Antipsychotic Agents
Clozapine
Risperidone
Haloperidol
Benzodiazepines
Schizophrenia
Isoindoles
Receptors, Dopamine D2
Dopamine Antagonists
Pirenzepine
Raclopride
Psychotic Disorders
Apomorphine
Receptors, Dopamine D3
Receptors, Dopamine
Isoxazoles
Receptors, Serotonin
Serotonin Antagonists
Dose-Response Relationship, Drug
Dopamine
Thioridazine
Rats, Sprague-Dawley
Catalepsy
Rats, Wistar
Basal Ganglia Diseases
Chlorpromazine
Perphenazine
Polypharmacy
Dyskinesia, Drug-Induced
Fluphenazine
Phencyclidine
Startle Reaction
Receptor, Serotonin, 5-HT2A
Quinolones
Off-Label Use
Akathisia, Drug-Induced
Sulpiride
Psychomotor Agitation
Psychiatric Status Rating Scales
Receptors, Serotonin, 5-HT2
Neuroleptic Malignant Syndrome
Psychotropic Drugs
Neurotensin
The social and economic effects of manic depressive illness and of its treatment in lithium clinics. (1/3659)
Advising about the employment of those who have had manic depressive episodes requires Occupational Health Physicians to obtain, with consent, an objective account of previous episodes and to appreciate the enormous range of manic and depressive manifestations. Familiarity is needed with the likely effects of treatment of episodes and the benefits and problems of prophylaxis--not just in general but in individual cases, for example, where driving is required. This article summarizes research into the effects of lithium preparations on the course of the illness, thyroid and renal function and the risk of suicide. The author found that changing from treatment of episodes to continuous prophylaxis benefited employment and personal relationships without causing body weight problems. Many patients do well in life if supported by an experienced professional team, with 61% requiring no further admissions once on lithium, and with an 86% reduction in admissions achieved in our local clinic. (+info)S-16924 [(R)-2-[1-[2-(2,3-dihydro-benzo[1,4]dioxin-5-yloxy)-ethyl]- pyrrolidin-3yl]-1-(4-fluorophenyl)-ethanone], a novel, potential antipsychotic with marked serotonin1A agonist properties: III. Anxiolytic actions in comparison with clozapine and haloperidol. (2/3659)
S-16924 is a potential antipsychotic that displays agonist and antagonist properties at serotonin (5-HT)1A and 5-HT2A/2C receptors, respectively. In a pigeon conflict procedure, the benzodiazepine clorazepate (CLZ) increased punished responses, an action mimicked by S-16924, whereas the atypical antipsychotic clozapine and the neuroleptic haloperidol were inactive. Similarly, in a Vogel conflict paradigm in rats, CLZ increased punished responses, an action shared by S-16924 but not by clozapine or haloperidol. This action of S-16924 was abolished by the 5-HT1A antagonist WAY-100,635. Ultrasonic vocalizations in rats were inhibited by CLZ, S-16924, clozapine, and haloperidol. However, although WAY-100,635 abolished the action of S-16924, it did not affect clozapine and haloperidol. In a rat elevated plus-maze, CLZ, but not S-16924, clozapine, and haloperidol, increased open-arm entries. Like CLZ, S-16924 increased social interaction in rats, whereas clozapine and haloperidol were inactive. WAY-100,635 abolished this action of S-16924. CLZ, S-16924, clozapine, and haloperidol decreased aggressive interactions in isolated mice, but this effect of S-16924 was not blocked by WAY-100, 635. All drugs inhibited motor behavior, but the separation to anxiolytic doses was more pronounced for S-16924 than for CLZ. Finally, in freely moving rats, CLZ and S-16924, but not clozapine and haloperidol, decreased dialysis levels of 5-HT in the nucleus accumbens: this action of S-16924 was blocked by WAY-100,165. In conclusion, in contrast to haloperidol and clozapine, S-16924 possessed a broad-based profile of anxiolytic activity at doses lower than those provoking motor disruption. Its principal mechanism of action was activation of 5-HT1A (auto)receptors. (+info)Ergoline derivative LEK-8829-induced turning behavior in rats with unilateral striatal ibotenic acid lesions: interaction with bromocriptine. (3/3659)
LEK-8829 [9,10-didehydro-N-methyl-(2-propynyl)-6-methyl-8- aminomethylergoline bimaleinate] is an antagonist of dopamine D2 receptors and serotonin (5-HT)2 and 5-HT1A receptors in intact animals and a D1 receptor agonist in dopamine-depleted animals. In the present study, we used rats with unilateral striatal lesions with ibotenic acid (IA) to investigate the dopamine receptor activities of LEK-8829 in a model with innervated dopamine receptors. The IA-lesioned rats circled ipsilaterally when challenged with apomorphine, the mixed agonist on D1/D2 receptors. LEK-8829 induced a dose-dependent contralateral turning that was blocked by D1 receptor antagonist SCH-23390. The treatment with D1 receptor agonist SKF-82958 induced ipsilateral turning, whereas the treatment with D2 receptor antagonist haloperidol induced contralateral posture. The combined treatment with SKF-82958 and haloperidol resulted in a weak contralateral turning, indicating the