Instructions Risperon film-coated tablets 2 mg blister No. 30
Composition
active ingredient: risperidone;
1 film-coated tablet contains 2 mg or 4 mg of risperidone;
excipients: anhydrous lactose, microcrystalline cellulose, pregelatinized starch, magnesium stearate, hypromellose 6, macrogol 6000, titanium dioxide (E 171).
Dosage form
Film-coated tablets.
Main physicochemical properties:
2 mg film-coated tablets: white, oval, biconvex tablets with a score, with the inscription T2;
4 mg film-coated tablets: white, oval, biconvex tablets with a score, with the inscription T4.
Pharmacotherapeutic group
Antipsychotic drugs.
ATX code N05A X08.
Pharmacological properties
Pharmacodynamics
Risperidone is a selective monoaminergic antagonist with characteristic properties.
It has high affinity for both serotonergic 5-HT2 receptors and dopaminergic D2 receptors. Risperidone also binds to α1-adrenergic receptors and (with lower affinity) to H1-histaminergic and α2-adrenergic receptors. Risperidone has no affinity for cholinergic receptors. Although risperidone is a potent D2 receptor antagonist, which reduces the severity of positive symptoms of schizophrenia, it is less likely to cause motor depression and catalepsy than classical neuroleptics. Balanced central antagonism of serotonin and dopamine may lead to a decrease in the incidence of extrapyramidal side effects and an expansion of therapeutic activity against the negative and affective symptoms of schizophrenia.
Pharmacokinetics
Risperidone is metabolized to 9-hydroxyrisperidone, which has similar pharmacological effects to risperidone.
Absorption.
After oral administration, risperidone is completely absorbed and reaches peak plasma concentrations within 1-2 hours, in elderly patients within 2-3 hours. Absolute bioavailability after oral administration of risperidone is 70% (CV=25%). Relative bioavailability after oral administration of risperidone in tablets is 94% (CV=10%) compared to the solution form. Food does not affect the absorption of the drug, so risperidone can be administered regardless of meals. Absolute bioavailability is 66% in extensive metabolizers and 82% in poor metabolizers.
Distribution.
Risperidone is rapidly distributed in the body. The volume of distribution is 1-2 l/kg. In blood plasma, risperidone binds to albumin and acid α1-glycoprotein. Risperidone is 90% bound to plasma proteins, 9-hydroxyrisperidone is 77%. The equilibrium concentration of risperidone in the body is achieved in most patients within 1 day. The equilibrium concentration of 9-hydroxyrisperidone is achieved within 4-5 days.
Biotransformation and excretion.
Risperidone is metabolized by cytochrome CYP2D6 to 9-hydroxyrisperidone, which has similar pharmacological effects to risperidone. Risperidone and 9-hydroxyrisperidone form the active antipsychotic fraction. Cytochrome CYP2D6 is subject to genetic polymorphism. In extensive CYP2D6 metabolizers, risperidone is rapidly converted to 9-hydroxyrisperidone, whereas in poor metabolizers, risperidone is converted much more slowly. Although extensive metabolizers have lower concentrations of risperidone and 9-hydroxyrisperidone than in poor metabolizers, the pharmacokinetics of risperidone and 9-hydroxyrisperidone in combination (i.e., the active antipsychotic fraction) after single and multiple doses are similar in extensive and poor metabolizers of CYP2D6.
Another route of metabolism of risperidone is N-dealkylation. In vitro studies with human liver microsomes have shown that risperidone at clinically relevant concentrations does not significantly inhibit the metabolism of drugs metabolized by cytochrome P450 isoenzymes, including CYP1A2, CYP2A6, CYP2C8/9/10, CYP2D6, CYP2E1, CYP3A4, and CYP3A5. One week after administration, 70% of the dose is excreted in the urine and 14% in the feces. The concentration of risperidone and 9-hydroxyrisperidone in the urine is 35-45% of the dose taken. The rest is made up of inactive metabolites. After oral administration in psychotic patients, the half-life is approximately 3 hours. The half-life of 9-hydroxyrisperidone and the active antipsychotic fraction reaches 24 hours, and in elderly patients - 34 hours.
Linearity.
