1;Preface;62;Contents;103;Contributors;144;Part I: Function, Outcome and Treatmentin Schizophrenia;204.1;Assessing Function and Functional Outcome in Schizophrenia;214.1.1;1 Introduction;224.1.1.1;1.1 Functional Dimensions;224.1.1.2;1.2 Recent Reviews and Overviews of Measures of Functioning in Schizophrenia;244.1.2;2 Construct Validity;254.1.2.1;2.1 Functional Outcome as an Experiential Process;264.1.2.2;2.2 Environmental Moderators of the Functional Dimensions;284.1.3;3 Ecological Validity;294.1.3.1;3.1 Verisimilitude and Veridicality;304.1.3.2;3.2 Observation in Naturalistic Environments;324.1.4;4 Conclusion;344.1.5;References;344.2;Antipsychotics and Metabolics in the Post-CATIE Era;404.2.1;1 Introduction;414.2.2;2 Sources of Cardiovascular Risk;434.2.3;3 The Cardiovascular and Metabolic Risk Profile of Subjects Entering the CATIE Schizophrenia Trial;464.2.4;4 The Impact of Antipsychotic Treatment on Cardiovascular and Metabolic Outcomes in the CATIE Schizophrenia Trial;474.2.4.1;4.1 Metabolic Outcomes;474.2.4.2;4.2 Framingham Cardiovascular Risk;484.2.4.3;4.3 Outcomes with Novel Biomarkers;504.2.5;5 The Post-CATIE Era;504.2.5.1;5.1 Clinical Conclusions;504.2.5.2;5.2 Hypotheses on Schizophrenia and Metabolic Risk, and Adiposity-Independent Drug Effects;524.2.6;6 Conclusions;544.2.7;References;544.3;Pharmacological Strategies for Enhancing Cognition in Schizophrenia;604.3.1;1 Introduction;614.3.2;2 Cholinergic Agents;634.3.2.1;2.1 Cholinesterase Inhibitors;644.3.2.2;2.2 Nicotine, Nicotinic Receptor Agonists, and Muscarinic Receptor Agonists;684.3.3;3 Glutamatergic Agents;774.3.3.1;3.1 Glycine Allosteric Modulators;774.3.3.2;3.2 AMPA Receptor Modulators;784.3.3.3;3.3 Phosphodiesterase 5 Inhibitors;834.3.3.4;3.4 NMDA Receptor Antagonists;834.3.4;4 Gamma-Aminobutyric Acid Modulating Agents;844.3.5;5 Dopaminergic Agents;874.3.5.1;5.1 Indirect Dopamine Agonists;884.3.5.2;5.2 Atomoxetine and Amantadine;884.3.5.3;5.3 Selective Dopamine Agonists;934.3.6;6 Modafinil;944.3.7;7 Other Agents;974.3.8;8 Conclusions;1004.3.9;References;1024.4;Treatment Implications of the Schizophrenia Prodrome;1144.4.1;1 Introduction;1154.4.1.1;1.1 Early Identification of Psychotic Illness;1174.4.1.2;1.2 Duration of Untreated Psychosis: Individual and Public Health Concern;1174.4.1.3;1.3 Identifying and Predicting Risk for Psychotic Illnesses;1184.4.1.4;1.4 Review of Treatment Studies in the Psychotic Prodrome;1214.4.1.5;1.5 Nonpharmacologic Interventions;1224.4.1.6;1.6 Psychopharmacologic Interventions;1234.4.1.7;1.7 Pharmacologic Potential for Neuroprotection;1244.4.1.8;1.8 Preliminary Treatment Recommendations;1264.4.1.9;1.9 Ethical Implications;1264.4.1.10;1.10 Development of Clinical Staging Criteria;1284.4.1.11;1.11 Recommended Treatment Guidelines;1294.4.1.12;1.12 General Summary;1324.4.2;References;1324.5;Antipsychotic Drug Development;1394.5.1;1 Introduction;1404.5.2;2 Dopamine D2 Receptors: Antagonism, Inverse Agonism, and Partial Agonism;1414.5.3;3 Dopamine D3 Receptors: Cognition and ``Optimized Antagonism´´ at D3 Versus D2 Receptors;1454.5.4;4 Serotonin 5-HT2A Receptors: Dopamine Brakes;1464.5.5;5 Serotonin 5-HT1A Receptors: Dopamine Accelerators;1464.5.6;6 Serotonin 5-HT2C Receptors;1474.5.7;7 Serotonin 5-HT7 Receptors;1484.5.8;8 Glutamatergic Receptors: NMDA and mGluR;1484.5.9;9 Glycine Agonists;1504.5.10;10 Receptors That Mediate Side Effects;1504.5.11;11 Conclusion;1514.5.12;References;1514.6;Antipsychotic Dosing and Drug Delivery;1564.6.1;1 Background;1574.6.2;2 History;1584.6.3;3 Dopamine Hypothesis;1584.6.4;4 D2 Mechanism of Antipsychotic Medication;1594.6.5;5 Clozapine;1604.6.6;6 Genesis and Interpretation of ``Atypicality´´;1604.6.7;7 Current State of Affairs;1614.6.8;8 Dosing;1614.6.8.1;8.1 Chlorpromazine Equivalents;1614.6.8.2;8.2 Other Contributions (Non-D2) to Efficacy;1644.6.8.2.1;8.2.1 Potential Benefits of Continuous Infusion;1664.6.8.2.2;