possible receptor mechanism of contralateral turning induced by LEK-8829. Bromocriptine induced a weak ipsilateral turning that was blocked by haloperidol. The ipsilateral turning induced by bromocriptine was significantly potentiated by the coadministration of a low dose but not by a high dose of LEK-8829. The potentiation of turning was blocked either by SCH-23390 or by haloperidol. The potentiation of ipsilateral turning suggests the costimulation of D2 and D1 receptors by bromocriptine and LEK-8829, respectively, whereas the lack of potentiation by the highest dose of LEK-8829 may be explained by the opposing activity of LEK-8829 and bromocriptine at D2 receptors. We propose that the D2 and 5HT2 receptor-blocking and D1 receptor-stimulating profile of LEK-8829 is promising for the treatment of negative symptoms of schizophrenia. (+info)Mixed agonist-antagonist properties of clozapine at different human cloned muscarinic receptor subtypes expressed in Chinese hamster ovary cells. (4/3659)
We recently reported that clozapine behaves as a partial agonist at the cloned human m4 muscarinic receptor subtype. In the present study, we investigated whether the drug could elicit similar effects at the cloned human m1, m2, and m3 muscarinic receptor subtypes expressed in the Chinese hamster ovary (CHO) cells. Clozapine elicited a concentration-dependent stimulation of [3H]inositol phosphates accumulation in CHO cells expressing either the m1 or the m3 receptor subtype. Moreover, clozapine inhibited forskolin-stimulated cyclic AMP accumulation and enhanced [35S] GTP gamma S binding to membrane G proteins in CHO cells expressing the m2 receptor. These agonist effects of clozapine were antagonized by atropine. The intrinsic activity of clozapine was lower than that of the full cholinergic agonist carbachol, and, when the compounds were combined, clozapine potently reduced the receptor responses to carbachol. These data indicate that clozapine behaves as a partial agonist at different muscarinic receptor subtypes and may provide new hints for understanding the receptor mechanisms underlying the antipsychotic efficacy of the drug. (+info)Low-dose clozapine for the treatment of drug-induced psychosis in Parkinson's disease. The Parkinson Study Group. (5/3659)
BACKGROUND: Drug-induced psychosis is a difficult problem to manage in patients with Parkinson's disease. Multiple open-label studies have reported that treatment with clozapine at low doses ameliorates psychosis without worsening parkinsonism. METHODS: We conducted a randomized, double-blind, placebo-controlled trial of low doses of clozapine (6.25 to 50 mg per day) in 60 patients at six sites over a period of 14 months. The patients (mean age, 72 years) had idiopathic Parkinson's disease and drug-induced psychosis of at least four weeks' duration. All the patients continued to receive fixed doses of antiparkinsonian drugs during the four weeks of the trial. Blood counts were monitored weekly in all the patients. RESULTS: The mean dose of clozapine was 24.7 mg per day. The patients in the clozapine group had significantly more improvement than those in the placebo group in all three of the measures used to determine the severity of psychosis. The mean (+/-SE) scores on the Clinical Global Impression Scale improved by 1.6+/-0.3 points for the patients receiving clozapine, as compared with 0.5+/-0.2 point for those receiving placebo (P<0.001). The score on the Brief Psychiatric Rating Scale improved by 9.3+/-1.5 points for the patients receiving clozapine, as compared with 2.6+/-1.3 points for those receiving placebo (P=0.002). The score on the Scale for the Assessment of Positive Symptoms improved by 11.8+/-2.0 points for the patients receiving clozapine, as compared with 3.8+/-1.9 points for those receiving placebo (P=0.01). Seven patients treated with clozapine had an improvement of at least three on the seven-point Clinical Global Impression Scale, as compared with only one patient given placebo. Clozapine treatment improved tremor and had no deleterious effect on the severity of parkinsonism. In one patient, clozapine was discontinued because of leukopenia. CONCLUSIONS: Clozapine, at daily doses of 50 mg or less, is safe and significantly improves drug-induced psychosis without worsening parkinsonism. (+info)Antagonistic effects of trifluoperazine, imipramine, and chlorpromazine against acetylcholine-induced contractions in isolated rat uterus. (6/3659)
