2010, English, Book, Illustrated edition: Pharmacotherapy for depression and treatment-resistant depression / George I. Papakostas, Maurizio Fava. Papakostas, George I.

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Pharmacotherapy for depression and treatment-resistant depression / George I. Papakostas, Maurizio Fava
 
Bookmark: https://trove.nla.gov.au/version/50401594
Physical Description
  • xxv, 699 p. : ill. ; 24 cm.
Published
  • Hackensack, NJ : World Scientific, c2010.
Language
  • English

Edition details

Title
  • Pharmacotherapy for depression and treatment-resistant depression /​ George I. Papakostas, Maurizio Fava.
Author
  • Papakostas, George I.
Other Authors
  • Fava, M. (Maurizio)
Published
  • Hackensack, NJ : World Scientific, c2010.
Content Types
  • text
Carrier Types
  • volume
Physical Description
  • xxv, 699 p. : ill. ; 24 cm.
Subjects
Summary
  • This unique and ground-breaking work, authored by renowned Harvard-and Massachusetts General Hospital based researchers G. I. Papakostas and M. Fava, represents the most comprehensive compilation to date of medical studies and reports involving the use of antidepressants for the treatment of major depressive disorder, one of the most prevalent and devastating medical illnesses afflicting mankind. Given the breadth of the scientific literature focusing on the use of antidepressants for major depressive disorder, this work represents an invaluable tool for clinicians as well as scientists in search of a reference manual to help guide them through the field. The book is organized into four parts; each part focusing on a separate theme that will facilitate the reader to precisely access particular information of interest, whether be it clinical or scientific in nature. Each part is then sub-divided into several thematic chapters, which are enriched with tables and figures citing --
  • results from the most influential studies in the field. Finally, clinical and research "pearls" are listed throughout the book in bullet-point fashion to help summarize the available knowledge-base in a user-friendly format. --Book Jacket.
Contents
  • Machine generated contents note: 1.Major Depressive Disorder and Treatment-Resistant Depression
  • 1.1.Major Depressive Disorder
  • 1.1.1.Definition
  • 1.1.2.Prevalence and disease burden
  • 1.2.Treatment-Resistant Depression (TRD)
  • 1.2.1.Definition and staging
  • 1.2.2.Prevalence
  • 1.2.3."Pseudo-resistance"
  • 1.3.Demographic and Clinical Risk Factors for Resistant Depression
  • 1.3.1.Studies focusing on SSRI therapy
  • 1.3.2.Studies focusing on therapy with older antidepressants
  • 1.3.3.Studies focusing on therapy with newer antidepressants
  • Summary and Conclusion of Chapter 1
  • pt. I First-Line Pharmacotherapy Strategies
  • 2.Monoaminergic-Based Strategies: "Single-Acting" Agents
  • 2.1.Monoamine Precursors for Depression
  • 2.2.Selective Serotonin Reuptake Inhibitors (SSRIs)
  • 2.2.1.Neuropharmacology
  • 2.2.2.Efficacy (general)
  • 2.2.3.Efficacy in patients with medical conditions
  • 2.2.3.1.Diabetes mellitus
  • Contents note continued: 2.2.3.2.Coronary artery disease and myocardial infarction
  • 2.2.3.3.Pulmonary and sleep disorders
  • 2.2.3.4.Cerebrovascular illness and stroke
  • 2.2.3.5.Movement disorders
  • 2.2.3.6.Epilepsy
  • 2.2.3.7.Dementia
  • 2.2.3.8.Renal insufficiency
  • 2.2.3.9.Hepatitis, cirrhosis, and interferon therapy
