taking other mood stabilisers. Use of both typical and atypical antipsychotics is associated with risk of cognitive impairment, but the risk is higher for antipsychotics with more sedating effects.
Among bipolar patients taking anticonvulsants, those on lamotrigine have a better cognitive profile than those on carbamazepine, valproate, topiramate, and zonisamide.
Although decreased verbal memory and slowed psychomotor speed are common side effects of lithium use these side effects usually disappear after discontinuation of lithium. Lithium may be protective of cognitive function in the long term since it promotes neurogenesis in the hippocampus and increases grey matter volume in the prefrontal cortex.
Antidepressants
Antidepressants should only be used with caution in bipolar disorder, as they may not be effective and may even induce mania. They should not be used alone, but may be considered as an adjunct to lithium.
A recent large-scale study found that severe depression in patients with bipolar disorder responds no better to a combination of antidepressant medications and mood stabilisers than it does to mood stabilisers alone and that antidepressant use does not hasten the emergence of manic symptoms in patients with bipolar disorder.
The concurrent use of an antidepressant and a mood stabiliser, instead of mood stabiliser monotherapy, may lower the risk of further bipolar depressive episodes in patients whose most recent depressive episode has been resolved. However, some studies have also found that antidepressants pose a risk of inducing hypomania or mania, sometimes in individuals with no prior history of mania. Saint John’s Wort, although a naturally occurring compound, is thought to function in a fashion similar to man-made antidepressants, and so unsurprisingly, there are reports that suggest that it can also induce mania. For these reasons, some psychiatrists are hesitant to prescribe antidepressants for the treatment of bipolar disorder unless mood stabilisers have failed to have an effect, however, others feel that antidepressants still have an important role to play in treatment of bipolar disorder.
Side effects vary greatly among different classes of antidepressants.
Antidepressants are helpful in preventing suicides in people suffering from bipolar disorder when they go in for the depressive phase.
NMDA-Receptor Antagonists
In a double-blind, placebo-controlled, proof-of-concept study, researchers administered an N-methyl-d-aspartate-receptor antagonist (ketamine) to 18 patients already on treatment with lithium (10 patients) or valproate (8 patients) for bipolar depression. From 40 minutes following intravenous injection of ketamine hydrochloride (0.5 mg/kg), the researchers observed significant improvements in depressive symptoms, as measured by standard tools, that were maintained for up to 3 days, an effect not observed in subjects who received the placebo. Five subjects dropped out of the ketamine study; of these, four were taking valproate and one was being treated with lithium. One patient showed signs of hypomania following ketamine administration and two experienced low mood. This study demonstrates a rapid-onset antidepressant effect of ketamine in a small group of patients with bipolar depression. The authors acknowledged the study’s limitations, including the dissociative disturbances in patients receiving ketamine that could have compromised the study blinding, and they emphasised the need for further research.
A more recent double-blind, placebo-controlled study by the same group found that ketamine treatment resulted in a similarly rapid alleviation of suicidal ideation in 15 patients with bipolar depression.
Ketamine is used as a dissociative anaesthetic, and is a Class C substance in the United Kingdom; as such, it should only be used under the direction of a health professional.
Dopamine Agonists
In a single controlled study of twenty one patients, the dopamine D3 receptor agonist pramipexole was found to be highly effective in the treatment of bipolar depression. Treatment was initiated at 0.125 mg t.i.d. and increased at a rate of 0.125 mg t.i.d. to a limit of 4.5 mg qd until the patients’ condition satisfactorily responded to the medication or they could not abide the side effects. The final average dosage was 1.7 mg ± .90 mg qd. The incidence of hypomania in the treatment group was no greater than in the control group.
Psychotherapy
Certain types of psychotherapy, used in combination with medication, may provide some benefit in the treatment of bipolar disorders. Psychoeducation has been shown to be effective in improving patients’ compliance with their lithium treatment. Evidence of the efficacy of family therapy is not adequate to support unrestricted recommendation of its use. There is “fair support” for the utility of cognitive therapy. Evidence for the efficacy of other psychotherapies is absent or weak, often not being performed under randomised and controlled conditions. Well-designed studies have found interpersonal and social rhythm therapy to be effective.
Although medication and psychotherapy cannot cure the illness, therapy can often be valuable in helping to address the effects of disruptive manic or depressive episodes that have hurt a patient’s career, relationships or self-esteem. Therapy is available not only from psychiatrists but from social workers, psychologists and other licensed counsellors.