AIM: To examine the effects and affinity of some phenothizines (trifluoperazine, Tri and chlorpromazine, Chl) and antidepressant (imipramine, Imi) drugs on acetylcholine (ACh)-induced uterine contraction. METHODS: Isotonic contractions of rat uterine strips were recorded. ACh was administrated to induce maximal contraction before exchange of nutrient solution. ACh was added 5 min after the testing drugs. The nutrient solution was exchanged 4 times after each agonist (ACh or other agents) to produce maximal contraction. RESULTS: Atropine (Atr, 0.029-2.9 mumol.L-1), 4-DAMP (3.6-360 nmol.L-1), pirenzepine (Pir, 0.23-23.5 mumol.L-1), and AF-DX 116 (0.7-35.6 mumol.L-1) competitively antagonized the muscular uterine concentration induced by ACh (0.068-36068 mumol.L-1). The Schild plot was linear (r = 1.00). The pKB and slopes values (95% confidence limits) were 9.28 +/- 0.12 and 1.00 +/- 0.10 to Atr, 9.06 +/- 0.10 and 1.10 +/- 0.08 to 4-DAMP, 7.03 +/- 0.15 and 0.99 +/- 0.12 to Pir, and 5.60 +/- 0.08 and 1.00 +/- 0.19 to AF-DX 116. Tri 0.01-2 mumol.L-1 (pKB = 8.39 +/- 0.04) and Imi 94-940 nmol.L-1 (pKB = 7.21 +/- 0.10) produced also a competitive antagonism of the muscular uterine contraction induced by ACh (r = 1.00), but the slope was only 0.60 +/- 0.03 to Tri or 0.83 +/- 0.16 to Imi. Chl 2.8-5.6 mumol.L-1 produced a weak antagonism on amplitude of muscular contraction induced by the cholinomimetic. CONCLUSION: The muscarinic receptors on uterus behaved as M3 subtype. Tri and Imi, but not Chl, were competitive antagonist of muscarinic receptors of uterus. Imi behaved a simple competitive antagonist at a single site on myometrium, but Tri was not a simple competitive agent at a single site. (+info)The use of atypical antipsychotics in the management of schizophrenia. (7/3659)
Long-term drug treatment of schizophrenia with conventional antipsychotics has limitations: an estimated quarter to one third of patients are treatment-resistant; conventional antipsychotics have only a modest impact upon negative symptoms (poverty of thought, social withdrawal and loss of affect); and adverse effects, particularly extrapyramidal symptoms (EPS). Newer, so-called atypical, antipsychotics such as olanzapine, risperidone, sertindole and clozapine (an old drug which was re-introduced in 1990) are claimed to address these limitations. Atypical agents are, at a minimum, at least as effective as conventional drugs such as haloperidol. They also cause substantially fewer extrapyramidal symptoms. However, some other adverse effects are more common than with conventional drugs. For example, clozapine carries a significant risk of serious blood disorders, for which special monitoring is mandatory; it also causes troublesome drowsiness and increased salivation more often than conventional agents. Some atypical agents cause more weight gain or QT prolongation than older agents. The choice of therapy is, therefore, not straightforward. At present, atypical agents represent an advance for patients with severe or intolerable EPS. Most published evidence exists to support the use of clozapine, which has also been shown to be effective in schizophrenia refractory to conventional agents. However, the need for compliance with blood count monitoring and its sedative properties make careful patient selection important. The extent of any additional direct benefit offered by atypical agents on negative symptoms is not yet clear. The lack of a depot formulation for atypical drugs may pose a significant practical problem. To date, only two double-blind studies in which atypical agents were compared directly have been published. Neither provides compelling evidence for the choice of one agent over another. Atypical agents are many times more expensive than conventional drugs. Although drug treatment constitutes only a small proportion of the costs of managing schizophrenia, the additional annual cost of the use of atypical agents in, say, a quarter of the likely U.K. schizophrenic population would be about 56 M pound sterling. There is only limited evidence of cost-effectiveness. Atypical antipsychotics are not currently licensed for other conditions where conventional antipsychotics are commonly used, such as behaviour disturbance or dementia in the elderly. Their dose, and place in treatment in such cases have yet to be determined. (+info)Synergistic interactions between ampakines and antipsychotic drugs. (8/3659)
Tests were made for interactions between antipsychotic drugs and compounds that enhance synaptic currents mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid-type glutamate receptors ("ampakines"). Typical and atypical antipsychotic drugs decreased methamphetamine-induced hyperactivity in rats; the effects of near or even subthreshold doses of the antipsychotics were greatly enhanced by the ampakines. Interactions between the ampakine CX516 and low doses of different antipsychotics were generally additive and often synergistic. The ampakine did not exacerbate neuroleptic-induced catalepsy, indicating that the interaction between the different pharmacological classes was selective. These results suggest that positive modulators of cortical glutamatergic systems may be useful adjuncts in treating schizophrenia. (+info)The term "schizophrenia" was first used by the Swiss psychiatrist Eugen Bleuler in 1908 to describe the splitting of mental functions, which he believed was a key feature of the disorder. The word is derived from the Greek words "schizein," meaning "to split," and "phrenos," meaning "mind."
