133 Sentences With "neuroleptic" | Random Sentence Generator

Lunsers refers to the Liverpool University Neuroleptic Side Effect Rating Scale.

These mothers require sedation with anti-psychotic (neuroleptic) agents, but are liable to extrapyramidal symptoms name="Cambridge 2017, p228." , including the neuroleptic malignant syndrome Price D K, Turnbull G J, Gregory R P, Stevens D R (1989). Neuroleptic malignant syndrome in a case of postpartum psychosis. British Journal of Psychiatry 155: 849-852. . Since the link with bipolar disorder was recognized (about 1970), treatment with mood-stabilizing agents, such as lithium name="Bergink 2013, p20-3." and anti-convulsant drugs, has been employed with success.

Dixyrazine, also known as dixypazin (oxalate), sold under the brand names Ansiolene, Esocalm, Esucos, Metronal, and Roscal, is a typical antipsychotic of the phenothiazine group described as a neuroleptic and antihistamine. It was first introduced in Germany in 1969. It is used as a neuroleptic, anxiolytic, and antihistamine in doses between 12.5 and 75 mg a day.

A rare but life-threatening side effect is neuroleptic malignant syndrome (NMS). The symptoms of NMS include muscle stiffness, convulsions and fever.

Serious side effects of triflupromazine can be akathisia and tardive dyskinesia as well as the rare, but potentially fatal, neuroleptic malignant syndrome.

A combined depot (Flupenthixol and Zuclopenthixol) in neuroleptic non- responsive schizophrenics. Current Psychiatry.1996. Vol. 3. No. 1, p.p. 113-122 177\.

Overdoses, drug interactions, and dangerous reactions from psychiatric medications, especially antipsychotics, are considered psychiatric emergencies. Neuroleptic malignant syndrome is a potentially lethal complication of first or second generation antipsychotics. If untreated, neuroleptic malignant syndrome can result in fever, muscle rigidity, confusion, unstable vital signs, or even death. Serotonin syndrome can result when selective serotonin reuptake inhibitors or monoamine oxidase inhibitors mix with buspirone.

Frank Ayd studied, in his words, "practically speaking, every neuroleptic that ever got on the market in this country except for Clozaril and Risperdal".

NMS was known about as early as 1956, shortly after the introduction of the first phenothiazines.Friedberg JM. Neuroleptic malignant syndrome. URL: . Accessed: July 3, 2006.

Neuroleptic malignant syndrome (NMS) is a life-threatening reaction that can occur in response to neuroleptic or antipsychotic medication. Symptoms include high fever, confusion, rigid muscles, variable blood pressure, sweating, and fast heart rate. Complications may include rhabdomyolysis, high blood potassium, kidney failure, or seizures. Any medications within the family of neuroleptics can cause the condition, though typical antipsychotics appear to have a higher risk than atypicals.

The term major tranquilizer was used for older antipsychotic drugs. The term neuroleptic is often used as a synonym for antipsychotic, even though – strictly speaking – the two terms are not interchangeable. Antipsychotic drugs are a subgroup of neuroleptic drugs, because the latter have a wider range of effects.R. Elliott Ingersoll, Carl F. Rak (2015): Psychopharmacology for Mental Health Professionals: An Integrative Approach, Cengage Learning, Boston, pp.

Nerisopam (GYKI-52322, EGIS-6775) is a drug which is a 2,3-benzodiazepine derivative, related to tofisopam. It has potent anxiolytic and neuroleptic effects in animal studies.

Levomepromazine, also known as methotrimeprazine, is a phenothiazine neuroleptic drug. Brand names include Nozinan, Levoprome, Detenler, Hirnamin, Levotomin and Neurocil. It is a low-potency antipsychotic (approximately half as potent as chlorpromazine) with strong analgesic, hypnotic and antiemetic properties that are primarily used in palliative care. Serious side effects include tardive dyskinesia, akathisia, abnormalities in the electrical cycle of the heart, low blood pressure and the potentially fatal neuroleptic malignant syndrome.

In 1937, Daniel Bovet and Anne-Marie Staub discovered the first antihistamine (Neuroleptic). In 1951 Paul Charpentier synthesized chlorpromazine (Neuroleptic). Different perspectives on the causes of psychological disorders arose. Some believed that stated that psychological disorders are caused by specific abnormalities of the brain and nervous system and that is, in principle, they should be approached for treatments in the same way as physical illness (arose from Hippocrates's ideas).

The first police doctor who saw him treated his nausea and vomiting with Stemetil, a drug that the manufacturer says can cause neuroleptic malignant syndrome, a rare but potentially fatal condition.

Chemically, it is an indole and phenylpiperazine derivative. Like reserpine and tetrabenazine, oxypertine depletes catecholamines, though not serotonin, possibly underlying its neuroleptic efficacy. Its structure is similar to solypertine and milipertine.

4-Bromofluorobenzene forms a Grignard reagent used in the synthesis of 4-fluorophenyl containing compounds,Patent US4605655 - Neuroleptic agents; no movement disorder side effects - Google Patents such as the pesticides Flusilazole.

It also has special neurologic indications for Tourette syndrome and resistant tics. The side effects include akathisia, tardive dyskinesia, and, more rarely, neuroleptic malignant syndrome and prolongation of the QT interval.

Dysphoria, sedation, hypotension resulting from peripheral alpha adrenoceptor blockade, prolongation of QT interval which can lead to torsades de pointes, and extrapyramidal side effects such as dystonic reactions/neuroleptic malignant syndrome.

There is little evidence regarding consistent benefits from their use beyond two or three years. Treatment of schizophrenia changed dramatically in the mid-1950s with the development and introduction of the first antipsychotic chlorpromazine. Others such as haloperidol and trifluoperazine soon followed. It remains unclear whether the newer antipsychotics reduce the chances of developing neuroleptic malignant syndrome, a rare but serious and potentially fatal neurological disorder most often caused by an adverse reaction to neuroleptic or antipsychotic drugs.

Perathiepin is a neuroleptic drug of the tricyclic family which was developed in the 1960s but was never marketed. In animal studies it was found to possess central depressant, antihistamine, antiserotonergic, and analgesic effects.

Bromperidol (marketed as Bromidol, Bromodol) is a butyrophenone derivative. It is a potent and long-acting neuroleptic, used as an antipsychotic in the treatment of schizophrenia. It was discovered at Janssen Pharmaceutica in 1966.

Moreover, its selectivity for the dopaminergic system is thought to account for its avoidance of the side effects typically associated with other neuroleptic drugs, such as chlorpromazine, which act on a number of neurotransmitter systems.

It should not be used concomitantly with medications known to prolong the QTc interval (e.g. 5-HT3 antagonists, tricyclic antidepressants, citalopram, etc.) as this may lead to an increased risk of QTc interval prolongation. Neither should it be given concurrently with lithium (medication) as it may increase the risk of lithium toxicity and neuroleptic malignant syndrome. It should not be given concurrently with other antipsychotics due to the potential for this to increase the risk of side effects, especially neurological side effects such as neuroleptic malignant syndrome.

Serotonin toxicity has a characteristic picture which is generally hard to confuse with other medical conditions, but in some situations it may go unrecognized because it may be mistaken for a viral illness, anxiety disorders, neurological disorder, anticholinergic poisoning, sympathomimetic toxicity, or worsening psychiatric condition. The condition most often confused with serotonin syndrome is neuroleptic malignant syndrome (NMS). The clinical features of neuroleptic malignant syndrome and serotonin syndrome share some features which can make differentiating them difficult. In both conditions, autonomic dysfunction and altered mental status develop.