Risperidone plasma concentrations are proportional to the drug dose (within the therapeutic dose range).
Elderly patients and patients with impaired renal or hepatic function.
A single-dose study in elderly patients and patients with renal insufficiency revealed higher plasma concentrations (AUC and Cmax 2-2.5 times higher) and a decrease in clearance of the active antipsychotic fraction by 30% in elderly patients and by 60% in patients with renal insufficiency (see section "Special warnings and precautions for use").
A lower degree of risperidone binding to plasma proteins was observed in patients with impaired liver function.
In patients with hepatic insufficiency, normal plasma risperidone concentrations were observed, but the mean free fraction of risperidone in plasma was increased by 35%.
The pharmacokinetics of risperidone, 9-hydroxyrisperidone and the active antipsychotic fraction in children are similar to those in adults.
Gender, race, and smoking.
Population pharmacokinetic analysis revealed no apparent effect of gender, age, or smoking habit on the pharmacokinetics of risperidone or the active antipsychotic fraction.
Indication
Treatment of schizophrenia and other psychiatric disorders, including maintenance therapy, in patients who have responded to therapy, in order to prevent relapse of the disease;
treatment of manic episodes in bipolar disorders (adjunctive therapy in combination with mood stabilizers as initial treatment or as monotherapy for a period of up to 12 weeks);
short-term treatment of severe aggression or severe psychiatric symptoms in patients with dementia who are at risk of harm to themselves or others;
symptomatic treatment of oppositional defiant disorder or other social behavior disorders in children, adolescents and adults with below average mental development or mental retardation who have manifestations of destructive behavior (impulsivity, autoaggression);
symptomatic treatment of autistic disorders in children aged 5 years and older, in whom symptoms range from hyperactivity to irritability (including aggression, self-harm, anxiety and pathological cyclic actions).
Contraindication
Hypersensitivity to the active ingredient or to any of the excipients of the drug.
Dementia and symptoms of Parkinson's disease (rigidity, bradykinesia and parkinsonian postural disorders).
Dementia and suspected dementia with Lewy bodies (in addition to symptoms of dementia, at least two of the following symptoms: parkinsonism, visual hallucinations, unsteadiness of gait).
Interaction with other medicinal products and other types of interactions
In vitro metabolism studies have shown that the breakdown of risperidone to 9-hydroxyrisperidone can be inhibited by phenothiazines, tricyclic antidepressants, and some beta-blockers that bind to CYP 2D6. Such inhibition may result in increased plasma concentrations of risperidone and decreased levels of the active metabolite 9-hydroxyrisperidone. Although clinical data from 12 patients showed that amitriptyline did not inhibit the breakdown of risperidone to 9-hydroxyrisperidone, analysis of data from a small number of patients receiving these drugs concomitantly confirms that the clinical effect is not altered.
Risperidone is a weak inhibitor of CYP 2D6 in vitro. Therefore, Risperidone is not expected to significantly inhibit the elimination of drugs that are metabolized by these enzymes.
With the simultaneous use of drugs that are enzyme inducers, the metabolism of risperidone may increase. Carbamazepine reduces the concentration of the active antipsychotic fraction in the blood plasma. Clinical data have shown that in patients who used carbamazepine simultaneously, the plasma concentrations of risperidone and 9-hydroxyrisperidone were 1.7-3.7 times lower. Similar effects (reduction in the plasma concentration of the active antipsychotic fraction) may be observed with the use of other inducers of hepatic CYP 3A4 enzymes, such as rifampicin, phenytoin and phenobarbital. When canceling or resuming the intake of carbamazepine or other inducers of CYP 3A4 enzymes, the dosage of Risperdal® should be re-evaluated and, if necessary, adjusted. In isolated cases, toxic serum concentrations of carbamazepine have been observed with the simultaneous use of carbamazepine and risperidone.
Risperdal® may have antagonistic effects on levodopa and other dopamine antagonists. If such a combination is considered necessary, especially in the end-stage of Parkinson's disease, the lowest effective doses of each drug should be used.