There are several subtypes of schizophrenia, including:
1. Paranoid Schizophrenia: Characterized by delusions of persecution and suspicion, and a tendency to be hostile and defensive.
2. Hallucinatory Schizophrenia: Characterized by hearing voices or seeing things that are not there.
3. Disorganized Schizophrenia: Characterized by disorganized thinking and behavior, and a lack of motivation or interest in activities.
4. Catatonic Schizophrenia: Characterized by immobility, mutism, and other unusual movements or postures.
5. Undifferentiated Schizophrenia: Characterized by a combination of symptoms from the above subtypes.
The exact cause of schizophrenia is still not fully understood, but it is believed to involve a combination of genetic, environmental, and neurochemical factors. It is important to note that schizophrenia is not caused by poor parenting or a person's upbringing.
There are several risk factors for developing schizophrenia, including:
1. Genetics: A person with a family history of schizophrenia is more likely to develop the disorder.
2. Brain chemistry: Imbalances in neurotransmitters such as dopamine and serotonin have been linked to schizophrenia.
3. Prenatal factors: Factors such as maternal malnutrition or exposure to certain viruses during pregnancy may increase the risk of schizophrenia in offspring.
4. Childhood trauma: Traumatic events during childhood, such as abuse or neglect, have been linked to an increased risk of developing schizophrenia.
5. Substance use: Substance use has been linked to an increased risk of developing schizophrenia, particularly cannabis and other psychotic substances.
There is no cure for schizophrenia, but treatment can help manage symptoms and improve quality of life. Treatment options include:
1. Medications: Antipsychotic medications are the primary treatment for schizophrenia. They can help reduce positive symptoms such as hallucinations and delusions, and negative symptoms such as a lack of motivation or interest in activities.
2. Therapy: Cognitive-behavioral therapy (CBT) and other forms of talk therapy can help individuals with schizophrenia manage their symptoms and improve their quality of life.
3. Social support: Support from family, friends, and support groups can be an important part of the treatment plan for individuals with schizophrenia.
4. Self-care: Engaging in activities that bring pleasure and fulfillment, such as hobbies or exercise, can help individuals with schizophrenia improve their overall well-being.
It is important to note that schizophrenia is a complex condition, and treatment should be tailored to the individual's specific needs and circumstances. With appropriate treatment and support, many people with schizophrenia are able to lead fulfilling lives and achieve their goals.
Some common types of psychotic disorders include:
1. Schizophrenia: A chronic and severe mental disorder that affects how a person thinks, feels, and behaves. It can cause hallucinations, delusions, and disorganized thinking.
2. Bipolar Disorder: A mood disorder that causes extreme changes in mood, energy, and behavior. It can lead to manic or hypomanic episodes, as well as depression.
3. Schizoaffective Disorder: A mental disorder that combines symptoms of schizophrenia and a mood disorder. It can cause hallucinations, delusions, and mood swings.
4. Brief Psychotic Disorder: A short-term episode of psychosis that can be triggered by a stressful event. It can cause hallucinations, delusions, and a break from reality.
5. Postpartum Psychosis: A rare condition that occurs in some new mothers after childbirth. It can cause hallucinations, delusions, and a break from reality.
6. Drug-Induced Psychosis: A psychotic episode caused by taking certain medications or drugs. It can cause hallucinations, delusions, and a break from reality.
7. Alcohol-Related Psychosis: A psychotic episode caused by alcohol use disorder. It can cause hallucinations, delusions, and a break from reality.
8. Trauma-Related Psychosis: A psychotic episode caused by a traumatic event. It can cause hallucinations, delusions, and a break from reality.
9. Psychotic Disorder Not Otherwise Specified (NOS): A catch-all diagnosis for psychotic episodes that do not meet the criteria for any other specific psychotic disorder.
Symptoms of psychotic disorders can vary depending on the individual and the specific disorder. Common symptoms include:
1. Hallucinations: Seeing, hearing, or feeling things that are not there.
2. Delusions: False beliefs that are not based in reality.
3. Disorganized thinking and speech: Difficulty organizing thoughts and expressing them in a clear and logical manner.
4. Disorganized behavior: Incoherent or bizarre behavior, such as dressing inappropriately for the weather or neglecting personal hygiene.
5. Catatonia: A state of immobility or abnormal movement, such as rigidity or agitation.
6. Negative symptoms: A decrease in emotional expression or motivation, such as a flat affect or a lack of interest in activities.