The most effective drugs belong to the neuroleptic variety such as monoamine-depleting drugs and dopamine receptor-blocking drugs. Of the monoamine-depleting drugs, tetrabenazine is most powerful against tics and results in fewest side effects. A non-neuroleptic drug found to be safe and effective in treating tics is topiramate. Botulinum toxin injection in affected muscles can successfully treat tics; involuntary movements and vocalizations can be reduced, as well as life-threatening tics that have the potential of causing compressive myelopathy or radiculopathy.

Key signs of excited delirium are aggression, altered mental status, and diaphoresis/hyperthermia. Other conditions which can resemble excited delirium are mania, neuroleptic malignant syndrome, hypoglycemia, thyroid storm, and catatonia of the malignant or excited type.

Dysfunction of dopaminergic neurotransmission in the CNS has been implicated in a variety of neuropsychiatric disorders, including social phobia, Tourette's syndrome, Parkinson's disease, schizophrenia, neuroleptic malignant syndrome, attention-deficit hyperactivity disorder (ADHD), and drug and alcohol dependence.

Asymmetrical olfactory acuity and neuroleptic treatment in schizophrenia. Schizophrenia Research, Sep 1; 44(3): 221 – 232. Purdon, S., Klein, S., FLOR-HENRY, P. (2001). Menstrual effects on asymmetrical olfactory acuity. Journal of the International Neuropsychological Society, 7: 703 – 709.

All antipsychotics can cause the rare and sometimes fatal neuroleptic malignant syndrome. Trifluoperazine can lower the seizure threshold. The antimuscarinic action of trifluoperazine can cause excessive dilation of the pupils (mydriasis), which increases the chances of patients with hyperopia developing glaucoma.

In its role as a synthetic acetylcholine antagonist, biperiden has been analyzed as an alternative anticonvulsant for usage in the treatment of intoxication by organophosphorus nerve agents, such as sarin. It was also suggested by IV route for neuroleptic malignant syndrome.

Differential diagnosis may become difficult in patients recently exposed to both serotonergic and neuroleptic drugs. Bradykinesia and extrapyramidal "lead pipe" rigidity are classically present in NMS, whereas serotonin syndrome causes hyperkinesia and clonus; these distinct symptoms can aid in differentiation.

The word neuroleptic originates from the Greek word lepsis ("seizure"). Antipsychotics ( neuroleptics or tranquilizers) were investigated by the anesthesiologists De Castro and Mundeleer who coined the term neuroleptanalgesia, an anesthetic process that involves combining a major neuroleptic tranquilizer/antipsychotic with a potent opioid analgesic to produce a detached, pain-free state. This technique was widely used from the 1960s onwards, initially using a combination of phenoperidine and haloperidol, which was subsequently replaced in the early 1980s by a combination of fentanyl and droperidol. Efforts were also made to develop compounds which combined both types of activity in a single molecule.

USB provides services in all fields of medicine apart from pediatrics. In 1953 the hospital was one of the first that did extensive research on the first neuroleptic Chlorpromazine.Hans C. Bangen: Geschichte der medikamentösen Therapie der Schizophrenie. VWB, Berlin 1992, , Page 83.

NMS was first described in 1960 by French clinicians who had been working on a study involving haloperidol. They characterized the condition that was associated with the side effects of haloperidol "syndrome malin des neuroleptiques", which was translated to neuroleptic malignant syndrome.

Carpipramine (Prazinil, Defekton) is an atypical antipsychotic used for the treatment of schizophrenia and anxiety in France and Japan. In addition to its neuroleptic and anxiolytic effects, carpipramine also has hypnotic properties. It is structurally related to both tricyclics like imipramine and butyrophenones like haloperidol.

Kandel, E. R. (2007). In Search of Memory. The Emergence of a New Science of Mind. W. W. Norton & Co. See also A review in Spanish about Kandel's book Known first as a "ganglio-plegic", he first called the drug "neuroplégique" then finally a "neuroleptic".

In 1953, Bayer brought the first neuroleptic (chlorpromazine) onto the German market.Bangen, Hans: Geschichte der medikamentösen Therapie der Schizophrenie. Berlin 1992, p. 98 In the 1960s, Bayer introduced a pregnancy test, Primodos, that consisted of two pills that contained norethisterone (as acetate) and ethinylestradiol.

Veralipride (Agreal, Agradil) is a benzamide neuroleptic medicine indicated in the treatment of vasomotor symptoms associated with the menopause. It was first authorised for use in 1979. Veralipride has never gained approval in the United States. In September 2006, it was withdrawn from the Spanish market.

Serious side effects include akathisia, tardive dyskinesia and the potentially fatal neuroleptic malignant syndrome. Mesoridazine was withdrawn from the United States market in 2004 due to dangerous side effects, namely irregular heart beat and QT-prolongation of the electrocardiogram. It currently appears to be unavailable worldwide.

He also explored the behavior and symptomatology of those in the pre-terminal stages of the illness, and the eventual terminal stage, noting that patients in these stages are rarely seen in modern times, thanks to the widespread use of neuroleptic medication, which prevent such levels of regression.

Bromocriptine (originally marketed as Parlodel, subsequently under many names) is an ergoline derivative and dopamine agonist that is used in the treatment of pituitary tumors, Parkinson's disease (PD), hyperprolactinaemia, neuroleptic malignant syndrome, and type 2 diabetes. It was patented in 1968 and approved for medical use in 1975.

Most infections can cause some degree of diaphoresis and it is a very common symptom in some serious infections such as malaria and tuberculosis. In addition, pneumothorax can cause diaphoresis with splinting of the chest wall. Neuroleptic malignant syndrome and other malignant diseases (e.g. leukemias) can also cause diaphoresis.

Drug treatment is indicated for patients with severe disabling chorea. It is treated with haloperidol, chlorpromazine alone or in combination with diazepam, and also pimozide, which is another neuroleptic drug which may have fewer adverse effects than haloperidol. Valproic acid, chloral hydrate, risperidone, or phenobarbital can also be used.

However, some psychology professionals still push for the reduction of neuroleptic drugs, as there is a popular belief that post-schizophrenic depression is caused by neuroleptic treatment. Therapists are also believed to engage the depression in people with schizophrenia, having given too much psychotherapy after the patient had overcome their schizophrenic symptoms. Schizophrenia itself should not be overlooked as a key player in causing post-schizophrenic depression, though. A study done over a two-year time period shadowing patients with schizophrenia and monitoring their depression was unable to locate possible triggers such as the ones previously listed, so it is possible the nature of schizophrenia itself is the primary cause of post-schizophrenic depression.

Before prescribing medication for these conditions which often resolve spontaneously, recommendations have pointed to improved skin hygiene, good hydration via fluids, good nutrition, and installation of padded bed rails with use of proper mattresses. Pharmacological treatments include the typical neuroleptic agents such as fluphenazine, pimozide, haloperidol and perphenazine which block dopamine receptors; these are the first line of treatment for hemiballismus. Quetiapine, sulpiride and olanzapine, the atypical neuroleptic agents, are less likely to yield drug-induced parkinsonism and tardive dyskinesia. Tetrabenazine works by depleting presynaptic dopamine and blocking postsynaptic dopamine receptors, while reserpine depletes the presynaptic catecholamine and serotonin stores; both of these drugs treat hemiballismus successfully but may cause depression, hypotension and parkinsonism.