Phenothiazines, tricyclic antidepressants and some β-blockers may increase the plasma concentration of risperidone, but not the concentration of the antipsychotic fraction. Cimetidine 400 mg twice daily and ranitidine 150 mg twice daily increased the AUC of the active antipsychotic fraction (risperidone and 9-hydroxyrisperidone) by 8% and 20%, respectively, although this is not clinically significant.
Fluoxetine (20 mg/day) and paroxetine (20 mg/day) have been shown to increase risperidone plasma concentrations by 2.5-2.8 and 3-9 times, respectively. Fluoxetine has no effect on 9-hydroxyrisperidone plasma concentrations. Paroxetine reduces 9-hydroxyrisperidone plasma concentrations by an average of 13%. Overall, the concentration of the active antipsychotic fraction increases by 50% when fluoxetine and paroxetine are coadministered. If fluoxetine and paroxetine are initiated or discontinued during Risperdal® therapy, the physician should review the dose of Risperdal®. The effect of discontinuation of fluoxetine and paroxetine on the pharmacokinetics of risperidone or 9-hydroxyrisperidone has not been studied.
Erythromycin (CYP 3A4 inhibitor) does not affect the pharmacokinetics of risperidone and the active antipsychotic fraction.
As with other antipsychotics, caution should be exercised when prescribing risperidone with drugs that prolong the QT interval, such as class Ia antiarrhythmics (quinidine, procainamide), class III antiarrhythmics (amiodarone, solatole), tricyclic antidepressants (amitriptyline), tetracyclic antidepressants (maprolitine), some antihistamines, other antipsychotics, some antimalarials (quinine, mefloquine), and drugs that cause electrolyte imbalance (hypokalemia, hypomagnesemia), bradycardia, or drugs that inhibit the hepatic metabolism of risperidone. This list is not exhaustive.
The cholinesterase inhibitors galantamine and donepezil do not have clinically significant effects on the pharmacokinetics of risperidone and the active antipsychotic fraction.
A clinical study in 13 patients demonstrated that the pharmacokinetics of lithium were not significantly altered when the concomitant neuroleptic was replaced by Risperidone 3 mg twice daily. The compatibility of risperidone with lithium has not been studied. Encephalopathies, extrapyramidal disorders, and neuroleptic malignant syndrome have been reported with concomitant use of neuroleptics and lithium. In clinical trials, extrapyramidal disorders and hyperkinesia were reported more frequently with lithium in combination with neuroleptics than with lithium alone.
Risperdal® had no clinically significant effects on the pharmacokinetics of valproate in a parallel-group study and digoxin in a crossover interaction study.
Topiramate significantly reduces the bioavailability of risperidone, but has little to no effect on the bioavailability of the active antipsychotic fraction. Therefore, this interaction is unlikely to be clinically significant.
Clonazepam, gabapentin, lamotrigine, methylphenidate: given the pharmacokinetics of risperidone and these active substances, interactions between them are not expected, although relevant studies have not been conducted.
The risks of using Risperidone® concomitantly with other drugs have not been systematically studied. Interactions are theoretically possible with all active substances that act on the central nervous system. Until further research is available, caution should be exercised when prescribing risperidone concomitantly with other drugs.
For information on increased mortality when used concomitantly with furosemide in elderly patients with dementia, see section "Special warnings and precautions for use".
Risperidone should be used with caution in combination with other centrally acting substances, including alcohol, opiates, antihistamines and benzodiazepines, due to an increased risk of sedation.
Verapamil, an inhibitor of CYP3A4 and P-glycoprotein, increases the plasma concentration of risperidone.
Concomitant use of oral Risperidone with paliperidone is not recommended because paliperidone is the active metabolite of risperidone and their combination may result in additive effects of the active antipsychotic fraction.
Application features
Elderly patients with dementia.
Increased mortality rate.
Elderly patients with dementia treated with atypical antipsychotics had an increased mortality rate compared with placebo in a meta-analysis of 17 controlled trials of atypical antipsychotics, including Risperdal. In a placebo-controlled trial of Risperdal, the mortality rate in this group was 4.0% compared with 3.1% in the placebo group. The median age of patients who died was 86 years (range 67-100 years). The specific risk factor profile for mortality in the Risperdal group has not been determined. The causes of death were typical for this age group (65 years and older) and included: cardiovascular and cerebrovascular diseases, neoplasms, infections (e.g. pneumonia), and diabetes.