Jungian Therapy
Jungian authors have likened the mania and depression of bipolar disorder to the Jungian archetypes ‘puer’ and ‘senex’. The puer archetype is defined by the behaviours of spontaneity, impulsiveness, enthusiasm or mania and is symbolised by characters such as Peter Pan or the Greek god Hermes. The senex archetype is defined by behaviours of order, systematic thought, caution, and depression and is symbolised by characters such as the Roman god Saturn or the Greek god Kronos. Jungians conceptualise the puer and senex as a coexistent bipolarity appearing in human behaviour and imagination, but in neurotic manifestations appears as extreme oscillations and as unipolar manifestations. In the case of the split puer-senex bipolarity the therapeutic task is to bring the puer and senex back into correlation by working with the patient’s mental imagery.”
Lifestyle Changes
Sufficient Sleep
If sleeping is disturbed, the symptoms can occur. Sleep disruption may actually exacerbate the mental illness state. Those who do not get enough sleep at night, sleep late and wake up late, or go to sleep with some disturbance (e.g. music or charging devices) have a greater chance of having the symptoms and, in addition, depression. It is highly advised to not sleep too late and to get enough high quality sleep.
Self-Management and Self-Awareness
Understanding the symptoms, when they occur and ways to control them using appropriate medications and psychotherapy has given many people diagnosed with bipolar disorder a chance at a better life. Prodrome symptom detection has been shown to be used effectively to anticipate onset of manic episodes and requires high degree of understanding of one’s illness. Because the offset of the symptoms is often gradual, recognising even subtle mood changes and activity levels is important in avoiding a relapse. Maintaining a mood chart is a specific method used by patients and doctors to identify mood, environmental and activity triggers.
Stress Reduction
Forms of stress may include having too much to do, too much complexity and conflicting demands among others. There are also stresses that come from the absence of elements such as human contact, a sense of achievement, constructive creative outlets, and occasions or circumstances that will naturally elicit positive emotions. Stress reduction will involve reducing things that cause anxiety and increasing those that generate happiness. It is not enough to just reduce the anxiety.
Co-Morbid Substance Use Disorder
Co-occurring substance misuse disorders, which are extremely common in bipolar patients can cause a significant worsening of bipolar symptomatology and can cause the emergence of affective symptoms. The treatment options and recommendations for substance use disorders is wide but may include certain pharmacological and nonpharmacological treatment options.
Other Treatments
Omega-3 Fatty Acids
Omega-3 fatty acids may also be used as a treatment for bipolar disorder, particularly as a supplement to medication. An initial clinical trial by Stoll et al. (1999) produced positive results. However, since 1999 attempts to confirm this finding of beneficial effects of omega-3 fatty acids in several larger double-blind clinical trials have produced inconclusive results. It was hypothesized that the therapeutic ingredient in omega-3 fatty acid preparations is eicosapentaenoic acid (EPA) and that supplements should be high in this compound to be beneficial. A 2008 Cochrane systematic review found limited evidence to support the use of Omega-3 fatty acids to improve depression but not mania as an adjunct treatment for bipolar disorder.
Omega-3 fatty acids may be found in fish, fish oils, algae, and to a lesser degree in other foods such as flaxseed, flaxseed oil and walnuts. Although the benefits of Omega-3 fatty acids remain debated, they are readily available at drugstores and supermarkets, relatively inexpensive, and have few known side effects (All of these oils, however, have the capacity to exacerbate GERD (gastroesophageal reflux disease) – food sources may be a good alternative in such cases).
Exercise
Exercise has also been shown to have antidepressant effects.
Electroconvulsive Therapy
Electroconvulsive therapy (ECT) may have some effectiveness in mixed mania states, and good effectiveness in bipolar depression, particularly in the presence of psychosis. It may also be useful in the treatment of severe mania that is non-responsive to medications.
The most frequent side effects of ECT include memory impairment, headaches, and muscle aches. In some instances, ECT can produce significant and long-lasting cognitive impairment, including anterograde amnesia, and retrograde amnesia.
Ketogenic Diet
Because many of the medications that are effective in treating epilepsy are also effective as mood stabilizers, it has been suggested that the ketogenic diet – used for treating paediatric epilepsy – could have mood stabilising effects. Ketogenic diets are diets that are high in fat and low in carbohydrates, and force the body to use fat for energy instead of sugars from carbohydrates. This causes a metabolic response similar to that seen in the body during fasting. This idea has not been tested by clinical research, and until recently, was entirely hypothetical. Recently, however, two case studies have been described where ketogenic diets were used to treat bipolar II. In each case, the patients found that the ketogenic diet was more effective for treating their disorder than medication and were able to discontinue the use of medication. The key to efficacy appears to be ketosis (a metabolic state characterised by elevated levels of ketone bodies in the blood or urine), which can be achieved either with a classic high-fat ketogenic diet, or with a low-carbohydrate diet similar to the induction phase of the Atkins Diet. The mechanism of action is not well understood. It is unclear whether the benefits of the diet produce a lasting improvement in symptoms (as is sometimes the case in treatment for epilepsy) or whether the diet would need to be continued indefinitely to maintain symptom remission.
