Aripiprazole versus other atypical antipsychotics for schizophrenia

Klinik und Poliklinik für Psychiatrie und Psychotherapie, Technische Universität München Klinikum rechts der Isar, Moehlstrasse 26, München, Germany, 81675.
Cochrane database of systematic reviews (Online) (Impact Factor: 6.03). 10/2009; DOI: 10.1002/14651858.CD006569.pub3
Source: PubMed


This review compares aripiprazole with other second generation antipsychotic drugs. There were only four studies on two comparisons - aripiprazole compared to olanzapine and aripiprazole compared to risperidone. On the basis of very limited data aripiprazole was not as effective as olanzapine but as good as risperidone. Aripiprazole was associated with less weight gain, cholesterol increase, sedation and prolactin related effects than olanzapine. Compared to risperidone aripiprazole produced fewer dystonias, cardiac arrhythmias, prolactin and cholesterol increase.

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    • "In most cases, we tried risperidone but other agents could be tried as well. Aripiprazole might be somewhat less sedating and have less weight gain than other antipsychotics (30). Unlike other antipsychotics, it is a D2-receptor partial agonist acting as functional antagonist in brain areas of high levels of dopamine and an agonist in regions with low dopamine concentration (31). "
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    ABSTRACT: Aim: Hypnagogic and hypnopompic hallucinations are characteristic symptoms of narcolepsy, as are excessive daytime sleepiness, cataplexy, and sleep paralysis. Narcolepsy patients may also experience daytime hallucinations unrelated to sleep–wake transitions. The effect of medication on hallucinations is of interest since treatment of narcolepsy may provoke psychotic symptoms. We aim to analyze the relation between sodium oxybate (SXB) treatment and psychotic symptoms in narcolepsy patients. Furthermore, we analyze the characteristics of hallucinations to determine their nature as mainly psychotic or hypnagogic and raise a discussion about whether SXB causes psychosis or if psychosis occurs as an endogenous complication in narcolepsy. Method: We present altogether four patients with narcolepsy who experienced psychotic symptoms during treatment with SXB. In addition, we searched the literature for descriptions of hallucinations in narcolepsy and similarities and differences with psychotic symptoms in schizophrenia. Results: Three out of four patients had hallucinations typical for psychosis and one had symptoms that resembled aggravated hypnagogic hallucinations. Two patients also had delusional symptoms primarily associated with mental disorders. Tapering down SXB was tried and helped in two out of four cases. Adding antipsychotic treatment (risperidone) alleviated psychotic symptoms in two cases. Conclusion: Psychotic symptoms in narcolepsy may appear during SXB treatment. Hallucinations resemble those seen in schizophrenia; however, the insight that symptoms are delusional is usually preserved. In case of SXB-induced psychotic symptoms or hallucinations, reducing SXB dose or adding antipsychotic medication can be tried.
    Frontiers in Neurology 08/2014; 5:136. DOI:10.3389/fneur.2014.00136
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    • "Treatment of schizophrenia with aripiprazole has been shown to induce fewer side effects compared with treatment using first-generation antipsychotics34 as well as with olanzapine and risperidone with regard to metabolic, prolactin-related, and dystonic side effects or QTc prolongation. 32,35 Conversely, switching treatment to aripiprazole could reduce weight gain under olanzapine or clozapine according to a recent meta-analysis including 784 patients. However, mean weight reduction was modest (−2.55 ± 1.5 kg).36 "
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    ABSTRACT: About one third of patients with schizophrenia respond unsatisfactorily to antipsychotic treatment and are termed "treatment-resistant". Clozapine is still the gold standard in these cases. However, 40%-70% of patients do not improve sufficiently on clozapine either. In the search for more efficacious strategies for treatment-resistant schizophrenia, drugs with different pharmacological profiles seem to raise new hopes, but are they valid? The aim of this review was to evaluate the evidence for aripiprazole as a potential strategy in monotherapy or combination therapy for patients with treatment-resistant schizophrenia. The evidence for aripiprazole monotherapy and for the combination of aripiprazole with psychotropics other than clozapine is scant, and no recommendation can be made on the basis of the currently available data. More effort has been made in describing combinations of aripiprazole and clozapine. Most of the open-label and case studies as well as case reports have shown positive effects of this combination on overall psychopathology and to some extent on negative symptoms. Several reports describe the possibility of dose reduction for clozapine in combination with aripiprazole, a strategy that might help so-called "treatment-intolerant" patients. The findings of four randomized controlled trials with respect to changes in psychopathology seem less conclusive. The most commonly found beneficial effects are better metabolic outcomes and indicators of the possibility of reducing the clozapine dose. However, other side effects, such as akathisia, are repeatedly reported. Further, none of the studies report longer-term outcomes. In the absence of alternatives, polypharmacy is a common strategy in clinical practice. Combining aripiprazole with clozapine in clozapine-resistant or clozapine-intolerant patients seems to be worthy of further investigation from the pharmacological and clinical points of view.
    Neuropsychiatric Disease and Treatment 05/2012; 8:235-44. DOI:10.2147/NDT.S13830 · 1.74 Impact Factor
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    • "Therefore, drugs acting on presynaptic D2 autoreceptors are supposed to act more closely to the actual pathology. Despite a substantial amount of research, only one partial agonist, aripiprazole, has shown successful clinical efficacy,3 while the clinical effect of bifeprunox,4 a partial agonist very similar to aripiprazole, is much more limited, leading to its premature clinical development halt. This suggests that it is difficult to identify the correct range of pharmacology parameters for partial agonism. "
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    ABSTRACT: Species differences in physiology and unique active human metabolites contribute to the limited predictive value of preclinical rodent models for many central nervous system (CNS) drugs. In order to explore possible drivers for this translational disconnect, we developed a computer model of a dopaminergic synapse that simulates the competition among three agents and their binding to pre- and postsynaptic receptors, based on the affinities for their targets and their actual concentrations. The model includes presynaptic autoreceptor effects on neurotransmitter release and modulation by presynaptic firing frequency and is calibrated with actual experimental data on free dopamine levels in the striatum of the rodent and the primate. Using this model, we simulated the postsynaptic dopamine D(2) receptor activation levels of bifeprunox and aripiprazole, two relatively similar dopamine D(2) receptor agonists. The results indicate a substantial difference in dose-response for the two compounds when applying primate calibration parameters as opposed to rodent calibration parameters. In addition, when introducing the major human and rodent metabolites of aripiprazole with their specific pharmacological activities, the model predicts that while bifeprunox would result in a higher postsynaptic D(2) receptor antagonism in the rodent, aripiprazole would result in a higher D(2) receptor antagonism in the primate model. Furthermore, only the highest dose of aripiprazole, but not bifeprunox, reaches postsynaptic functional D(2) receptor antagonism similar to 4 mg haloperidol in the primate model. The model further identifies a limited optimal window of functionality for dopamine D(2) receptor partial agonists. These results suggest that computer modeling of key CNS processes, using well-validated calibration paradigms, can increase the predictive value in the clinical setting of preclinical animal model outcomes.
    Neuropsychiatric Disease and Treatment 09/2010; 6:589-603. DOI:10.2147/NDT.S12460 · 1.74 Impact Factor
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