A. Okasha Read at the fourth WHO seminar on Biological Psychiatry in Cairo, November 1986. 104\. Tardive dyskinesia in psychosis. A study of its prevalence, psychodemographic and clinical aspects among neuroleptic – treared Egytptian patients. Okasha, A.H Khalil, A Ashour and M.R Elfiky Egypt. J. Psychiatry, 1986, 9: 8-17 105\.

Other conditions that can produce similar symptoms such as neuroleptic malignant syndrome, malignant hyperthermia, anticholinergic toxicity, heat stroke, and meningitis should be ruled out. No laboratory tests can confirm the diagnosis. Initial treatment consists of discontinuing medications which may be contributing. In those who are agitated, benzodiazepines may be used.

Serious side effects may include movement disorders including tardive dyskinesia and neuroleptic malignant syndrome. Use in pregnancy and breastfeeding is generally not recommended. It is a typical antipsychotic which is believed to work by affecting levels of dopamine in the brain. Prochlorperazine was approved for medical use in the United States in 1956.

Amisulpride should not be used in conjunction with drugs that prolong the QT interval (such as citalopram, venlafaxine, bupropion, clozapine, tricyclic antidepressants, sertindole, ziprasidone, etc.), reduce heart rate and those that can induce hypokalaemia. Likewise it is imprudent to combine antipsychotics due to the additive risk for tardive dyskinesia and neuroleptic malignant syndrome.

The International Classification of Diseases (ICD) also developed a section on mental disorders. The term stress, having emerged from endocrinology work in the 1930s, was increasingly applied to mental disorders. Electroconvulsive therapy, insulin shock therapy, lobotomies and the "neuroleptic" chlorpromazine came to be used by mid-century.Bangen, Hans: Geschichte der medikamentösen Therapie der Schizophrenie.

Mesoridazine (Serentil) is a piperidine neuroleptic drug belonging to the class of drugs called phenothiazines, used in the treatment of schizophrenia. It is a metabolite of thioridazine. The drug's name is derived from the methylsulfoxy and piperidine functional groups in its chemical structure. It has central antiadrenergic, antidopaminergic, antiserotonergic and weak muscarinic anticholinergic effects.

Levosulpiride, sold under the brand name Neoprad is a substituted benzamide antipsychotic, reported to be a selective antagonist of dopamine D2 receptor activity on both central and peripheral levels. It is an atypical neuroleptic and a prokinetic agent. Levosulpiride is also claimed to have mood elevating properties. Chemically, it is the (S)-(−)-enantiomer of sulpiride.

Side effects include amenorrhea, gynecomastia, galactorrhea, changes in libido, and neuroleptic malignant syndrome. In the U.S., as of 2013 only one case of adverse reaction to levosulpiride had been recorded on the FDA Adverse Event Reporting System Database. A case of rapid onset resistant dystonia caused by low dose levosulpiride was reported in India.

Proposed causes for demyelination include genetics and environmental factors such as being triggered by a viral infection or chemical exposure. Organophosphate poisoning by commercial insecticides such as sheep dip, weed killers, and flea treatment preparations for pets, can also result in nerve demyelination. Chronic neuroleptic exposure may cause demyelination. Vitamin B12 deficiency may also result in dysmyelination.

The second-generation antipsychotic olanzapine is thought to have a rebound-induced hyperthermia, which may be mediated by serotonin receptors. Hyperthermia, or elevated core body temperature, is associated with neuroleptic malignant syndrome, a potentially lethal syndrome that commonly occurs due to excessive D2R antagonism. In general, rebound D2R activity may induce rebound parkinsonism and rebound akathisia.

The high temperatures of hyperpyrexia are considered medical emergencies, as they may indicate a serious underlying condition or lead to severe morbidity (including permanent brain damage), or to death. A common cause of hyperpyrexia is an intracranial hemorrhage. Other causes in emergency room settings include sepsis, Kawasaki syndrome,Marx (2006), p. 2506. neuroleptic malignant syndrome, drug overdose, serotonin syndrome, and thyroid storm.

Propiomazine (Largon, Propavan, Indorm, Serentin, Dorevane, Dorevan) is an antihistamine blocking H1 receptors. It is used to treat insomnia, and to produce sleepiness or drowsiness and to relieve anxiety before or during surgery or other procedures and in combination with analgetics also during labor. Propiomazine is a phenothiazine, but is not used as a neuroleptic because it does not block dopamine receptors well.

Sepsis, encephalitis, neuroleptic malignant syndrome, malignant hyperthermia, lethal catatonia, spinal cord injury (not associated with PSH), seizures, and hydrocephalus (this can be associated with PSH) are examples of diagnoses that should be considered due to the manifestation of similar symptoms before confirming a diagnosis of PSH. PSH has no simple radiological features that can be observed or detected on a scan.

A former strategy to reduce motor complications was to withdraw patients from L-DOPA for some time. It is discouraged now since it can bring dangerous side effects such as neuroleptic malignant syndrome. Most people eventually need levodopa and later develop motor complications. The on-off phenomenon is an almost invariable consequence of sustained levodopa treatment in patients with Parkinson's disease.

Lobotomies, Insulin shock therapy, Electro convulsive therapy, and the "neuroleptic" chlorpromazine came into use mid-century. An antipsychiatry movement came to the fore in the 1960s. Deinstitutionalization gradually occurred in the West, with isolated psychiatric hospitals being closed down in favor of community mental health services. However, inadequate services and continued social exclusion often led to many being homeless or in prison.

Ocaperidone (R 79598) is a benzisoxazole antipsychotic. It was initially developed by Janssen, later licensed to French laboratory Neuro3D and then acquired in 2007 by German company Evotec. It was found to be more potent than risperidone in animal studies,Megens AA, Awouters FH, Meert TF, Schellekens KH, Niemegeers CJ, Janssen PA. Pharmacological profile of the new potent neuroleptic ocaperidone (R 79,598). J Pharmacol Exp Ther.

More serious side effects include: movement disorder like tardive dyskinesia, a condition called neuroleptic malignant syndrome, and depression. It is thus rarely recommended that people take the medication for longer than twelve weeks. No evidence of harm has been found after being taken by many pregnant women. It belongs to the group of medications known as dopamine-receptor antagonists and works as a prokinetic.

Overall adverse effects in treatment are similar between men, women, geriatric, pediatric and racial groups. Lamotrigine has been associated with a decrease in white blood cell count (leukopenia). Lamotrigine does not prolong QT/QTc in TQT studies in healthy subjects.Lamotrigine does not prolong QTc in a thorough QT/QTc study in healthy subjects In people taking antipsychotics, cases of lamotrigine- precipitated neuroleptic malignant syndrome have been reported.

A Combined Depot (FLupenthixol and Zuclopenthixol) in Neuroleptic Non-responsive Schizophrenia, Current Psychiatry, vol., 1, 1994 157\. Postgraduate Psychiatric Education in the Middle East, International Conference on Postgraduate Education, Al Ain, 1994. 158\. Sertraline in OCD: A twelve week, non-comparative study of the safety, efficacy and toleration of Sertraline in the treatment of obsessive compulsive disorder with or without concurrent depression in outpatients 1995 159\.

About 7% of people with parkinsonism developed symptoms as a result of side effects of medications, mainly neuroleptic antipsychotics especially the phenothiazines (such as perphenazine and chlorpromazine), thioxanthenes (such as flupenthixol and zuclopenthixol) and butyrophenones (such as haloperidol), and rarely, antidepressants. The incidence of drug-induced parkinsonism increases with age. Drug-induced parkinsonism tends to remain at its presenting level and does not worsen like Parkinson's disease.

