Olanzapine Versus Placebo and Haloperidol: Quality of Life and Efficacy Results of the North American Double-Blind Trial

Hamilton, S.H.; Revicki, Dennis A.; Genduso, L.A.; Beasley, Charles M.

doi:10.1016/s0893-133x(97)00111-5

Cited by 109 publications

(43 citation statements)

References 28 publications

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“…Olanzapine displayed efficacy in treating negative symptoms in a 24-week extension study, but there was no statistically significant difference between olanzapine and haloperidol in reducing negative symptoms (Hamilton et al 1998). A path-analysis of acute-phase studies found that most of the changes in negative symptoms could not be explained by other compounds (positive symptoms, depression, EPS) .…”

Section: Negative Symptomsmentioning

confidence: 92%

World Federation of Societies of Biological Psychiatry (WFSBP) Guidelines for Biological Treatment of Schizophrenia, Part 2: Long-term treatment of schizophrenia

Falkai

Wobrock

Lieberman

et al. 2006

The World Journal of Biological Psychiatry

201

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These guidelines for the biological treatment of schizophrenia were developed by an international Task Force of the World Federation of Societies of Biological Psychiatry (WFSBP). The goal during the development of these guidelines was to review systematically all available evidence pertaining to the treatment of schizophrenia, and to reach a consensus on a series of practice recommendations that are clinically and scientifically meaningful based on the available evidence. These guidelines are intended for use by all physicians seeing and treating people with schizophrenia. The data used for developing these guidelines have been extracted primarily from various national treatment guidelines and panels for schizophrenia, as well as from meta-analyses, reviews and randomised clinical trials on the efficacy of pharmacological and other biological treatment interventions identified by a search of the MEDLINE database and Cochrane Library. The identified literature was evaluated with respect to the strength of evidence for its efficacy and then categorised into four levels of evidence (A Á/D). This second part of the guidelines covers the long-term treatment as well as the management of relevant side effects. These guidelines are primarily concerned with the biological treatment (including antipsychotic medication, other pharmacological treatment options, electroconvulsive therapy, adjunctive and novel therapeutic strategies) of adults suffering from schizophrenia.Key words: Schizophrenia, long-term treatment, evidence-based medicine, practice guidelines, biological treatment, antipsychotics EXECUTIVE SUMMARY OF RECOMMENDATIONS General recommendationsSpecific treatment strategies are required not only for patients suffering from acute schizophrenia, but also in the stabilisation and stable phase of the disease. The stabilisation period follows the acute phase and constitutes a time-limited transition to continuing treatment in the stable phase. The stable phase represents a prolonged period of treatment and rehabilitation during which symptoms are under adequate control and the focus is on improving functioning and recovery. The goals of long-term therapy have to be discussed with the patient on the background of adequately provided information and his personal goals in order to find common ground to encourage a long-term medication strategy (shared-decision making). In this regard a treatment plan must be formulated and implemented. During the stabilisation phase, the main goals of treatment are to facilitate continued reduction in symptoms, consolidate remission, and promote the process of recovery. The main goals of treatment during the stable phase are to ensure that symptom remission or control is sustained, that the patient is maintaining or improving the level of functioning and quality of life, to prevent relapse, and to ensure that monitoring for adverse treatment effects continues. The antipsychotic pharmacological therapy should be accompanied by psychosocial interventions. A number of psychosocial...

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Section: Negative Symptomsmentioning

confidence: 92%

World Federation of Societies of Biological Psychiatry (WFSBP) Guidelines for Biological Treatment of Schizophrenia, Part 2: Long-term treatment of schizophrenia

Falkai

Wobrock

Lieberman

et al. 2006

The World Journal of Biological Psychiatry

201

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“…The recently developed clozapine-like atypical neuroleptic, olanzapine, is also effective in treating the negative symptoms of schizophrenia (Beasley et al 1996;Hamilton et al 1998) and shares similar neuropharmacological profiles with clozapine, including receptor binding (Bymaster et al 1996a), noradrenaline release in the mPFC (Li et al 1998;Westerink et al 1998) and preferential Fos induction in the mPFC (Robertson and Fibiger 1996;Sebens et al 1998). Previous studies have shown that Fos expression induced by noradrenaline in the frontal cortex is mediated mainly by ␤ -adrenoceptors (Bing et al 1992;Stone and Zhang 1995).…”

Section: The Atypical Neuroleptics Clozapine and Olanzapine Have Sumentioning

confidence: 99%

“…Although clozapine is known to have an affinity for various neurotransmitter receptors, such as noradrenergic, dopaminergic, histaminergic, muscarinic and 5-hydroxytryptamine (5-HT) receptors, the precise neuropharmacological action of clozapine that results in the induction of Fos expression in the mPFC is unknown. Since clozapine administration increases the firing rate of noradrenergic cells in the locus coeruleus (LC) and noradrenaline release from nerve terminals in the mPFC (Ramirez and Wang 1986;Li et al 1998;Westerink et al 1998), it is possible that clozapine-induced noradrenaline release activates cortical neurons in the mPFC.The recently developed clozapine-like atypical neuroleptic, olanzapine, is also effective in treating the negative symptoms of schizophrenia (Beasley et al 1996;Hamilton et al 1998) and shares similar neuropharmacological profiles with clozapine, including receptor binding (Bymaster et al 1996a), noradrenaline release in the mPFC (Li et al 1998;Westerink et al 1998) and preferential Fos induction in the mPFC (Robertson and Fibiger 1996;Sebens et al 1998). Previous studies have shown that Fos expression induced by noradrenaline in the frontal cortex is mediated mainly by ␤ -adrenoceptors (Bing et al 1992;Stone and Zhang 1995).…”

mentioning

confidence: 99%

Clozapine- and Olanzapine-induced Fos Expression in the Rat Medial Prefrontal Cortex is Mediated by β-Adrenoceptors