Concomitant use with furosemide.
In a placebo-controlled study in elderly patients with dementia, an increased mortality rate was observed with the concomitant use of risperidone with furosemide (7.3%; mean age 89 years, range 75-97 years) compared with patients treated with risperidone alone (3.1%; mean age 84 years, range 70-96 years) or furosemide alone (4.1%; mean age 80 years, range 67-90 years). An increased mortality rate among patients treated with risperidone and furosemide concomitantly was observed in two of the four clinical trials. There was no increased mortality rate among patients treated with risperidone and other diuretics concomitantly.
No pathophysiological mechanisms have been identified to explain this finding. The cause of death was not uniform either. However, caution should be exercised when prescribing in such cases, and the risks and benefits of this combination or of other potential diuretics should be assessed before prescribing. Regardless of treatment, dehydration was a common risk factor for mortality and should be carefully monitored in patients with dementia.
In placebo-controlled clinical trials, a higher rate of fatal cerebrovascular adverse events (strokes and transient ischemic attacks) was observed in patients with dementia treated with Risperdal® compared to those treated with placebo (mean age 85 years; range 73-97 years).
Pooled data from six placebo-controlled studies in elderly patients with dementia (aged 65 years and older) showed that cerebrovascular events (including serious events) occurred in 3.3% (33/989) of patients treated with Risperidone compared with 1.2% (8/693) of patients treated with placebo. The ratio between the Risperidone and placebo groups (odds ratio; 95% CI) was 2.96 (1.33, 7.45), and in the subgroup of patients with vascular dementia it was 5.26 (1.18, 48.11).
The risk of cerebrovascular adverse events is significantly higher in patients with mixed or vascular dementia compared with Alzheimer's dementia. The risks and benefits of prescribing Risperdal® to elderly patients with dementia should be carefully weighed, especially the risk of stroke. Risperdal® should be prescribed with particular caution to patients with dementia who have hypertension, cardiovascular disease, and vascular dementia. Patients and caregivers should be instructed to immediately report signs of possible cardiovascular events, such as sudden weakness, numbness of the face, arms, or legs, and speech and vision disorders. All possible treatment options, including discontinuation of Risperdal®, should be considered immediately.
Children.
Before prescribing Risperdal® to children, the risk-benefit ratio should be carefully weighed. The need for continued treatment should be carefully assessed regularly. The indications “symptomatic treatment of social conduct disorders, oppositional defiant disorder and/or other social conduct disorders” and “autistic disorders” have only been studied in children aged 5 years and older. Therefore, Risperdal® should not be prescribed for these indications in children under 5 years of age.
There is no experience with the use of Risperdal® in children under 15 years of age for the treatment of schizophrenia and in children under 10 years of age for the treatment of manic episodes in bipolar disorder.
For children, the available data are based on clinical studies of 1 year duration. These data show that there is no effect on growth and development. The effect on growth and development with treatment lasting more than one year is unknown. Therefore, clinical monitoring of the endocrine system should be carried out, including measurement of height and weight, monitoring of sexual development, potential prolactin-dependent effects, and investigation of extrapyramidal symptoms and other motor disorders.
Drowsiness.
In placebo-controlled studies, somnolence was commonly observed in children with autism. Most cases were mild to moderate in severity. Somnolence was predominantly observed at the start of treatment, with the highest frequency occurring within the first two weeks of treatment, and resolved spontaneously, with a median duration of 16 days. In patients with somnolence, a change in dosing regimen may be considered.
Orthostatic hypotension.
Due to the α1-lytic activity of risperidone, orthostatic hypotension may occur, especially at the beginning of treatment. In the post-marketing period, clinically significant hypotension has been observed with the simultaneous use of risperidone and antihypertensive agents. Risperidone should be used with caution in patients with cardiovascular diseases (such as heart failure, myocardial infarction, conduction disorders, dehydration, hypovolemia or cerebrovascular disease). In these cases, the dose should be adjusted gradually (see section "Method of administration and dosage"). If hypotension occurs, a dose reduction should be considered.