Neuroleptic drugs often cause dystonia, including oculogyric crisis. Malfunction of the sodium- potassium pump may be a factor in some dystonias. The - pump has been shown to control and set the intrinsic activity mode of cerebellar Purkinje neurons. This suggests that the pump might not simply be a homeostatic, "housekeeping" molecule for ionic gradients; but could be a computational element in the cerebellum and the brain.

Others highlight negative effects of treatment. Still others point to disparities in the way these laws are applied. The psychiatric survivors movement opposes compulsory treatment on the basis that the ordered drugs often have serious or unpleasant side-effects such as anhedonia, tardive dyskinesia, neuroleptic malignant syndrome, excessive weight gain leading to diabetes, addiction, sexual side effects, and increased risk of suicide. John M. Grohol, Psy.

The hydantoin group can be found in several medicinally important compounds. In pharmaceuticals, hydantoin derivatives form a class of anticonvulsants; phenytoin and fosphenytoin both contain hydantoin moieties and are both used as anticonvulsants in the treatment of seizure disorders. The hydantoin derivative dantrolene is used as a muscle relaxant to treat malignant hyperthermia, neuroleptic malignant syndrome, spasticity, and ecstasy intoxication. Ropitoin is an example of an antiarrhythmic hydantoin.

Antidopaminergic ergolines have found use in antiemetics and in the treatment of schizophrenia. These substances are neuroleptic and are either an antagonist of dopamine at the postsynaptic level at the D2 receptor site or an agonist of dopamine at the presynaptic level at the D1 receptor site. The antagonist or agonist behavior of the ergolines are substrate dependent and mixed agonist/antagonist behaviors of ergoline derivatives have been reported.

Benzodiazepines themselves can trigger or worsen delirium, and there is no reliable evidence for use in non-alcohol-related delirium. If the delirium involves alcohol withdrawal, benzodiazepine withdrawal, or contraindications to antipsychotics (e.g. in Parkinson's disease or neuroleptic malignant syndrome), then benzodiazepines are recommended. Similarly, people with dementia with Lewy bodies may have significant side effects to antipsychotics, and should either be treated with a none or small doses of benzodiazepines.

CNS side effects include drowsiness, vertigo, headache, tremor, syncope, sleep disturbances, nightmares, restlessness, akinesia, agitation, seizures, rigidity, akathisia, confusion, fatigue, insomnia, hyperkinesia, weakness, lethargy, ataxia, slurred speech, depression, myoclonic jerks, and anxiety. Rarely seen are delusions, hallucinations, delirium, amnesia, libido increase or decrease, paranoia and irritability, abnormal EEG, worsening of psychosis, paresthesia, status epilepticus, and obsessive compulsive symptoms. Similar to other antipsychotics clozapine rarely has been known to cause neuroleptic malignant syndrome.

Serious side effects may include the potentially permanent movement disorder tardive dyskinesia, as well as neuroleptic malignant syndrome, an increased risk of suicide, angioedema, and high blood sugar levels. In older people with psychosis as a result of dementia, it may increase the risk of dying. Use during pregnancy is of unclear safety. How it works is not clear but is believed to involve effects on dopamine and serotonin in the brain.

In the clinical trial that lead to the cessation of its development as a drug, flumezapine was noted to be toxic. The administration of flumezapine led to the adverse effects of elevating the plasma concentration of creatine phosphokinase (CPK) and the liver enzymes aspartate transaminase (AST) and alanine transaminase (ALT). These liver enzyme elevation risks are similar to that of the neuroleptic drug chlorpromazine. Flumezapine also induced extrapyramidal symptoms (EPS) in patients during early clinical trials.

It is also used in the management of neuroleptic malignant syndrome, muscle spasticity (e.g. after strokes, in paraplegia, cerebral palsy, or patients with multiple sclerosis), and poisoning by 2,4-dinitrophenol or by the related compounds dinoseb and dinoterb. The most frequently occurring side effects include drowsiness, dizziness, weakness, general malaise, fatigue, and diarrhea. It is marketed by Par Pharmaceuticals LLC as Dantrium (in North America) and by Norgine BV as Dantrium, Dantamacrin, or Dantrolen (in Europe).

The most common effects of overdose are drowsiness and tachycardia. Rare but potentially critical complications are cardiac arrest, abnormal heart rhythms, severe low blood pressure, seizures, and neuroleptic malignant syndrome. Life- threatening overdose is rare, however, as the median lethal dose is about 338 milligrams/kilogram in mice and 425 mg/kg in rats. The potential harm is increased when central nervous system depressants and antidepressants are also used; deliberate overdose often includes alcohol among other drugs.

Insulin shock therapy or insulin coma therapy (ICT) was a form of psychiatric treatment in which patients were repeatedly injected with large doses of insulin in order to produce daily comas over several weeks.Neustatter WL (1948) Modern psychiatry in practice. London: 224. It was introduced in 1927 by Austrian-American psychiatrist Manfred Sakel and used extensively in the 1940s and 1950s, mainly for schizophrenia, before falling out of favour and being replaced by neuroleptic drugs in the 1960s.

MacDonald Tow's research on the survivors demonstrated that the operation often caused serious intellectual damage.P MacDonald Tow 1955 Personality changes following frontal leucotomy: a clinical and experimental study of the frontal lobes in man. Oxford University Press. When the Board of Control published their second survey in 1961 the use of psychosurgery had declined by more than half; the decline being attributed to an awareness of the risks of irreversible effects and the introduction in 1955 of neuroleptic drugs.

Affected individuals typically experience limited relief from standard pain relieving medication, with the exception of some neuroleptic agents. Patients frequently experience 'pseudovisceral' phenomena or symptoms of altered autonomic nervous system function including nausea, bloating, abdominal swelling, loss of appetite with consecutively lowered body weight or an altered defecation process. Pain is typically related to tensing the abdominal wall muscles, so any type of movement is prone to aggravate pain. Lying quietly can be the least painful position.

Aceperone is a neuroleptic drug of the butyrophenone class. It is an α-noradrenergic blocking drug developed by Janssen Pharmaceutica in the 1960s. Aceperone has been used as a tool in the study of the biochemical basis of learning. Although aceperone does not block learning per se, it blocks access to an attentional mechanism by which animals ‘tune in’ to the relevant visual dimension when learning a visual discrimination task at doses below those that affect general behaviour.

Until the 1970s there was considerable debate within psychiatry on the most appropriate term to use to describe the new drugs. In the late 1950s the most widely used term was "neuroleptic", followed by "major tranquilizer" and then "ataraxic". The first recorded use of the term tranquilizer dates from the early nineteenth century. In 1953 Frederik F. Yonkman, a chemist at the Swiss-based Cibapharmaceutical company, first used the term tranquilizer to differentiate reserpine from the older sedatives.

The word neuroleptic was coined in 1955 by Delay and Deniker after their discovery (1952) of the antipsychotic effects of chlorpromazine. It is derived from the (neuron, originally meaning "sinew" but today referring to the nerves) and "λαμβάνω" (lambanō, meaning "take hold of"). Thus, the word means taking hold of one's nerves. It was often taken to refer also to common side effects such as reduced activity in general, as well as lethargy and impaired motor control.