7. Cognitive impairment: Difficulty with attention, memory, and other cognitive functions.
8. Social withdrawal: Avoidance of social interactions and relationships.
9. Lack of self-care: Neglecting personal hygiene, nutrition, and other basic needs.
10. Suicidal or homicidal ideation: Thoughts of harming oneself or others.
It's important to note that not everyone with schizophrenia will experience all of these symptoms, and some people may experience additional symptoms not listed here. Additionally, the severity and frequency of symptoms can vary widely from person to person. With proper treatment and support, many people with schizophrenia are able to manage their symptoms and lead fulfilling lives.
It is important to note that catalepsy is not the same as catatonia, which is a more specific condition characterized by a wide range of symptoms, including immobility, mutism, negativism, and emotional dysregulation. However, catalepsy and catatonia do share some similarities, and the terms are often used interchangeably in clinical practice.
The exact cause of catalepsy is not fully understood, but it is thought to be related to dysfunction in certain areas of the brain, such as the neocortex and basal ganglia. In some cases, catalepsy may be a side effect of medication or drug intoxication.
Treatment for catalepsy typically focuses on addressing the underlying cause, such as managing seizures or withdrawing from drugs. In some cases, medications such as benzodiazepines or antipsychotics may be used to help manage symptoms. Other approaches, such as physical therapy and behavioral interventions, may also be helpful in improving mobility and function.
Some examples of basal ganglia diseases include:
1. Parkinson's disease: A neurodegenerative disorder characterized by tremors, rigidity, bradykinesia (slow movement), and postural instability.
2. Huntington's disease: An autosomal dominant disorder that causes progressive degeneration of the basal ganglia and a decline in cognitive, motor, and psychiatric functions.
3. Dystonia: A movement disorder characterized by sustained or intermittent muscle contractions that cause abnormal postures or movements.
4. Tourette's syndrome: A neurodevelopmental disorder characterized by multiple motor tics and at least one vocal tic, such as repeated sounds or words.
5. Obsessive-compulsive disorder (OCD): An anxiety disorder characterized by recurring thoughts or compulsions to perform repetitive behaviors.
6. Schizophrenia: A psychotic disorder characterized by hallucinations, delusions, and cognitive impairments.
7. Kleine-Levin syndrome: A rare sleep disorder characterized by recurring periods of excessive sleepiness and automatic behaviors.
8. Wilson's disease: A rare genetic disorder caused by copper accumulation in the basal ganglia, leading to cognitive and motor impairments.
9. Hemiballism: A rare movement disorder characterized by unilateral or bilateral involuntary movements of the upper limbs.
10. Chorea-acanthocytosis: A rare genetic disorder characterized by chorea (involuntary movements), acanthocytosis (abnormal red blood cell shape), and cognitive decline.
These conditions are often challenging to diagnose and manage, and may require a comprehensive evaluation by a multidisciplinary team of healthcare professionals, including neurologists, psychiatrists, geneticists, and other specialists. Early diagnosis and appropriate treatment can help improve outcomes for individuals with these conditions.
Dyskinesias can be caused by a variety of drugs, including:
1. Antipsychotic medications: These drugs are commonly used to treat conditions such as schizophrenia and bipolar disorder.
2. Antidepressant medications: Certain antidepressants, such as selective serotonin reuptake inhibitors (SSRIs), can cause dyskinesias.
3. Anti-anxiety medications: Benzodiazepines can cause dyskinesias, especially at high doses or with long-term use.
4. Opioids: These drugs can cause dyskinesias as a side effect, particularly when taken in high doses or for prolonged periods.
5. Antihistamines: Some antihistamines can cause dyskinesias, especially in older adults.
6. Anticonvulsants: Certain anticonvulsant medications, such as valproate and carbamazepine, can cause dyskinesias.
7. Corticosteroids: Long-term use of corticosteroids can lead to dyskinesias, especially in the face and limbs.
The symptoms of drug-induced dyskinesias can vary depending on the type of medication being taken and the individual's response to it. Common symptoms include:
1. Involuntary movements of the face, arms, legs, or trunk
2. Jerky or twitching movements
3. Tremors or shaking
4. Slow, rigid movements
5. Lack of coordination and balance
6. Difficulty with speech and swallowing
7. Fatigue and weakness
If you are experiencing dyskinesias as a result of medication, it is important to speak with your healthcare provider. They may be able to adjust your medication regimen or recommend alternative treatments to help manage the symptoms. In some cases, discontinuing the medication that is causing the dyskinesias may be necessary. Additionally, your healthcare provider may recommend other therapies, such as physical therapy or speech therapy, to help improve your mobility and communication skills.
The exact mechanism by which drugs can cause akathisia is not fully understood, but it is believed to involve changes in the levels of certain neurotransmitters (such as dopamine and serotonin) in the brain. These changes can affect the normal functioning of the nervous system, leading to symptoms such as agitation, restlessness, and an excessive desire to move about.
