A Meta-analysis of the Efficacy of Second-Generation Antipsychotics

Davis, John M.; Chen, Nancy; Glick, Ira D.

doi:10.1001/archpsyc.60.6.553

Cited by 911 publications

(567 citation statements)

References 150 publications

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“…The equivalence of olanzapine and amisulpride with regard to positive and negative symptoms has also been demonstrated in another randomized comparison study with 377 acutely psychotic schizophrenic patients, where 2 months after treatment onset no differences in BPRS total or BPRS factor scores, or depressive symptoms (Martin et al, 2002) were evident. A meta-analysis by Davis et al (2003) indicated that olanzapine and amisulpride are both equally superior to conventional antipsychotics regarding PANSS or BPRS total scores (effect sizes, olanzapine,…”

Section: Discussionmentioning

confidence: 99%

Cognitive Improvement in Schizophrenic Patients does not Require a Serotonergic Mechanism: Randomized Controlled Trial of Olanzapine vs Amisulpride

Wagner

Quednow

Westheide

et al. 2004

Neuropsychopharmacol

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Combined serotonin-2A (5-HT 2A ) and dopamine-2 (D 2 ) receptor blockade has been proposed as a candidate mechanism by which second-generation antipsychotics (SGAs) improve both cognition and negative symptoms in schizophrenic patients, in contrast to antipsychotics of the first generation. The SGA amisulpride, however, only binds to D 2 /D 3 receptors, which makes it an interesting tool to test this assumption. In a randomized controlled trial, 52 schizophrenic patients were allocated to treatment with either olanzapine (10-20 mg/day) or amisulpride (400-800 mg/day). A comprehensive neuropsychological test battery and clinical ratings were used to assess participants at inclusion and after 4 and 8 weeks. Cognitive improvements of moderate size were observed, with effect sizes similar to those obtained in previous studies on the cognitive effects of SGAs. Importantly, amisulpride was not inferior to olanzapine for any cognitive domain. Combined 5-HT 2A /D 2 receptor blockade is probably not necessary for cognitive improvement by SGAs.

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Section: Discussionmentioning

confidence: 99%

Cognitive Improvement in Schizophrenic Patients does not Require a Serotonergic Mechanism: Randomized Controlled Trial of Olanzapine vs Amisulpride

Wagner

Quednow

Westheide

et al. 2004

Neuropsychopharmacol

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“…Roughly speaking, clozapine has been found to be almost 0.5 effect size units better than FGAs; and olanzapine, risperidone, and amisulpride about 0.25 effect size units better than FGAs (Davis et al, 2003). For these empirical results to be completely explained by such an artifact, the bias would need to produce approximately a 0.5 effect size unit (which corresponds essentially to a 12-point PANSS total score) difference of SGA vs FGA to explain clozapine's greater efficacy (or one-half that to explain the difference of olanzapine or risperidone vs an FGA (Davis and Chen, 2002)).…”

Section: Interpretation Of Meta-analysis Size Effectsmentioning

confidence: 99%

“…We used a previously published dataset from our metaanalysis of SGAs vs FGAs of 124 RCTs and the methodology has been previously reported in detail (Davis et al, 2003). Our primary outcome was improvement as measured with the Positive and Negative Syndrome Scale (PANSS; Kay et al, 1987).…”

Section: Source Of Datamentioning

confidence: 99%

“…First, we constructed a continuous 5-point semiquantitative scale to measure the degree to which FGAs produce EPS, scored from high to low: ie 5 ¼ high dose of high potency FGAs (high dose is defined as above 12 mg haloperidol, the cutoff point proposed by Geddes et al (2000)); 4 ¼ low dose of high potency FGAs (p12.5 mg haloperidol); 3 ¼ high dose (defined as above 600 mg chlorpromazine equivalents) of low potency FGAs; 2 ¼ low dose of low potency FGAs; or 1 ¼ receiving thioridazine (which has a particularly low incidence of EPS). Second, we also classified the SGAs by their propensity to cause EPS on a four-point semiquantitative scale: ie 4 ¼ amisulpride, risperidone, or remoxipride (which do cause some EPS, although less than FGAs; Marder et al, 1997;Davis et al, 2003;Davis and Chen, 2004); 3 ¼ olanzapine, sertindole, ziprasidone, or aripiprazole; 2 ¼ quetiapine; or 1 ¼ clozapine. The propensity scale was based primarily on the double-blind, randomized registrational studies of FGA or SGA vs placebo.…”

Section: Evaluation Of Three Types Of Moderator Variables As Potentiamentioning

confidence: 99%

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Issues that May Determine the Outcome of Antipsychotic Trials: Industry Sponsorship and Extrapyramidal Side Effect