QT prolongation.
In clinical trials, QT prolongation was not associated with risperidone. In the post-marketing period, very rare cases of QT prolongation have been reported. Risperidone®, as with other antipsychotics, should be used with caution in patients with cardiovascular disease, electrolyte disturbances (hypokalemia, hypomagnesemia), or a family history of QT prolongation. Caution should also be exercised when co-administered with drugs that prolong the QT interval.
Leukopenia, neutropenia, agranulocytosis.
Leukopenia, neutropenia and agranulocytosis have been reported with antipsychotics, including risperidone. Agranulocytosis has been reported very rarely (<1/10,000 patients) in the post-marketing setting.
Patients with a history of significant leukopenia or drug-induced leukopenia/neutropenia should be closely monitored during the first few months of treatment and risperidone should be discontinued if signs of significant leukopenia appear and if no other cause for the decrease is found.
Patients with clinically significant neutropenia should be monitored for fever and other signs of infection and treated appropriately if symptoms develop. In case of severe neutropenia (<1×109/L), risperidone treatment should be discontinued and the white blood cell count monitored until recovery.
Cases of venous thromboembolism have been described with the use of antipsychotic drugs. Since patients treated with antipsychotic drugs often have acquired risk factors for venous thromboembolism, all possible factors for the development of thromboembolism should be identified before and during treatment with Risperdal® and appropriate preventive measures should be taken.
Tardive dyskinesia/extrapyramidal symptoms.
Tardive dyskinesia, characterized by involuntary rhythmic movements (predominantly of the tongue and/or face), has been reported with dopamine receptor antagonists. The occurrence of extrapyramidal symptoms is a risk factor for the development of tardive dyskinesia. If signs and symptoms of tardive dyskinesia develop, discontinuation of all antipsychotic medications should be considered.
Parkinson's disease and dementia with Lewy bodies.
Physicians should weigh the risks and benefits when prescribing antipsychotics, including Risperidone®, to patients with Parkinson's disease or dementia with Lewy bodies. Risperidone may worsen Parkinson's disease. Patients with any of the above conditions may be at increased risk of neuroleptic malignant syndrome and may be more sensitive to antipsychotic drugs (e.g., confusion, pain sensitivity, and postural instability with frequent falls in addition to extrapyramidal symptoms).
Neuroleptic malignant syndrome.
Rare cases of neuroleptic malignant syndrome, characterized by hyperthermia, muscle rigidity, autonomic instability, impaired consciousness, and elevated creatine phosphokinase levels, have been reported with classical neuroleptic drugs. Additional features include myoglobinuria (rhabdomyolysis) and acute renal failure. If neuroleptic malignant syndrome develops, all antipsychotic drugs, including Risperdal®, should be discontinued.
Hyperglycemia and diabetes.
Hyperglycemia, diabetes mellitus, or exacerbation of pre-existing diabetes mellitus have been reported with Risperidone. The association between the use of atypical antipsychotics and glucose abnormalities is complicated by the increased risk of diabetes mellitus in patients with schizophrenia and the increased incidence of diabetes mellitus in the general population. Therefore, the association between the use of atypical antipsychotics and adverse reactions related to hyperglycemia is not fully understood. Although epidemiological studies indicate an increased risk of adverse reactions related to hyperglycemia in patients treated with atypical neuroleptics. All patients taking atypical antipsychotics should be monitored for symptoms of hyperglycemia and diabetes mellitus.
Weight gain.
Significant weight gain has been reported with Risperdal®. Weight monitoring is recommended.
Priapism.
Priapism may occur during treatment with Risperdal due to its alpha-adrenergic blocking effects. Cases of priapism have been reported in the post-marketing period.
Body temperature regulation.
Antipsychotic drugs may impair the body's ability to lower its core temperature. Appropriate care is recommended for patients prescribed Risperdal if they are exposed to conditions that may cause an increase in core body temperature, such as intense physical exercise, exposure to high ambient temperatures, concomitant therapy with drugs with anticholinergic activity, or exposure to dehydration.
Antiemetic effect.