The Role of Cannabinoids
Acute cannabis intoxication transiently produces perceptual distortions, psychotic symptoms and reduction in cognitive abilities in healthy persons and in severe mental disorder, and may impair the ability to safely operate a motor vehicle.
Cannabis use is common in bipolar disorder, and is a risk factor for a more severe course of the disease by increasing frequency and duration of episodes. It is also reported to reduce age at onset.
Alternative Medicine
Several studies have suggested that omega-3 fatty acids may have beneficial effects on depressive symptoms, but not manic symptoms. However, only a few small studies of variable quality have been published and there is not enough evidence to draw any firm conclusions.
1915 – John C. Lilly, American psychoanalyst, physician, and philosopher (d. 2001).
People (Deaths)
2014 – Julian Rotter, American psychologist and academic (b. 1916).
John C. Lilly
John Cunningham Lilly (06 January 1915 to 30 September 2001) was an American physician, neuroscientist, psychoanalyst, psychonaut, philosopher, writer and inventor. He was a member of a generation of counterculture scientists and thinkers that included Ram Dass, Werner Erhard and Timothy Leary, all frequent visitors to the Lilly home. He often stirred controversy, especially among mainstream scientists.
Lilly conducted high-altitude research during World War II and later trained as a psychoanalyst. He gained renown in the 1950s after developing the isolation tank. He saw the tanks, in which users are isolated from almost all external stimuli, as a means to explore the nature of human consciousness. He later combined that work with his efforts to communicate with dolphins. He began studying how bottlenose dolphins vocalize, establishing centres in the US Virgin Islands, and later San Francisco, to study dolphins. A decade later, he began experimenting with psychedelics, including LSD, often while floating in isolation. His work inspired two Hollywood movies, The Day of the Dolphin (1973) and Altered States (1980).
Julian Rotter
Julian B. Rotter (22 October 1916 to 06 January 2014) was an American psychologist known for developing social learning theory and research into locus of control. He was a faculty member at The Ohio State University and then the University of Connecticut. A Review of General Psychology survey, published in 2002, ranked Rotter as the 64th most eminent and 18th most widely cited psychologist of the 20th century. A 2014 study published in 2014 placed at #54 among psychologists whose careers spanned the post-World War II era.
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.
Closed-Head Injury
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.
HIV/AIDS
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.
Drugs
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.
Other
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.
Controversy
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.
Description
Racing thoughts may be experienced as background or take over a person’s consciousness. Thoughts, music, and voices might be zooming through one’s mind as they jump tangentially from one to the next. There also might be a repetitive pattern of voice or of pressure without any associated “sound”. It is a very overwhelming and irritating feeling, and can result in losing track of time. In some cases, it may also be frightening to the person experiencing it, as there is a loss of control. If one is experiencing these thoughts at night when going to sleep, they may suddenly awaken, startled and confused by the very random and sudden nature of the thoughts.
Racing thoughts differ in manifestation according to the individual’s perspective. These manifestations can vary from unnoticed or minor distractions to debilitating stress, preventing the sufferer from maintaining a thought.
Generally, racing thoughts are described by an individual who has had an episode where the mind uncontrollably brings up random thoughts and memories and switches between them very quickly. Sometimes they are related, as one thought leads to another; other times they seem completely random. A person suffering from an episode of racing thoughts has no control over their train of thought, and it stops them from focusing on one topic or prevents sleeping.
Associated Conditions
The causes of racing thoughts are most often associated with anxiety disorders, but many influences can cause these rapid, racing thoughts. There are also many associated conditions, in addition to anxiety disorders, which can be classified as having secondary relationships with causing racing thoughts. The conditions most commonly linked to racing thoughts are bipolar disorder, anxiety disorder, attention deficit hyperactivity disorder, sleep deprivation, amphetamine dependence, and hyperthyroidism.
Anxiety Disorders
Racing thoughts associated with anxiety disorders can be caused by many different conditions, such as obsessive-compulsive disorder (OCD), panic disorder, generalised anxiety disorder, or posttraumatic stress disorder.
In people with OCD, racing thoughts can be brought on by stressors, or triggers, causing disturbing thoughts in the individual. These disturbing thoughts, then, result in compulsions characterising OCD in order to lower the stress and gain some sort of control over these stressful, racing thoughts.