Davis

Chen

Glick

2007

Neuropsychopharmacol

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This study presents a meta-analysis of the influence of several potentially biasing factors (eg industry support, extrapyramidal side effects) on efficacy of studies comparing second-generation antipsychotic (SGA) with first-generation antipsychotic (FGA) medications. We used the dataset from our previously published meta-analysis of 124 randomized controlled trials (RCTs) comparing SGAs with FGAs, to evaluate whether certain possible biases could influence the actual outcome on the total score of the Positive and Negative Syndrome Scale (PANSS), Brief Psychiatric Rating Scale (BPRS), and Clinical Global Impressions (CGI) scores. Industry sponsorship was determined by contact with authors or publication statement. We calculated whether (1) industry sponsorship, (2) study quality, (3) extrapyramidal symptoms (EPS) properties, or (4) prophylactic antiparkinsonian medications influenced SGA vs FGA efficacy for each drug and averaged overall by two Hedges and Olkin-based meta-analyses. The analysis found that none of the factors was significantly associated with a particular outcome. While industry-sponsored articles may conclude their medication to be more favorable than that of a competitor in an RCT, we found that the observed efficacy was not influenced by sponsorship. Many attribute the finding that SGAs appears to be more efficacious than FGAs to be a result of EPS-decreasing efficacy (or its measurement). We were unable to confirm that the drug's EPS properties or antiparkinsonian management altered actual efficacy.

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“…At a population level several studies have reported an association between increasing antidepressant use and a reduction in suicide rates, though the potential effect of confounders makes it impossible to prove that this is a causal relationship (Henriksson and Isacsson, 2006;Olfson et al, 2003). Antipsychotic drugs have proven efficacy in the acute (Davis et al, 2003) and long-term treatment of schizophrenia (Leucht et al, 2003b) and the treatment of mania (Perlis et al, 2006). There is increasing evidence that specific atypical antipsychotics may have benefit in other phases of bipolar illness Tohen et al, 2005).…”

Section: Avoiding Adverse Effectsmentioning

confidence: 99%

Neurological complications of psychiatric drugs: clinical features and management

Haddad

Dursun

2007

Hum. Psychopharmacol. Clin. Exp.

190

106

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This paper reviews the main neurological complications of psychiatric drugs, in particular antipsychotics and antidepressants. Extrapyramidal syndromes include acute dystonia, parkinsonism, akathisia, tardive dyskinesia and tardive dystonia. Extrapyramidal symptoms (EPS) are less frequent with atypical than with conventional antipsychotics but remain common in clinical practice partly due to lack of screening by health professionals. Neuroleptic malignant syndrome (NMS) consists of severe muscle rigidity, pyrexia, change in conscious level and autonomic disturbance but partial forms also occur. NMS is particularly associated with the initiation and rapid increase in dose of high-potency antipsychotics but it has been reported with all the atypical antipsychotics and rarely with other drugs including antidepressants. Serotonin toxicity comprises altered mental state (agitation, excitement, confusion), neuromuscular hyperactivity (tremor, clonus, myoclonus, hyperreflexia) and autonomic hyperactivity and occurs on a spectrum. Severe cases, termed serotonin syndrome, usually follow the co-prescription of drugs that increase serotonergic transmission by different pathways, for example a monoamine oxidase inhibitor (MAOI) and a selective serotonin reuptake inhibitor (SSRI). Most antipsychotics and antidepressants lower the seizure threshold and can cause seizures; the risk is greater with clozapine than with other atypical antipsychotics and greater with tricyclic antidepressants (TCAs) than with SSRIs. In randomised controlled trials in elderly patients with dementia atypical antipsychotics are associated with a higher risk of stroke and death than placebo. Cohort studies suggest that conventional drugs carry at least the same risk. Cessation of treatment with antipsychotics and antidepressants can lead to a wide range of discontinuation symptoms which include movement disorders and other neurological symptoms. Clinicians need to be familiar with strategies to reduce the risk of these adverse events and to manage them when they arise. Their occurrence needs to be balanced against the benefits of psychiatric drugs in terms of efficacy and improved quality of life in a range of disorders.

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A Meta-analysis of the Efficacy of Second-Generation Antipsychotics

Abstract: Some SGAs are more efficacious than FGAs, and, therefore, SGAs are not a homogeneous group.

Cited by 911 publications

References 150 publications

Cognitive Improvement in Schizophrenic Patients does not Require a Serotonergic Mechanism: Randomized Controlled Trial of Olanzapine vs Amisulpride

Cognitive Improvement in Schizophrenic Patients does not Require a Serotonergic Mechanism: Randomized Controlled Trial of Olanzapine vs Amisulpride

Issues that May Determine the Outcome of Antipsychotic Trials: Industry Sponsorship and Extrapyramidal Side Effect

Neurological complications of psychiatric drugs: clinical features and management

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