In preclinical studies, risperidone has been shown to have an antiemetic effect. This property may mask symptoms of overdose with certain drugs or conditions such as intestinal obstruction, Reye's syndrome, and brain tumors.
Convulsions.
Risperdal should be used with caution in patients with a history of seizures or other conditions that potentially lower the seizure threshold.
Intraoperative atonic iris syndrome (ISAR).
During cataract surgery, intraoperative atonic iris syndrome has been observed in patients treated with drugs with alpha-adrenergic blocking properties, including Risperdal®.
ISAR may increase the risk of complications during and after eye surgery. The ophthalmologist should be informed of any previous or current use of antipsychotic medications. The potential benefits of discontinuing alpha-blocking medications prior to surgery have not been established, and the risks of discontinuing antipsychotic medications should be weighed against the risks of discontinuing antipsychotic medications.
Liver and kidney dysfunction.
Patients with impaired liver and kidney function are recommended to prescribe half the initial and maintenance doses (see section "Method of administration and dosage").
Tissue culture studies suggest that cell growth in human breast tumors may be stimulated by prolactin. Although a clear association with antipsychotic use has not yet been established by clinical or epidemiological studies, caution is advised when prescribing risperidone to patients with a history of such conditions. Risperidone should be used with caution in patients with hyperprolactinemia and prolactin-dependent tumors, such as pituitary prolactinomas, or suspected prolactin-dependent tumors, such as epithelial tumors of the breast.
Excipients.
The film-coated tablets contain lactose. Patients with rare hereditary problems of galactose intolerance, the Lapp lactase deficiency or glucose-galactose malabsorption should not take Risperdal film-coated tablets.
Patients with hypersensitivity to azo dyes (E 110), acetylsalicylic acid and other prostaglandin synthesis inhibitors should use Risperdal® film-coated tablets with caution.
The product contains orange-yellow S (E 110). May cause allergic reactions.
Use during pregnancy or breastfeeding
Pregnancy.
Controlled studies in pregnant women have not been conducted. Although no teratogenic effects were observed in animal studies, an indirect effect on prolactin levels was observed.
Newborns whose mothers have used antipsychotics (including risperidone) during the last trimester of pregnancy are at risk of developing reversible extrapyramidal symptoms and/or drug withdrawal syndrome. These symptoms include agitation, unusually high or low muscle tone, tremor, drowsiness, respiratory distress, or feeding difficulties. These complications may vary in severity. In some cases, they resolved spontaneously over time, while in others, monitoring of the infant's condition in the intensive care unit or prolonged hospitalization was required.
Risperidone is not recommended for use during pregnancy unless clearly necessary. If it is necessary to discontinue Risperidone during pregnancy, this should not be done abruptly.
Breastfeeding period.
In animal studies, risperidone and 9-hydroxyrisperidone were excreted in milk. There are observations that risperidone and 9-hydroxyrisperidone may also be excreted in human breast milk. In individual cases, 4.3% of the maternal dose was detected in breast milk as the active antipsychotic fraction of the active substance. If treatment is necessary, breastfeeding should be discontinued.
Ability to influence reaction speed when driving vehicles or other mechanisms
The drug may affect the reaction rate when performing work that requires special attention. Therefore, it is recommended to refrain from driving a car or operating other mechanical devices.
Method of administration and doses
Usual dose
Risperdal® can be taken once or twice daily. Doses greater than 8 mg should be taken in two divided doses (morning and evening). Food intake does not affect the absorption of Risperdal®.
Gradual discontinuation of treatment is recommended. Acute withdrawal symptoms, including nausea, vomiting, sweating, insomnia, have been observed very rarely after abrupt discontinuation of high doses of antipsychotics. Recurrence of psychotic symptoms may also occur, and involuntary movements (e.g. akathisia, dystonia and dyskinesia) have been reported.
To achieve a dose of 0.25–2.5 mg, it is recommended to use risperidone as an oral solution.
Schizophrenia
Adults
Risperdal® can be administered once or twice daily.
The dose should be started with 2 mg of Risperdal® per day, on the second day the dose can be increased to 4 mg. After that, the dose can be maintained unchanged or, if necessary, individual dose adjustment can be continued. For most patients, the recommended dose is 4-6 mg per day. Some patients may require a gradual increase in dose or a lower initial dose.