Promethazine, a phenothiazine derivative, is structurally different from the neuroleptic phenothiazines, with similar but different effects. It acts primarily as a strong antagonist of the H1 receptor (antihistamine) and a moderate mACh receptor antagonist (anticholinergic), and also has weak to moderate affinity for the 5-HT2A, 5-HT2C, D2, and α1-adrenergic receptors, where it acts as an antagonist at all sites, as well. Another notable use of promethazine is as a local anesthetic, by blockade of sodium channels.

It may also be seen in many medical disorders including infections (such as encephalitis), autoimmune disorders, meningitis, focal neurological lesions (including strokes), alcohol withdrawal, abrupt or overly rapid benzodiazepine withdrawal, cerebrovascular disease, neoplasms, head injury, and some metabolic conditions: homocystinuria, diabetic ketoacidosis, hepatic encephalopathy and hypercalcaemia. It can be an adverse reaction to prescribed medication. It bears similarity to conditions such as encephalitis lethargica and neuroleptic malignant syndrome. There are a variety of treatments available; benzodiazepines are a first-line treatment strategy.

Hyperthermia is an increase in body temperature over the temperature set point, due to either too much heat production or not enough heat loss. It is an example of a high temperature phenomenon that is not a fever; rather, it occurs from a number of causes including heatstroke, neuroleptic malignant syndrome, malignant hyperthermia, as well as in response to stimulants such as substituted amphetamines and cocaine, and in idiosyncratic drug reactions, and serotonin syndrome. Hyperthermia differs from hyperpyrexia, see section following.

A variety of conditions have similar symptoms to SPS, including myelopathies, dystonias, spinocerebellar degenerations, primary lateral sclerosis, neuromyotonia, and some psychogenic disorders. Tetanus, neuroleptic malignant syndrome, malignant hyperpyrexia, chronic spinal interneuronitis, serotonin syndrome, Multiple sclerosis, Parkinson's disease, and Isaacs syndrome should also be excluded. Patients' fears and phobias often incorrectly lead doctors to think their symptoms are psychogenic, and they are sometimes suspected of malingering. It takes an average of six years after the onset of symptoms before the disease is diagnosed.

With the goal of inducing lifelong changes in humans, Cameron used different methods of depatterning and repatterning the brain. The procedures included psychic driving, drug-induced sleep, intensive electroconvulsive therapy, sensory deprivation and the administration of neuroleptic Thorazine. Drug-Induced Sleep Cameron used doses of thorazine to put patients into an artificial coma. The drug-induced sleep, which took place in the “sleep room”, usually lasted from a few days up to 86 days; longer than expected by the patients.

Delay pioneered research on drugs including LSD, mescaline, and psilocybin. Delay's name came first on these papers in part because he was the leader of a department with strong hierarchy. Delay's team studied isoniazid (INH) and its effect on depression, around 1952. Delay discovered, jointly with J. M. Harl and Pierre Deniker, who was Delay's co-worker and also a psychiatrist, that chlorpromazine, the first neuroleptic, produced a considerable reduction in the agitation and aggression of those patients with symptoms of schizophrenia.

The most common side effects are akathisia. According to the drug’s warning label and safety information, the side effects are large in variety. The complete list of side effects include: akathisia, Contraindication Cerebrovascular Adverse Reactions (Including Stroke), Neuroleptic Malignant Syndrome, Tardive Dyskinesia, metabolic changes, Hyperglycemia/Diabetes Mellitus, Dyslipidemia, weight gain, Orthostatic Hypotension, Leukopenia, Neutropenia, Agranulocytosis, seizures, potential for Cognitive and Motor Impairment, difficulties with body temperature regulation, Dysphagia, Injection-Site Reactions (rash, swelling, redness, irritation at the point of injection), Dystonia and pregnancy and nursing complications.

First-generation antipsychotics, known as typical antipsychotics, were first introduced in the 1950s, and others were developed until the early 1970s. Second-generation drugs, known as atypical antipsychotics, were introduced firstly with clozapine in the early 1970s followed by others. Both generations of medication block receptors in the brain for dopamine, but atypicals tend to act on serotonin receptors as well. Neuroleptic, originating from (neuron) and (take hold of)—thus meaning "which takes the nerve"—refers to both common neurological effects and side effects.

When fluctuations occur, a person can cycle through phases with good response to medication and reduced PD symptoms ("on" state), and phases with poor response to medication and significant PD symptoms ("off" state). Using lower doses of levodopa may reduce the risk and severity of these levodopa-induced complications. A former strategy to reduce levodopa-related dyskinesia and fluctuations was to withdraw levodopa medication for some time. This is now discouraged since it can bring on dangerous side effects such as neuroleptic malignant syndrome.

However, they are actually very different conditions with different underlying dysfunction (serotonin excess vs dopamine blockade). Both the time course and the clinical features of NMS differ significantly from those of serotonin toxicity. Serotonin toxicity has a rapid onset after the administration of a serotonergic drug and responds to serotonin blockade such as drugs like chlorpromazine and cyproheptadine. Dopamine receptor blockade (NMS) has a slow onset, typically evolves over several days after administration of a neuroleptic drug, and responds to dopamine agonists such as bromocriptine.

Fava and velvet beans are natural sources of L-DOPA and are taken by many people with PD. While they have shown some effectiveness, their intake is not free of risks. Life-threatening adverse reactions have been described, such as the neuroleptic malignant syndrome. Faecal transplants may have a beneficial impact on symptoms. While not a treatment per se, a wearable device developed by Haiyan Zhang of Microsoft Research Cambridge, can serve to dampen the tremors of a patient's hand and fingers thereby restoring normal functions.

The interplay between the prefrontal cortex and socioemotional system of the brain is relevant for adolescent development, as proposed by the Dual Systems Model. The medial prefrontal cortex has been implicated in the generation of slow- wave sleep (SWS), and prefrontal atrophy has been linked to decreases in SWS. Prefrontal atrophy occurs naturally as individuals age, and it has been demonstrated that older adults experience impairments in memory consolidation as their medial prefrontal cortices degrade. In monkeys, significant atrophy has been found as a result of neuroleptic or antipsychotic psychiatric medication.

In Britain a legal case involved the death of two children of a mother whose three children had all had hypernatraemia. She was charged with poisoning the children with salt. One of the children, who was born at 28 weeks gestation with respiratory complications and had a fundoplication for gastroesophageal reflux and failure to thrive was prescribed domperidone. An advocate for the mother suggested the child may have suffered neuroleptic malignant syndrome as a side effect of domperidone due to the drug crossing the child's immature blood-brain-barrier.

Lithium is known to be a potential precipitant of serotonin syndrome in people concurrently on serotonergic medications such as antidepressants, buspirone and certain opioids such as pethidine (meperidine), tramadol, oxycodone, fentanyl and others. Lithium co-treatment is also a risk factor for neuroleptic malignant syndrome in people on antipsychotics and other antidopaminergic medications. High doses of haloperidol, fluphenazine, or flupenthixol may be hazardous when used with lithium; irreversible toxic encephalopathy has been reported.Case reports: ()() Indeed, these and other antipsychotics have been associated with increased risk of lithium neurotoxicity, even with low therapeutic lithium doses.

Reasons for this decline included increasing concern about the deaths and damage caused by the operation, the introduction of neuroleptic drugs, and changing ideas about the nature and treatment of mental illness.J Pippard 1962 Leucotomy in Britain today. Journal of Mental Science 108: 249–55.WS Maclay 1953 Death due to treatment. Proceedings of the Royal Society of Medicine 46:13–20. By the mid-1970s the use of psychosurgery had declined still further to about 100–150 operations a year, and nearly all were of the modified type.