Ohashi

Hamamura

Lee

et al. 2000

Neuropsychopharmacology

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The atypical neuroleptics, clozapine and olanzapine, have superior therapeutic efficacy against the negative symptoms of schizophrenia, compared with the typical neuroleptics. Recently, it has been suggested that the ability of clozapine and olanzapine to induce Fos expression in the medialClozapine, a prototype atypical antipsychotic compound, is effective not only against the positive, but also against the negative symptoms of schizophrenia (Claghorn et al. 1987;Kane et al. 1988) which are usually resistant to typical neuroleptics. The mechanisms underlying this action, although investigated intensively, remain to be established. Recent studies involving the Fos protein have demonstrated that clozapine induces a much larger increase in the number of neurons that exhibit Fos-like immunoreactivity (LI) in the medial prefrontal cortex (mPFC) than do typical neuroleptics (Deutch and Duman 1996; Fink-Jensen and Kristensen 1994; Fink-Jensen et al. 1995;Guo et al. 1995;Kurokawa et al. 1997;Robertson and Fibiger 1992;Robertson et al. 1994;Wan et al. 1995). This regionally specific clozapine effect sets it apart from typical neuroleptics.Although simple neuronal depolarization or increase in firing rate per se are not enough to induce c-fos in many neurons, other factors such as phenotype of neuronal cell are also required for c-fos expression, Fos protein is thought to be a marker of activated neurons in specified subset of neurons (Sagar et al. 1988; Dragunow and Faull 1989;Grant et al. 1992;Sharp et al. 1993). Therefore, it can be postulate that clozapine may enhance neuronal activity in the mPFC. In connection with the hypothesis that hypofrontality may be responFrom the Department of Neuropsychiatry (KO, TH, YL, HS, SK), Okayama University Medical School, Shikata-cho Okayama, Japan; and Takaoka Hospital (YF), Nishi-imazyuku Himeji, Japan.Address correspondence to: Dr. T. Hamamura, Department of Neuropsychiatry, Okayama University Medical School, 2-5-1 Shikata-cho, Okayama, 700-8558 Japan.Received November 9, 1999; revised February 8, 2000; accepted February 17, 2000. N EUROPSYCHOPHARMACOLOGY 2000 -VOL . 23 , NO . 2 Clozapine-and Olanzapine-induced Fos in mPFC 163 sible for the negative or deficit symptoms of schizophrenia (Weinberger 1988), the preferential induction of Fos-LI in the mPFC is postulated to be one of the mechanisms by which clozapine reduces the negative symptoms of schizophrenia (Robertson et al. 1994). If this is the case, it is important to determine the neuropharmacological mechanisms by which clozapine induces Fos expression in the mPFC. Although clozapine is known to have an affinity for various neurotransmitter receptors, such as noradrenergic, dopaminergic, histaminergic, muscarinic and 5-hydroxytryptamine (5-HT) receptors, the precise neuropharmacological action of clozapine that results in the induction of Fos expression in the mPFC is unknown. Since clozapine administration increases the firing rate of noradrenergic cells in the locus coeruleus (LC) and noradrenaline release from...

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“…The utility of the QLS in assessing change in deficit status has been highlighted in treatment studies (eg Meltzer et al, 1990;Rosenheck et al, 1997;Hamilton et al, 1998). The importance of the QLS in assessing outcome in schizophrenia research has also been highlighted by the observed relation between neurocognitive impairment and psychosocial status (Green, 1996;Buchanan et al, 1994;Medalia et al, 1998;Wykes et al, 1999).…”

Section: Introductionmentioning

confidence: 99%

Development of an Abbreviated Schizophrenia Quality of Life Scale Using a New Method

Bilker

Brensinger

Kurtz

et al. 2002

Neuropsychopharmacol

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The goal of the study was to develop and apply a predictive model approach to reduce the number of items collected for scales that yield a total summary score. A parsimonious subset of items from the 21-item Quality of Life Scale (QLS) that can accurately predict the total scale score was sought and evaluated in 198 patients with schizophrenia, using a statistical modeling approach. Two additional data sets were used for model validation: the subset of 101 patients used in the model construction who had the QLS administered approximately 1 year later and a new sample of 37 patients. Using only seven QLS items as predictors, the correlation was 0.9831 between the predicted and true QLS totals. Applying the model based for these seven QLS items, the correlations from the first and second validation data sets were 0.9791 and 0.9637, respectively. The study demonstrates that a small subset of items of the QLS predicts the entire 21-item scale with high accuracy. Two validation samples have confirmed the finding. This reduces the effort associated with scale administration and is likely to increase the assessment of an important functional domain. Such models can guide efforts for item reduction in other rating instruments.

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Olanzapine Versus Placebo and Haloperidol: Quality of Life and Efficacy Results of the North American Double-Blind Trial

Cited by 109 publications

References 28 publications

World Federation of Societies of Biological Psychiatry (WFSBP) Guidelines for Biological Treatment of Schizophrenia, Part 2: Long-term treatment of schizophrenia

World Federation of Societies of Biological Psychiatry (WFSBP) Guidelines for Biological Treatment of Schizophrenia, Part 2: Long-term treatment of schizophrenia

Clozapine- and Olanzapine-induced Fos Expression in the Rat Medial Prefrontal Cortex is Mediated by β-Adrenoceptors

Development of an Abbreviated Schizophrenia Quality of Life Scale Using a New Method

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