Drug-induced akathisia can occur with a wide range of medications and drugs, including antipsychotic medications, antidepressants, stimulants, and certain illegal substances. It is important for healthcare professionals to be aware of the potential for drug-induced akathisia when prescribing these medications, as it can be a serious side effect that can negatively impact a person's quality of life.
Treatment for drug-induced akathisia typically involves stopping or reducing the medication that is causing the symptoms. In some cases, additional medications may be prescribed to help manage the symptoms and reduce discomfort. It is important for individuals experiencing drug-induced akathisia to work closely with their healthcare provider to find the best course of treatment.
Psychomotor agitation is a common symptom of many mental health disorders, including bipolar disorder, schizophrenia, and major depressive disorder. It can also be caused by medications such as stimulants, antipsychotics, and benzodiazepines.
Some common signs and symptoms of psychomotor agitation include:
* Fidgeting or restlessness
* Purposeless movement of limbs (e.g., pacing, fiddling with objects)
* Increased muscle tension
* Difficulty sitting still
* Excessive talking or movement
* Increased heart rate and blood pressure
* Agitation or irritability
Psychomotor agitation can be assessed through a combination of physical examination, medical history, and laboratory tests. Treatment options for psychomotor agitation depend on the underlying cause, but may include medication adjustments, behavioral interventions, or hospitalization in severe cases.
It is important to note that psychomotor agitation can be a symptom of an underlying medical condition, so it is essential to seek professional medical attention if you or someone you know is experiencing these symptoms. A healthcare professional can diagnose and treat the underlying cause of psychomotor agitation, reducing the risk of complications and improving quality of life.
The exact cause of NMS is not fully understood, but it is believed to be related to an immune-mediated response to the neuroleptic drug. The syndrome typically develops within 1 to 2 weeks of starting or increasing the dose of the medication, and it can progress rapidly if left untreated.
The symptoms of NMS can include:
* Fever (usually above 38°C)
* Muscle rigidity and stiffness
* Altered mental status, such as confusion, disorientation, or agitation
* Autonomic dysfunction, such as changes in heart rate, blood pressure, or respiration
* Delirium or coma
* Seizures or convulsions
The diagnosis of NMS is based on a combination of clinical findings and laboratory tests, such as electrolyte imbalances, liver function tests, and muscle enzymes. Treatment typically involves stopping the neuroleptic medication and providing supportive care, such as intravenous fluids, oxygen therapy, and sedation to manage agitation or seizures. In severe cases, hospitalization in an intensive care unit may be necessary.
Preventing NMS is important, and it involves careful monitoring of patients who are taking neuroleptic medications, particularly during the early stages of treatment. Regular check-ups with a healthcare provider can help identify any potential problems before they become severe. Additionally, it is essential to report any new or worsening symptoms promptly, as early intervention can improve outcomes.
Overall, neuroleptic malignant syndrome is a rare but potentially life-threatening side effect of neuroleptic medications. Prompt recognition and treatment are crucial to preventing serious complications and improving outcomes for affected individuals.
Perathiepin
Dopamine supersensitivity psychosis
Flumezapine
Lenperone
History of malaria
Clorotepine
Mania
Pharmacological torture
Butaperazine
Olanzapine
Chlorprothixene
Piquindone
Dosulepin
Prothipendyl
Pipamperone
Side effects of cyproterone acetate
Insomnia
Azapirone
Hyperprolactinaemia
Duffy antigen system
Umespirone
Depression in childhood and adolescence
Ziprasidone
Temazepam
Methdilazine
Noyori asymmetric hydrogenation
Perlapine
Topiramate
Benzodiazepine withdrawal syndrome
Management of schizophrenia
List of investigational anxiolytics
R-type calcium channel
Lawrence Bittaker and Roy Norris
Aspiration pneumonia
Fluperlapine
Doxepin
Dementia with Lewy bodies
Postpartum psychosis
Corey Haim
Sonepiprazole
Trump administration family separation policy
ABT-724
Henry McCollum and Leon Brown
Pharmaceutical industry
Drugs and sexual desire
List of drugs known for off-label use
Risk factors of schizophrenia
Generalized anxiety disorder
Benzodiazepine overdose
History of medicine
Primidone
Metformin
Midazolam
Atypical antipsychotic
Child psychopathology
Obesogen
Pharmaco-electroencephalography
Dyslipidemia
History of electroconvulsive therapy in the United States
Obsessive-Compulsive Disorder Medication: Selective Serotonin Reuptake Inhibitors, Tricyclic Antidepressants, Serotonin...