Neuroleptic medications (antipsychotics), such as haloperidol (brand name Haldol) or pimozide (brand name Orap), have historically been and continue to be the medications with the most proven efficacy in controlling tics. These medications work by blocking dopamine receptors, and are associated with a high side effect profile. The traditional antipsychotic drugs are associated with tardive dyskinesia when used long- term; and parkinsonism, dystonia, dyskinesia, and akathisia when used short- term. Additional side effects can be school phobia (a form of separation anxiety), depression, weight gain, and cognitive blunting (dulling of cognitive ability).

Valbenazine is known to cause reversible reduction of dopamine release by selectively inhibiting pre-synaptic human vesicular monoamine transporter type 2 (VMAT2). In vitro, valbenazine shows great selectivity for VMAT2 and little to no affinity for VMAT1 or other monoamine receptors. Although the exact cause of tardive dyskinesia is unknown, it is hypothesized that it may result from neuroleptic-induced dopamine hypersensitivity. By selectively reducing the ability of VMAT2 to load dopamine into synaptic vesicles, the drug reduces overall levels of available dopamine in the synaptic cleft, ideally alleviating the symptoms associated with dopamine hypersensitivity.

Sulfozin was not used in American psychiatry. The American delegation during its visit to the USSR in 1989 confirmed charges of the use of sulfozine injections. Psychiatrists in the USSR employed sulfozine treatment allegedly to increase treatment response to neuroleptic administration but were unable to present any research evidence of its efficiency for this purpose. The muscle necrosis, fever, immobility, and severe pain caused by sulfozine, as well as the pattern of its use in 10 persons, suggest that the medication was applied for punitive rather than therapeutic purposes.

In 1987, the National Alliance on Mental Illness (NAMI) brought a complaint against Breggin with the board of the State of Maryland. NAMI was upset about remarks he made on The Oprah Winfrey Show on April 2, 1987. On the TV show, Breggin stated that mental health clients should judge their clinicians in terms of their empathy and support; if they failed to show interest in them and tried to prescribe drugs during the first session, he advised such clients to seek assistance elsewhere. He also pointed out the iatrogenic effects of neuroleptic drugs.

A first European near-replication of the original Soteria approach was implemented in 1984 in Berne, Switzerland, on a somewhat different conceptual basis. Three Soteria-like environments focused on longer term rehabilitation were created in Sweden (Perris, 1989). Writing in 1999, Mosher described the core of Soteria as "the 24 hour a day application of interpersonal phenomenologic interventions by a nonprofessional staff, usually without neuroleptic drug treatment, in the context of a small, homelike, quiet, supportive, protective, and tolerant social environment." More recent adaptions sometimes employed professional staff.

The psychiatric survivors movement opposes compulsory treatment on the basis that the ordered drugs often have serious or unpleasant side-effects such as tardive dyskinesia, neuroleptic malignant syndrome, excessive weight gain leading to diabetes, addiction, sexual side effects, and increased risk of suicide. The New York Civil Liberties Union has denounced what they see as racial and socioeconomic biases in the issuing of outpatient commitment orders. The main opponents to any kind of coercion, including the outpatient commitment and any other form of involuntary commitment, are Giorgio Antonucci and Thomas Szasz.

Despite the critical success of his debut solo album, rumors abounded that Wilson had either suffered a stroke or had been permanently disabled due to excessive drug use. Wilson, who had been prescribed massive amounts of psychotropic drugs by Landy's staff since 1983, had developed tardive dyskinesia, a neurological condition marked by involuntary, repetitive movements, that develops in about 20 percent of patients treated with anti-psychotic drugs for an extended period of time.Sweet, R.A., Mulsant, B. H. Gupta, B., Rifai, A.H., Pasternak, R.E., et al. (1995). Duration of neuroleptic treatment and prevalence of tardive dyskinesia in late life.

Neurotensin is a potent mitogen for colorectal cancer. Neurotensin has been implicated in the modulation of dopamine signaling, and produces a spectrum of pharmacological effects resembling those of antipsychotic drugs, leading to the suggestion that neurotensin may be an endogenous neuroleptic. Neurotensin- deficient mice display defects in responses to several antipsychotic drugs consistent with the idea that neurotensin signaling is a key component underlying at least some antipsychotic drug actions. These mice exhibit modest defects in prepulse inhibition (PPI) of the startle reflex, a model that has been widely used to investigate antipsychotic drug action in animals.

Ultimately the underlying cause needs to be treated. Electroconvulsive therapy (ECT) is an effective treatment for catatonia, however, it has been pointed out that further high quality randomized controlled trials are needed to evaluate the efficacy, tolerance, and protocols of ECT in catatonia. Antipsychotics should be used with care as they can worsen catatonia and are the cause of neuroleptic malignant syndrome, a dangerous condition that can mimic catatonia and requires immediate discontinuation of the antipsychotic. Excessive glutamate activity is believed to be involved in catatonia; when first-line treatment options fail, NMDA antagonists such as amantadine or memantine may be used.

Combined with less inhibitory signalling from the thalamus and other basal ganglic structures, from hyoptrophy the abnormal activation of the cingulate cortex, specifically around Broca's and Wernicke's areas, abnormal D2 agonism can facilitate the self-reinforcing, illogical patterns of language found in such patients. In schizophrenia, this feedback loop has progressed, which produced the widespread neural atrophy characteristic of this disease. Patients on neuroleptic or antipsychotic medication have significantly less atrophy within these crucial areas. As such, early medical intervention is crucial in preventing the advancement of these profound deficits in bilateral communication at the root of all psychotic disorders.

" For those female animals with previous sexual experience, amphetamine stimulation happens faster than for virgins. There is no study on male equivalent because the studies are meant to explain why females experience addiction earlier than males. Even in 1986 the effect of antipsychotics on receptor measurement was controversial. An article in Science sought to clarify whether the increase was solely due to medication by using drug-naive schizophrenics: "The finding that D2 dopamine receptors are substantially increased in schizophrenic patients who have never been treated with neuroleptic drugs raises the possibility that dopamine receptors are involved in the schizophrenic disease process itself.

Mornidine advertisements for postoperative recovery claimed "unusually low side effects". However, contemporary comparative trials found that hypotension (low blood pressure) was a substantial concern when the drug was given at normal dosages for this indication; blood pressure reductions of up to 70 mmHg were reported. Reductions in dosage mitigated hypotension while maintaining antiemetic efficacy. In his book The Creation of Psychopharmacology, Irish psychiatrist David Healy states that the failure of pipamazine to perform as a neuroleptic and its negative side effect profile helped Searle lose interest in the antipsychotic sector, and contributed to the company's refusal to market haloperidol in the United States.

Benperidol, sold under the trade name Anquil among others, is a drug which is a highly potent butyrophenone derivative. It is the most potent neuroleptic on the European market, with chlorpromazine equivalency as high as 75 to 100 (about 150 to 200% potency in terms of dose compared to haloperidol).Möller; Müller; Bandelow: Neuroleptika, 2001, WVG; (in German) It is an antipsychotic, which can be used for the treatment of schizophrenia,Bobon J, Collard J, Lecoq R, Benperidol and promazine: a "double blind" comparative study in mental geriatrics, Acta Neurol Belg. 1963 Oct;63:839-43.

