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Risperidone

A Review of its Use in the Management of the Behavioural and Psychological Symptoms of Dementia

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Summary

Abstract

Risperidone is a benzisoxazole derivative which has proven efficacy against the positive and negative symptoms of schizophrenia. It has more recently been investigated and shown efficacy as a treatment for the behavioural and psychological symptoms associated with dementia in the elderly. Risperidone has pharmacological properties resembling those of the atypical antipsychotic clozapine and an improved tolerability profile compared with the conventional antipsychotic haloperidol. Risperidone has antagonistic activity primarily at serotonin 5-HT2A and dopamine D2 receptors.

In the first 2 large, well controlled trials of an antipsychotic agent used in the treatment of elderly patients with Alzheimer’s dementia, vascular dementia or mixed dementia, risperidone 1 mg/day was at least as effective as haloperidol and superior to placebo, as assessed by the rating scales for global behaviour, aggression and psychosis. In extension phases of the 2 trials, clinical benefits were maintained for treatment periods of up to 1 year, with an incidence rate of tardive dyskinesia (2.6%) one-tenth of that seen with conventional antipsychotics. Risperidone, administered at a low dosage of 1 mg/day was associated with fewer extrapyramidal symptoms compared with haloperidol in elderly patients. Risperidone was well tolerated with no clinically relevant abnormalities in laboratory tests, vital signs or electrocardiogram results.

Conclusion: The efficacy of risperidone has been demonstrated in the treatment of the behavioural and psychological symptoms associated with dementia in the elderly. Preliminary results from 1-year extension studies confirm the favourable efficacy and tolerability profile of risperidone 1 mg/day. Although head to head studies with other atypical antipsychotic agents are required and the long term use of the drug requires clarification, risperidone represents a generally well tolerated and effective treatment in the management of dementia-associated behavioural and psychological symptoms in the elderly.

Overview of Pharmacodynamic Properfies

Risperidone binds to both serotonin 5-HT2A and dopamine D2 receptors, with higher binding affinity for the serotonin receptor compared with other antipsychotics. It demonstrates high central serotonin 5-HT2A receptor antagonism at low doses and dose-related dopamine D2 receptor antagonism. The higher binding affinity of risperidone for serotonin 5-HT2A than dopamine D2 receptors, along with its mesolimbic specificity of action, is thought to account for the reduced incidence of extrapyramidal symptoms (EPS) relative to conventional antipsychotics. High to moderate binding is also seen at other neurotransmitter receptor binding sites and the drug therefore has potential to cause postural hypotension, sedation and drowsiness.

Risperidone, administered at low doses in the rat, causes central serotonin 5-HT2A antagonistic activity. At high doses, the drug demonstrates direct dopamine D2 blocking properties and suppression of apomorphine- and amphetamine-induced stereotyped rat behaviour and agitation, actions predictive of antipsychotic activity.

Low dose risperidone significantly increased slow-wave sleep and decreased wakefulness in rats. In isolated case studies, 2 elderly women with severe dementia in nursing care showed an improvement in the quality of sleep during treatment with low dose risperidone (1.5 mg/day).

Some cognitive impairment is typically present in patients with dementia and treatments that potentiate this impairment should be avoided or minimised. In 2 large 12-week, placebo-controlled, double-blind trials in elderly patients with dementia, risperidone treatment was not associated with cognitive decline.

Pharmacokinetic Properties

Risperidone is rapidly and extensively absorbed after oral administration in healthy volunteers. The drug is extensively metabolised in the liver by the cytochrome P450-IID6 (CYP2D6) isoenzyme to the major metabolite, 9-hydroxy-risperidone (9-OH-risperidone). This metabolite has equipotent pharmacological activity to the parent compound. Risperidone is also metabolised by CYP2D6 to 7-hydroxy-risperidone and di-hydroxy-risperidone.

The absolute oral bioavailability of risperidone is approximately 67 and 81% in normal and poor metabolisers, respectively. However, the absolute oral bioavailability of the active moiety (risperidone plus the active metabolite 9-OH-risperidone) is 100% regardless of the individual’s metabolic status.

Risperidone is rapidly distributed. Within the rat brain, the active moiety is preferentially distributed to regions known to have high concentrations of serotonin 5-HT2A and dopamine D2 receptors, the frontal cortex and striatum, respectively.

Risperidone and its metabolites are excreted mainly in the urine (70%) and partly in the faeces (14%). The elimination half-life (t½β) of risperidone is 2.8, 12.4 and 16.2 hours in extensive, intermediate and poor metabolisers, respectively, although t½β of the active moiety is approximately 20 hours irrespective of metabolic status.