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Associated with atypical antipsychotics1
- Hyperglycaemia is known occasionally to occur with conventional neuroleptics, but has more recently been associated with atypical antipsychotics especially clozapine and olanzapine. (nih.gov)
Schizophrenia9
- People with schizophrenia and other neuropsychiatric disorders are especially vulnerable to the development of TDs after exposure to conventional neuroleptics, anticholinergics, toxins, substances of abuse, and other agents. (medscape.com)
- TDs are most common in patients with schizophrenia, schizoaffective disorder, or bipolar disorder who have been treated with antipsychotic medication for long periods, but they occasionally occur in other patients as well. (medscape.com)
- In order to alleviate the positive symptoms of schizophrenia, all antipsychotic agents act on the dopaminergic system. (medscape.com)
- The novel atypical antipsychotic agent aripiprazole is a partial agonist at D 2 receptors that has been shown in clinical trials to be effective in treating both the positive and the negative symptoms of schizophrenia, and to be well tolerated, with a low propensity for EPS and no clinically significant weight gain, hyperprolactinaemia or corrected QT-interval prolongation. (medscape.com)
- We tested the hypothesis that patients with schizophrenia who are using khat will fail to respond to standard antipsychotic treatment. (who.int)
- Patients with newly diagnosed schizophrenia on antipsychotic monotherapy (n = 1007, 817 men) were included and categorized into khat and non-khat users. (who.int)
- Khat use hinders an individual's response to initial antipsychotic drug treatment for schizophrenia. (who.int)
- FANAPT is an atypical antipsychotic agent indicated for the treatment of schizophrenia in adults. (nih.gov)
- Although and response to antipsychotic treatment in schizophrenia limited use may not be accompanied by serious conse- patients. (who.int)
Medication1
- Switching to aripiprazole from maintenance therapy with another antipsychotic also works well, provided the change is made gradually, involving tapering of the original medication. (medscape.com)
Drugs8
- The use of antipsychotic drugs is common in the care of the elderly with dementia and associated behavioural problems, but until recently none of these agents had marketing authorisation for this indication. (rcpe.ac.uk)
- Tardive dyskinesia : report of the American Psychiatric Association Task Force on Late Neurological Effects of Antipsychotic Drugs. (who.int)
- Task Force on Late Neurological Effects of Antipsychotic Drugs. (who.int)
- Elderly patients with dementia-related psychosis treated with antipsychotic drugs are at an increased risk of death. (nih.gov)
- Elderly patients with dementia-related psychosis who are treated with atypical antipsychotic drugs are at an increased risk of death and cerebrovascular-related adverse events, including stroke. (nih.gov)
- Atypical antipsychotic drugs have been associated with metabolic changes that may increase cardiovascular/cerebrovascular risk. (nih.gov)
- The drugs benefit list includes four antipsychotic drugs that can be used only under limited conditions and require pre-approval from Health Canada. (thestar.com)
- These drugs are often referred to as neuroleptics alluding to the tendency to produce neurological side effects, but not all antipsychotics are likely to produce such effects. (bvsalud.org)
Weight Gain4
- However, other adverse effects such as weight gain and metabolic changes are cause for concern with some atypical antipsychotics. (medscape.com)
- Association of antipsychotic agent-induced weight gain with a polymorphism of the promotor region of the 5-HT2C receptor gene]. (cdc.gov)
- Association of HTR2C-759C/T and -697G/C polymorphisms with antipsychotic agent-induced weight gain]. (cdc.gov)
- Genetic predictors of antipsychotic-induced weight gain: a case-matched multi-gene study. (cdc.gov)
Medications5
- Maguire GA. Prolactin elevation with antipsychotic medications: Mechanisms of action and clinical consequences. (nih.gov)
- Antipsychotic medications were reviewed to determine their potential and the cause of substitution in association with khat use. (who.int)
- The National Pregnancy Registry for Atypical Antipsychotics was created in order to evaluate the safety of atypical antipsychotic medications taken by women during pregnancy. (womensmentalhealth.org)
- While the preliminary data from this study is reassuring, larger numbers of participants are needed to provide more complete data regarding the reproductive safety of atypical antipsychotics as a class of medications. (womensmentalhealth.org)
- The National Pregnancy Registry for Atypical Antipsychotics continues to recruit pregnant women taking atypical antipsychotic medications. (womensmentalhealth.org)
Olanzapine2
- Antipsychotics, such as haloperidol, olanzapine, and risperidone, have been used with some success in augmenting SSRIs in patients with OCD, particularly in patients with comorbid Tourette disorder or other tic disorders. (medscape.com)
- With olanzapine, other atypical antipsychotics may be considered. (nih.gov)
Benzodiazepines1
- Because of the risks of toxicity, use only as an alternative to other less toxic anxiolytic agents (e.g., benzodiazepines) in most patients. (drugs.com)
MeSH1
- Une recherche documentaire a été effectuée dans PubMed de 1980 à 2021 en utilisant diverses combinaisons de termes MeSH comme tabac, diabète, hypertension, dyslipidémie, trouble dépressif majeur, trouble bipolaire, schizophrénie. (who.int)