Tiapride is a dopamine D2 and D3 receptor antagonist. It is more selective than other neuroleptic drugs such as haloperidol and risperidone, which not only target four of the five known dopamine receptor subtypes (D1-4), but also block serotonin (5-HT2A, 2C), α1\- and α2-adrenergic, and histamine H1 receptors. Compared to these drugs, tiapride has a relatively moderate affinity for its target receptors, displacing 50 percent of 3H-raclopride binding at a concentration of 320 nM at D2 receptors and a concentration of 180 nM at D3 receptors. Tiapride displays a relatively high regional selectivity for limbic areas.

Equilibrium between mGlu2/5HT2A is altered against tendency towards of psychosis by neuroleptic-pattern 5HT2A antagonists and mGlu2 agonists; both display antipsychotic activity. AMPA, the most widely distributed receptor in the brain, is a tetrameric ionotropic receptor; alterations in equilibrium between constituent subunits are seen in mGlu2/5HT2A antagonist (antipsychotic) administration\- GluR2 is seen to be upregulated in the PFC while GluR1 downregulates in response to antipsychotic administration. Reelin abnormalities may also be involved in the pathogenesis of schizophrenia via a glutamate-dependent mechanism. Reelin expression deficits are seen in schizophrenia, and reelin enhances expression of AMPA and NMDA alike.

Sedation is very common, and extrapyramidal side effects are common and include restlessness, dystonic reactions, pseudoparkinsonism, and akathisia; the extrapyramidal symptoms can affect 2% of people at low doses, whereas higher doses may affect as many as 40% of people. Prochlorperazine can also cause a life-threatening condition called neuroleptic malignant syndrome (NMS). Some symptoms of NMS include high fever, stiff muscles, neck muscle spasm, confusion, irregular pulse or blood pressure, fast heart rate (tachycardia), sweating, abnormal heart rhythms (arrhythmias). Research from the Veterans Administration and United States Food and Drug Administration show injection site reactions.

This discovery opened the search for additional dopamine receptors, and, in the subsequent years, Civelli discovered and described the unexpected diversity of dopamine receptors by successively cloning the D1, D4 and D5 receptors. His discovery of the D4 receptor suggested that this receptor may have a particular affinity for the atypical neuroleptic clozapine. Civelli's research in this period did not focus solely on dopamine receptors; he also discovered the adenosine A3 receptor. By cloning G protein-coupled receptors on the basis of their genomic sequences, Civelli had faced receptors that were not matched to their ligands, the so-called orphan receptors.

This drug is contraindicated in people with cancers that secrete catecholamines (for example epinephrine), such as phaeochromocytoma or paraganglioma, because as a COMT inhibitor it blocks catecholamine degradation. Other contraindications are a history of neuroleptic malignant syndrome (NMS) or non-traumatic rhabdomyolysis, and combination with monoamine oxidase inhibitors that are not used as antiparkinsonians, because of possible drug interactions. NMS and associated rhabdomyolysis have been rarely observed under the older COMT inhibitors tolcapone and entacapone. This typically occurs shortly after the beginning of a COMT inhibitor add-on therapy when the levodopa dose has been reduced, or after discontinuation of a COMT inhibitor.

Abrupt or rapid discontinuation from etizolam, as with benzodiazepines, may result in the appearance of the benzodiazepine withdrawal syndrome, including rebound insomnia. Neuroleptic malignant syndrome, a rare event in benzodiazepine withdrawal, has been documented in a case of abrupt withdrawal from etizolam. This is particularly relevant given etizolam's short half life relative to benzodiazepines such as diazepam resulting in a more rapid drug level decrease in blood plasma levels. In a study that compared the effectiveness of etizolam, alprazolam, and bromazepam for the treatment of generalized anxiety disorder, all three drugs retained their effectiveness over 2 weeks, but etizolam became more effective from 2 weeks to 4 weeks.

In a comparative study sampling 313 patients, those with religious delusion were found to be aged older, and had been placed on a drug regime or started a treatment programme at an earlier stage. In the context of presentation, their global functioning was found to be worse than another group of patients without religious delusions. The first group also scored higher on the Scale for the Assessment of Positive Symptoms (SAPS), had a greater total on the Brief Psychiatric Rating Scale (BPRS), and were treated with a higher mean number of neuroleptic medications of differing types during their hospitalization. Religious delusion was found in 2007 to strongly correlate with "temporolimbic overactivity".

This is a general list of long-term side effects associated with Antipsychotic (neuroleptic) medication. Many patients will not develop these side effects, although there is still a significant possibility of risks associated with Antipsychotic usage. This is only a list of long term side effects, and many consumers of these drugs may experience a decline in these side effects over time if they continue to take their medicine. Some of these side effects are benign or temporary, but many remain a crucial concern for companies and healthcare professionals and substantial efforts are being encouraged to reduce the potential risks for future antipsychotics through more clinical trials and drug development.

Orthomolecular psychiatry began with Abram Hoffer and Humphry Osmond in the 1950s and was continued by Carl Pfeiffer, although proponents of orthomolecular psychiatry say that the ideas behind their approach can be traced back to the 1920s and '30s. as cited in Orthomolecular psychiatry's goal of weaning patients from conventional neuroleptic drugs follows "Pfeiffer's Law", "For every drug that benefits a patient, there is a natural substance that can achieve the same effect". In 1968, Linus Pauling first used the term orthomolecular. Hoffer's therapies focused on using niacin, among other nutrients, to treat what he diagnosed as acute schizophrenia based on an unaccepted test.

Originally developed to treat high blood pressure, these medications are a safer alternative to neuroleptic medications for the people with TS that respond to them. This class of medication is often the first tried for tics, as the antihypertensives have a lower side effect profile than some of the medications which more proven efficacy. The evidence for their safety and efficacy is not as strong as the evidence for some of the standard and atypical neuroleptics, but there is fair supportive evidence for their use, nonetheless. This class of medication takes about six weeks to begin to work on tics, so sustained trials are warranted.

Clocapramine's affinity for the 5-HT2A receptor is greater than that for the D2 receptor and it has a lower propensity for inducing extrapyramidal symptoms compared to typical antipsychotics, thus underlying its atypical nature. In several clinical trials, clocapramine has been compared to other neuroleptic agents. Against haloperidol, though there was no significant difference in efficacy at the end of the study, clocapramine tended to be superior in alleviating motor retardation, alogia, and thought disorder, and also produced fewer side effects. Against sulpiride, clocapramine demonstrated more favorable effects in the treatment of both positive and negative symptoms, including motor retardation, delusions, hallucinations, and social isolation, though it produced more side effects.

It is also known to possess a relatively high liability for causing orthostatic hypotension compared to other antipsychotics. Similarly to other first-generation antipsychotics it has a relatively high liability for causing prolactin elevation. It is moderate risk for causing weight gain. As with all antipsychotics thioridazine has been linked to cases of tardive dyskinesia (an often permanent neurological disorder characterised by slow, repetitive, purposeless and involuntary movements, most often of the facial muscles, that is usually brought on by years of continued treatment with antipsychotics, especially the first-generation (or typical) antipsychotics such as thioridazine) and neuroleptic malignant syndrome (a potentially fatal complication of antipsychotic treatment).