Panic disorder is an anxiety disorder characterised by repeated panic attacks of fear or nervousness, lasting several minutes. During these panic attacks, the response is out of proportion to the situation. The racing thoughts may feel catastrophic and intense, but they are a symptom of the panic attack and must be controlled in order to soothe the panic and minimise the panic attack.
Generalised anxiety disorder (GAD) is a neurological anxiety disorder that involves uncontrollable and excessive worrying about irrational topics or problems. These stressful thoughts must be present for at least six months in order to be diagnosed as GAD. Along with other symptoms, racing thoughts is one of the most common ones. With GAD, there is an inability to relax or let thoughts or worries go, persistent worrying and obsessions about small concerns that are out of proportion to the result, and even worrying about their excessive worrying.
Bipolar Disorder
Racing thoughts can be brought on by bipolar disorder, defined by mood instability that range from extreme emotional highs, mania, to severe depression. During the manic phase of bipolar disorder is when racing thoughts usually occur. Disjointed, constantly changing thoughts with no underlying theme can be a sign of the manic phase of bipolar disorder. Manic thoughts can prevent performance of daily routines due to their rapid, unfocused and overwhelming nature. Racing thoughts in people with bipolar disorder are generally accompanied with other symptoms associated with this disorder.
Amphetamines
Amphetamines are used as a stimulant to trigger the central nervous system, increasing heart rate and blood pressure while decreasing appetite. Since amphetamines are a stimulant, use of these drugs result in a state that resembles the manic phase of bipolar disorder and also produces similar symptoms, as stated above.
Attention Deficit Hyperactivity Disorder
Racing thoughts associated with ADHD is most common in adults. With ADHD, racing thoughts can occur and tend to cause insomnia. Racing thoughts in people with ADHD tend to be rapid, unstable thoughts which do not follow any sort of pattern, similar to racing thoughts in people with bipolar disorder. Medications used to treat ADHD, such as Adderall or Methylphenidate, can be prescribed to patients with ADHD to calm these racing thoughts, most commonly in the morning when people wake up but just as well in the evening before sleep.
Lack of Sleep
Racing thoughts, also referred to as “racing mind”, may prevent a person from falling asleep. Chronic sleep apnoea and prolonged disturbed sleep patterns may also induce racing thoughts. Treatment for sleep apnoea and obstructive airway disorder can improve airflow and improve sleep resulting in improved brain and REM (rapid eye movement) function and reduced racing thought patterns.
Hyperthyroidism
Hyperthyroidism is a condition in which the thyroid gland produces too much thyroid hormone, thyroxin. This overabundance of thyroxin causes irregular and rapid heartbeat, irritability, weight loss, nervousness, anxiety and racing thoughts. The anxiety and inability to focus is very common in hyperthyroidism and leads to racing thoughts, as well as panic attacks and difficulty concentrating.
Frequency
Anxiety disorder, the most common mental illness in the United States, affects 40 million people, ages 10 and older; this accounts for 18% of the US population. Most people suffering from anxiety disorder report some form of racing thoughts symptom.
The prevalence of OCD in every culture studied is at least 2% of the population, and the majority of those have obsessions, or racing thoughts. With these reports, estimates of more than 2 million people in the United States (as of 2000) suffer from racing thoughts.
Treatment
There are various treatments available to calm racing thoughts, some of which involve medication. One type of treatment involves writing out the thoughts onto paper. Some treatments suggest using activities, such as painting, cooking, and other hobbies, to keep the mind busy and distract from the racing thoughts. Exercise may be used to tire the person, thereby calming their mind. When racing thoughts are anxiety induced during panic or anxiety attacks, it is recommended that the person wait it out. Using breathing and meditation techniques to calm the breath and mind simultaneously is another tool for handling racing thoughts induced by anxiety attacks. Mindfulness meditation has also shown to help with racing thoughts by allowing practitioners to face their thoughts head-on, without reacting.
While all of these techniques can be useful to cope with racing thoughts, it may prove necessary to seek medical attention and counsel. Since racing thoughts are associated with many other underlying mental illnesses, such as bipolar disorder, anxiety disorder, and ADHD, medications used commonly to treat these disorders will help calm racing thoughts in patients.
Treatment for the underlying causes of racing thoughts is helpful and useful in order to calm the racing thoughts more permanently. For example, in people with ADHD, medications used to promote focus and calm distracting thoughts, will help them with their ADHD.
Some obstructive airway disorders may be relieved with nasal septoplasty which can improve sleep and lead to a reduction of racing mind. Insomnia may increase racing thoughts and those effected will find sleep apnoea treatment and nasal surgery helpful to eliminate their racing thoughts.
It is important to look at the underlying defect that may be causing racing thoughts in order to prevent them in the long-term.
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