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World Federation of Societies of Biological Psychiatry (WFSBP) guidelines for biological treatment of schizophrenia, part 2: Long-term treatment of schizophrenia

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TLDR
These guidelines for the biological treatment of schizophrenia were developed by an international Task Force of the World Federation of Societies of Biological Psychiatry to reach a consensus on a series of practice recommendations that are clinically and scientifically meaningful based on the available evidence.
Abstract
These guide lines for the biological treatment of schizophrenia were developed by an international Task Force of the World Federation of Societies of Biological Psychiatry (WFSBO). 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-D). This first part of the guidelines covers disease definition, classification, epidemiology and course of schizophrenia, as well as the management of the acute phase treatment. 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.

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AGNP Consensus Guidelines for Therapeutic Drug Monitoring in Psychiatry: Update 2011

TL;DR: Following guidelines for TDM in psychiatry will help to improve the outcomes of psychopharmacotherapy of many patients especially in case of pharmacokinetic problems, and one should never forget that TDM is an interdisciplinary task that sometimes requires the respectful discussion of apparently discrepant data.
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A Meta-Analysis of Head-to-Head Comparisons of Second-Generation Antipsychotics in the Treatment of Schizophrenia

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References
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Journal ArticleDOI

Oral olanzapine versus oral haloperidol in the maintenance treatment of schizophrenia and related psychoses

TL;DR: Olanzapine was superior to haloperidol in the maintenance therapy of schizophrenia and related psychoses and experienced less relapse.
Journal Article

Risperidone as an adjunct to clozapine therapy in chronic schizophrenics

TL;DR: In an open 4-week trial involving 12 treatment-resistant schizophrenic patients, the addition of risperidone to clozapine was well tolerated and produced significant reduction of symptoms, suggesting that this may be a useful clinical approach.
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A path-analytical approach to differentiate between direct and indirect drug effects on negative symptoms in schizophrenic patients. A re-evaluation of the North American risperidone study.

TL;DR: The relationship between shift in extrapyramidal symptoms and shift in negative symptoms failed to reach statistical significance; however, there was a clear tendency in the expected direction in both treatment groups.
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A Double‐Blind Study of Lorazepam versus the Combination of Haloperidol and Lorazepam in Managing Agitation

TL;DR: The utility of intramuscular lorazepam (LZ) with the combination of intamuscular haloperidol (HDL) and LZ to control acutely agitated behavior is compared.
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Augmenting antipsychotic treatment with lamotrigine or topiramate in patients with treatment-resistant schizophrenia: a naturalistic case-series outcome study.

TL;DR: Preliminary data support previous evidence that lamotrigine is an effective augmentation agent for clozapine and suggest glutamate hyperfunction in schizophrenia may have a presynaptic basis and that atypicals with low dopamine receptor occupancy may have antagonistic actions on glutamate function which confer additional antipsychotic activity.
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