Hyperthermia is generally diagnosed by the combination of unexpectedly high body temperature and a history that supports hyperthermia instead of a fever. Most commonly this means that the elevated temperature has occurred in a hot, humid environment (heat stroke) or in someone taking a drug for which hyperthermia is a known side effect (drug-induced hyperthermia). The presence of signs and symptoms related to hyperthermia syndromes, such as extrapyramidal symptoms characteristic of neuroleptic malignant syndrome, and the absence of signs and symptoms more commonly related to infection-related fevers, are also considered in making the diagnosis. If fever-reducing drugs lower the body temperature, even if the temperature does not return entirely to normal, then hyperthermia is excluded.

Exercise increases the outflow of creatine kinase to the blood stream for up to a week, and this is the most common cause of high CK in blood. Furthermore, high CK in the blood may be related to high intracellular CK such as in persons of African descent. Finally, high CK in the blood may be an indication of damage to CK-rich tissue, such as in rhabdomyolysis, myocardial infarction, myositis and myocarditis. This means creatine kinase in blood may be elevated in a wide range of clinical conditions including the use of medication such as statins; endocrine disorders such as hypothyroidism; and skeletal muscle diseases and disorders including malignant hyperthermia, and neuroleptic malignant syndrome.

TIK-301 is intended to be a take-as-need drug for primary insomnia, circadian rhythm disorders, depression, as well as sleep disorders in blind individuals and can be used to alleviate neuroleptic-induced tardive dyskinesia in schizophrenia patients. In a phase I clinical trial, TIK-301 was shown to be effective as a chronobiotic at a dose of 5 mg/L, but not in lower doses. In a phase II trial for primary insomnia, patients experienced objective and subjective improvements in sleep latency at 20 mg (31% improvement), 50 mg (32%) and 100 mg (41%) doses. The sleep latency improvement at the 100 mg dose is comparable to FDA approved zolpidem's effects.

As had been made clear several times before and during the trial, Lamb's court victory did not make him a free man. He was escorted by police back to Penetanguishene and placed in the hospital's maximum security unit at Oak Ridge, where he was to remain indefinitely pending an order from the Ontario Executive Council. Elliot Barker, the head of Oak Ridge's therapeutic division, had already interviewed Lamb in 1966 and spoken on his behalf at his trial. The doctor had arrived at Penetanguishene in 1959, and in 1965 stepped up his efforts to reform the unit's programmes, which on his arrival were still based around the traditional methods of neuroleptic tranquillisation and electroconvulsive therapy, supplemented by long periods of isolation for each inmate.

One of the clearest risk factors in the development of NMS is the course of drug therapy chosen to treat a condition. Use of high-potency neuroleptics, a rapid increase in the dosage of neuroleptics, and use of long-acting forms of neuroleptics are all known to increase the risk of developing NMS. It has been purported that there is a genetic risk factor for NMS, since identical twins have both presented with NMS in one case, and a mother and two of her daughters have presented with NMS in another case. Demographically, it appears that males, especially those under forty, are at greatest risk for developing NMS, although it is unclear if the increased incidence is a result of greater neuroleptic use in men under forty.

New York City, for example, has no dispensaries at all, and if a person broke the law, it is a problem of the police; only later psychiatrists investigate if there is concern of a mental health issue, Vladimir Pshizov writes. There have been many cases where orphans have been indicted to be sent to psychiatric hospitals, often when the accused are perfectly healthy. In 2010, 20 out of 72 orphans from an orphanage in Komsomolsk-on-Amur were placed in a psychiatric hospital and exposed to neuroleptic medication. The city prosecutor found that all the children were placed in the hospital to be treated for "emotional disorders" without having been examined by a commission of psychiatrists or provided for by a court judgment.

The family pathologist supported by an expert in drug withdrawal thought that Stemetil causing neuroleptic malignant syndrome was the most likely cause of death. The Home Office pathologist initially subscribed to the view that he had died from an overdose of nitrazepam, supported by evidence from a Manchester toxicologist. The Home Office pathologist presented this as his opinion both at the second inquest and in a report prepared for the Police Complaints Authority. The Manchester toxicologist then admitted that he had fabricated the data that led to this conclusion and at the third inquest, presenting his evidence as the last witness, the Home Office Pathologist presented a radically different opinion, that Patterson had died as a result of a complex metabolic disorder “resulting from drug withdrawal symptoms, dehydration and gastro-enteritis”.

Tardive Dysmentia is a rarely used term introduced in a 1983 paper to describe "changes in affect, activation level, and interpersonal interaction", and hypothesized to be caused by long-term exposure to neuroleptic drugs in the same way as the much better known syndrome of tardive dyskinesia. Several papers in the following years discussed the validity of the concept, and this small literature was reviewed in a 1993 publication by M. S. Myslobodsky, who drew attention to the "possibility that the syndrome of dysmentia is occasional excessive emotional reactivity, enhanced responsiveness to environmental stimuli, and indifference to or reduced awareness of the patient's abnormal involuntary movements", but concluded that the pathophysiology is uncertain. Since then, the term has fallen into disuse, receiving at most only passing mentions in the literature.

In reality this is not the case, as re-examinations of drug trial data in meta-analyses, especially where unpublished data are included (publication bias means that researchers and drug companies do not publish negative findings for obvious commercial reasons), have revealed that most of the benefits seen in active treatment groups are also seen in the placebo groups. NICE itself says that the difference between antidepressant medication and placebo is not clinically significant, yet continues to recommend them. As far as schizophrenia is concerned, neuroleptic drugs may have some short-term effects, but it is not the case that these drugs possess specific ‘anti-psychotic’ properties, and it is impossible to assess whether or not they confer advantages in long-term management of psychoses because of the severe disturbances that occur when people on long-term active treatment are withdrawn to placebos. These disturbances are traditionally interpreted as a ‘relapse’ of schizophrenia when in fact there are several possible interpretations for the phenomenon.

Dementia with Lewy bodies is characterised by the formation of Lewy bodies in the cerebral cortex, substantia nigra, locus coeruleus, and components of the basal forebrain cholinergic system. Clinical features include a cortical dementia and confusion, Parkinsonism, sensitivity to neuroleptic drugs, and psychiatric manifestations such as recurrent and well-formed hallucinations, particularly in the early stages of the disease. Because of an overlap in clinical symptoms, differentiating dementia with Lewy bodies from Alzheimer’s type dementia can sometimes prove to be difficult. However, differences in attentional functioning capacities in patients have been found to distinguish these two neurodegenerative disorders. Although areas of attentional processing such as divided attention, shifting processes, or inhibition are impaired in both Alzheimer’s disease and dementia with Lewy bodies (DLB), research has shown these deficits to be more prominent in DLB patients than AD patients, coinciding with impaired selective attention, particularly in the visual modality, or their ability to selectively allocate attention to specific stimuli.

Other contraindications include the administration of hydroxyzine alongside depressants and other compounds which affect the central nervous system; if absolutely necessary, it should only be administered concomitantly in small doses. If administered in small doses with other substances, such as mentioned, then patients should refrain from using dangerous machinery, motor vehicles or any other practice requiring absolute concentration, in accordance with safety law. Studies have also been conducted which show that long-term prescription of hydroxyzine can lead to tardive dyskinesia after years of use, but effects related to dyskinesia have also anecdotally been reported after periods of 7.5 months, such as continual head rolling, lip licking and other forms of athetoid movement. In certain cases, elderly patients' previous interactions with phenothiazine derivatives or pre-existing neuroleptic treatment may have had some contribution towards dyskinesia at the administration of hydroxyzine due to hypersensitivity caused due to the prolonged treatment, and therefore some contraindication is given to the short-term administration of hydroxyzine to those with previous phenothiazine use.