Risperidone1
- Risperidone is an atypical antipsychotic agent that displays 5-HT2A receptor antagonism. (fishersci.com)
Psychosis2
Bipolar disorder1
- The newer atypical or second-generation antipsychotic agents are used to treat a spectrum of psychiatric disorders, including psychotic disorders, bipolar disorder, major depression, PTSD and other anxiety disorders. (womensmentalhealth.org)
Patients4
- Analyses of 17 placebo-controlled trials in geriatric patients mainly receiving atypical antipsychotic agents revealed an approximate 1.6- to 1.7-fold increase in mortality compared with that in patients receiving placebo. (drugs.com)
- Observational studies suggest that conventional or first-generation antipsychotic agents also may increase mortality in such patients. (drugs.com)
- Undesirable alterations have been observed in patients treated with atypical antipsychotics. (nih.gov)
- Agents intervening against Delirium in the ICU (AID-ICU) is an international, multicentre, randomised, blinded, placebo-controlled trial investigates benefits and harms of treatment with haloperidol in patients with ICU-acquired delirium. (helsinki.fi)
Adverse1
- said some prescriptions used to treat severe mental illnesses are not covered by Health Canada unless the patient has tried other antipsychotic agents first and experienced no improvement or suffered adverse reactions. (thestar.com)
Clinical2
- Unlike conventional antipsychotic agents, atypical antipsychotics also exert activity at other receptors, and it is generally acknowledged that, compared with conventional antipsychotics, atypical agents are associated with a broader spectrum of clinical efficacy and are better tolerated. (medscape.com)
- When compared with conventional antipsychotic agents in clinical trials, it is acknowledged that atypical agents are associated with a broader spectrum of efficacy, including effects on both positive and negative symptoms and, possibly, cognitive function, and that they are better tolerated, particularly in relation to EPS. (medscape.com)
Neuroleptics1
- Although they are associated with the use of neuroleptics, TDs apparently existed before the development of these agents. (medscape.com)
Causative agent2
- The management of hyperglycaemia depends on the causative agent. (nih.gov)
- For example, people with fetal alcohol syndrome, other developmental disabilities, and other brain disorders are vulnerable to the development of TDs, even after receiving only 1 dose of the causative agent. (medscape.com)
Atypical agents1
- Our data on the reproductive safety of these newer atypical agents is growing. (womensmentalhealth.org)
Conventional2
- conventional (prototypical, first-generation) antipsychotic and antiemetic agent. (drugs.com)
- [ 16 ] There has also been some concern regarding corrected QT (QTc) prolongation observed with certain atypical anti- psychotic agents, although these agents may not be as arrhythmogenic as some conventional agents. (medscape.com)
Prolongation1
- Currently, treatment options are limited to counselling as antipsychotic agents are linked to QT interval prolongation (the prolongation of time between the heart contracting and relaxing) and sudden death if the user is also taking cocaine. (kcl.ac.uk)
Drug2
- however, optimum antipsychotic effect usually requires prolonged administration of the drug. (drugs.com)
- Prodrugs are used typically to reduce toxicity caused by functional groups such as the carboxylate ion, to alter release properties (e.g., prolonging action of antipsychotic agents), or to improve absorption (bioavailability) by making the drug more lipophilic. (cdc.gov)
Alleviate1
- Agents that control agitated psychotic behavior, alleviate acute psychotic states, reduce psychotic symptoms, and exert a quieting effect. (bvsalud.org)
Pregnant2
- 64367] In rare cases, when another antihypertensive agent cannot be used to treat a pregnant patient, serial ultrasound examinations should be performed to assess the intraamniotic environment. (pdr.net)
- The National Pregnancy Registry for Atypical Antipsychotics is a prospective pharmacovigilance program in which pregnant women between the ages of 18 and 45 are enrolled and interviewed during pregnancy. (womensmentalhealth.org)
Risk3
- Initially confined to new-generation atypical antipsychotics in which an approximately 1.6-1.7-fold increase in mortality has been demonstrated, recent evidence points to a risk of at least similar magnitude with older-generation typical agents, prompting warnings by UK and US medicines regulators about an increased risk of death associated with the entire class, atypical and typical. (rcpe.ac.uk)
- No studies thus far have demonstrated an increase in risk of malformations in children exposed to atypical antipsychotics. (womensmentalhealth.org)
- These findings, taken together with other studies , suggest that prenatal exposure to atypical antipsychotics does not appear to significantly increase the risk for congenital malformations, although we have very few documented exposures to some of the newest atypicals, including lurasidone (Latuda), iloperidone (Fanapt), brexpiprazole (Rexulti), and cariprazine (Vraylar). (womensmentalhealth.org)
Dose1
- Individuals taking antidepressants or antipsychotics should be observed during the initial phase of dose adjustment and advised not to drive if they show any evidence of drowsiness or hypotension. (caa.ca)