Doses greater than 10 mg/day have not been shown to be more effective than lower doses, but they may cause extrapyramidal symptoms. Since the safety of doses greater than 16 mg/day has not been studied, such doses should not be used.
If additional sedation is needed, a benzodiazepine can be used concurrently.
Elderly patients (65 years and older).
The recommended starting dose is 0.5 mg twice daily. If necessary, the dose can be increased to 1-2 mg twice daily by increasing by 0.5 mg twice daily.
Manic episodes in bipolar disorder
Adults.
As with other symptomatic treatments, long-term use of Risperdal® requires periodic dose review and adjustment throughout the course of therapy. There is no data on the efficacy of Risperdal® in the treatment of acute bipolar mania lasting more than 12 weeks. If Risperdal® is used in combination with mood stabilizers, therapy may be discontinued earlier, as the onset of the treatment effect can be expected within the first weeks of therapy. Even after a response to treatment, the possibility of recurrence of depressive symptoms should be considered due to the characteristics of the course of the disease and the adverse reactions of the drugs used for treatment, including Risperdal®.
Elderly patients (65 years and older).
The recommended initial dose is 0.5 mg twice daily. If necessary, the dose can be increased to 1-2 mg twice daily, increasing by 0.5 mg twice daily. Since experience in elderly patients is limited, caution is recommended.
Children aged 10 and over.
The recommended starting dose is 0.5 mg once daily, in the morning or evening. The dose can be individually increased by adding 0.5 to 1 mg/day no more frequently than every 24 hours until the recommended dose of 2.5 mg/day is reached. Efficacy of treatment has been demonstrated in the dose range of 0.5 to 6 mg/day; doses above 6 mg/day have not been studied.
Patients with drowsiness may be advised to divide the daily dose into 2 doses.
As with other types of symptomatic treatment, with long-term use of Risperdal®, doses should be periodically reviewed and adjusted throughout the course of therapy.
There is no experience with the use of Risperdal® for the treatment of manic episodes in bipolar disorder in children under 10 years of age.
Short-term treatment of severe aggression or severe psychiatric symptoms in patients with dementia
The recommended initial dose is 0.25 mg twice daily. If necessary, the dose can be increased by increasing the dose by 0.25 mg twice daily not more often than every other day. For most patients, the optimal dose is 0.5 mg twice daily. However, for some patients, the effective dose can be increased to 1 mg twice daily. After reaching the optimal dose, the possibility of taking the daily dose once daily can be considered. As with other types of symptomatic treatment, with long-term use of Risperdal®, the dose should be periodically reviewed and adjusted throughout the course of therapy.
Risperdal® treatment should be discontinued no later than 3 months after the start of therapy; therapy can only be resumed if behavioral disorders reappear.
Symptomatic treatment of social behavior disorders or aggressive behavior
Patients with body weight ≥ 50 kg
The recommended starting dose is 0.5 mg once daily. If necessary, the dose should be adjusted by adding 0.5 mg once daily no more than every other day. The optimal dose for most patients is 1 mg once daily. However, for some patients, no more than 0.5 mg once daily is sufficient to achieve a positive effect, while others may require 1.5 mg once daily.
Patients with body weight < 50 kg
The recommended starting dose is 0.25 mg once daily. If necessary, the dose can be adjusted by adding 0.25 mg once daily no more than every other day. The optimal dose for most patients is 0.5 mg once daily. However, for some patients, no more than 0.25 mg once daily is sufficient to achieve a positive effect, while others may require 0.75 mg once daily.
As with other types of symptomatic treatment, long-term use of Risperdal® should be periodically reviewed and adjusted throughout therapy.
There is no experience with the use of Risperdal® for the symptomatic treatment of social behavior disorders or aggressive behavior in children under 5 years of age.
Autism (children aged 5 and over)
The dose should be individualized, depending on the patient's condition and clinical response.
Patients with body weight <50 kg
The recommended starting dose is 0.25 mg once daily. From day 4, the dose can be increased by 0.25 mg. The dose should be maintained at 0.5 mg and on day 14, the dose should be increased by 0.5 mg.