In both the elderly and patients with renal disease, the renal (CLR) and total body clearances (CL) of the active moiety are significantly reduced and t½β prolonged compared with values in young volunteers.

Therapeutic Use

Most of the literature on risperidone for the treatment of dementia-related behavioural and psychological disturbances in the elderly consists of non-comparative trials, case studies, small controlled trials, or retrospective reviews. The largest of these studies have indicated efficacy for risperidone at doses ranging from 0.5 to 4.0 mg/day, with the optimal dose being 1.0 mg/day. Risperidone 0.5 to 1.0 mg/day was beneficial against a full range of target symptoms including aggression, agitation and psychosis.

The first 2 large, placebo-controlled, double-blind trials in which an antipsychotic has been used in the treatment of dementia-related behavioural and psychological disturbances in the elderly, utilised risperidone. Results from these multicentre studies of risperidone in elderly patients (≥55 years) with dementia (predominantly of the Alzheimer’s type) show the drug to reduce behavioural symptoms of the disease.

In 1 study, 625 nursing home patients were randomised to receive placebo or risperidone 0.5, 1.0 or 2.0 mg/day in divided doses for 12 weeks. Treatment response at end-point [≥50% reduction in the Behavioural Pathology in Alzheimer’s Disease rating scale (BEHAVE-AD) total score] was seen in significantly more patients receiving risperidone 1.0 and 2.0 mg/day than placebo.

Similarly, in the second 12-week study (n = 344), more risperidone (mean dose of 1.1 mg/day) or haloperidol (mean dose 1.2 mg/day) than placebo recipients achieved a treatment response, defined as a ≥30% reduction in BEHAVE-AD total score, although there was no statistical difference between treatments. In a post hoc analysis of patients who completed 12 weeks of treatment, significantly greater improvements were seen on the BEHAVE-AD aggressiveness score (p =0.05) and the Cohen-Mansfield Agitation Inventory total and verbal aggressive scores (p = 0.02) with risperidone- versus haloperidol-treated patients.

In both trials, significant reductions in aggression were seen with risperidone when compared with placebo at week 12 and end-point, with significant improvements seen as early as week 2 in 1 trial. At week 12, risperidone was superior to haloperidol for control of aggression. In 1 trial risperidone 1 or 2 mg/day was superior to placebo in reducing BEHAVE-AD psychosis subscale scores (p < 0.01).

Long term risperidone treatment was shown to sustain behavioural improvements in two 1-year noncomparative extensions of these 12-week studies.

Tolerability

In the 2 placebo-controlled 12-week trials, the most common adverse events reported by at least 10% of patients in any one group (risperidone, placebo or haloperidol) were injury, somnolence, fall, EPS, urinary tract infection, peripheral oedema and purpura. In one trial, 77% of risperidone (mean dose 1.1 mg/day) compared with 80% of haloperidol (mean dose 1.2 mg/day) and 73% of placebo recipients reported adverse events. However, there were no significant differences in the incidence of serious or severe adverse effects between the treatment and placebo groups. Study withdrawal rates were similar for both risperidone 1 mg/day and placebo groups.

There were no reports of clinically relevant abnormalities in laboratory tests, vital signs or electrocardiogram results in either study.

The incidence of EPS was dose-related in patients who received risperidone 0.5, 1 or 2 mg/day. However, the incidence of EPS-related adverse events was not significantly different in patients receiving placebo or risperidone 1 mg/day, but differed significantly between haloperidol and placebo recipients. There were no reports of tardive dyskinesia (TD) or neuroleptic malignant syndrome with risperidone treatment during the 12-week study period in both trials. In one of the long term (up to 1 year) follow-up trials there were no new cases of TD, whereas in the other only a low incidence of TD was reported.

Various instances of risperidone overdose (≤180mg) have been reported, with symptoms described as exaggerated therapeutic adverse effects. There were no reports of death directly relating to risperidone ingestion.

Dosage and Administration

The recommended starting dosage of risperidone is 0.5 mg/day as 2 divided doses. After ≥2 days, the dosage may be adjusted to a recommended dosage of 0.5 to 1.5 mg/day. The usual optimal dosage is 1mg administered once daily. The risk of orthostatic hypotension can be minimised by careful risperidone titration. This dosage schedule is also recommended for patients with hepatic or renal impairment.

Coadministration of risperidone with drugs that are likely to alter its metabolism is unlikely to be clinically important because the main metabolite of risperidone is also active.

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    Nila Bhana & Caroline M. Spencer

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Bhana, N., Spencer, C.M. Risperidone. Drugs & Aging 16, 451–471 (2000). https://doi.org/10.2165/00002512-200016060-00005

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