  • 2.2.3.10.Human immunodeficiency virus
  • 2.2.3.11.Malignancy
  • 2.2.3.12.Transplant recipients
  • 2.2.4.Side effect profile
  • 2.2.4.1.General
  • 2.2.4.2.Central nervous system
  • 2.2.4.3.Cardiovascular
  • 2.2.4.4.Hematologic
  • 2.2.4.5.Endocrine
  • 2.2.4.6.Metabolic
  • 2.2.4.7.Immunologic
  • 2.2.4.8.Dermatologic
  • 2.2.4.9.Risk of malignancy
  • 2.2.4.10.Risk of teratogenicity
  • 2.2.4.11.Risk of transmission during breastfeeding
  • 2.2.4.12.Discontinuation syndrome
  • 2.2.5.Dosing
  • 2.2.5.1.Initial and optimal dose
  • 2.2.5.2.Serotonin transporter occupancy as a function of dose
  • 2.2.5.3.Plasma levels and clinical efficacy
  • Contents note continued: 2.2.5.4.Cytochrome enzyme genotype and plasma levels
  • 2.2.5.5.P-glycoprotein interactions
  • 2.2.6.Drug interactions
  • 2.3.Serotonin Receptor Antagonists and Agonists
  • 2.3.1.Trazodone and nefazodone
  • 2.3.1.1.Neuropharmacology
  • 2.3.1.2.Efficacy
  • 2.3.1.3.Side effect profile
  • 2.3.1.4.Dosing
  • 2.3.2.Other 5HT-2 active agents
  • 2.3.2.1.Ritanserin
  • 2.3.2.2.Fenfluramine and dexfenfluramine
  • 2.3.2.3.Agomelatine
  • 2.3.3.5HT-1 active agents
  • 2.3.3.1.Agonists
  • 2.3.3.2.Antagonists
  • 2.3.4.Agents acting on 5HT-3 and 5HT-4
  • 2.4.Serotonin Reuptake Enhancers
  • 2.5.α-2 Adrenergic Receptor Agonists and Antagonists
  • 2.6.Norepinephrine Reuptake Inhibitors (NRIs)
  • 2.6.1.Reboxetine
  • 2.6.2.Atomoxetine
  • 2.6.3.Viloxazine
  • 2.7.Selective β Adrenergic Receptor Agonists
  • 2.8.Dopamine-Selective Agents
  • 2.8.1.Receptor agonists
  • 2.8.2.Reuptake inhibitors
  • 2.8.3.Receptor antagonists
  • Contents note continued: 3.Monoaminergic-Based Strategies: "Dual-Acting" Agents
  • 3.1.Tricyclic Antidepressants (TCAs)
  • 3.1.1.Neuropharmacology
  • 3.1.2.Classification
  • 3.1.3.Efficacy
  • 3.1.4.Side effect profile
  • 3.1.5.Dosing
  • 3.2.Serotonin-Norepinephrine Reuptake Inhibitors (SNRIs)
  • 3.2.1.Venlafaxine
  • 3.2.1.1.Neuropharmacology
  • 3.2.1.2.Efficacy
  • 3.2.1.3.Side effect profile
  • 3.2.1.4.Dosing
  • 3.2.2.Desvenlafaxine
  • 3.2.3.Duloxetine
  • 3.2.3.1.Efficacy
  • 3.2.3.2.Side effect profile
  • 3.2.3.3.Dosing
  • 3.2.4.Milnacipran
  • 3.3.5HT-2 and α-2 Adrenergic Receptor Antagonists
  • 3.3.1.Mirtazapine
  • 3.3.1.1.Neuropharmacology
  • 3.3.1.2.Efficacy
  • 3.3.1.3.Side effect profile
  • 3.3.1.4.Dosing
  • 3.3.2.Mianserin
  • 3.4.Norepinephrine-Dopamine Reuptake Inhibitors
  • 3.4.1.Bupropion
  • 3.4.1.1.Neuropharmacology
  • 3.4.1.2.Efficacy
  • 3.4.1.3.Side effect profile
  • 3.4.1.4.Dosing
  • 3.4.2.Nomifensine
  • Contents note continued: 4.Monoaminergic-Based Strategies: "Triple-Acting" Agents
  • 4.1.Monoamine Oxidase Inhibitors (MAOIs)
  • 4.1.1.Neuropharmacology
  • 4.1.2.Efficacy
  • 4.1.3.Side effect profile
  • 4.1.3.1.Dietary restrictions and drug interactions
  • 4.1.4.Dosing
  • 4.2.Serotonin-Norepinephrine-Dopamine Reuptake Inhibitors
  • 4.3.Catechol-O-Methyltransferase (COMT) Inhibitors
  • 5.Polypharmacy from the Onset of Treatment
  • 5.1.Adjunctive Treatment with Monoaminergic Agents
  • 5.1.1.Tryptophan
  • 5.1.2.Pindolol
  • 5.1.3.Typical antipsychotic agents
  • 5.1.4.5HT2 and α-2 adrenergic receptor antagonists
  • 5.1.5.Other antidepressants
  • 5.1.6.Atypical antipsychotic agents
  • 5.1.7.Dopaminergic agents
  • 5.1.8.Other monoaminergic agents
  • 5.2.Adjunctive Treatment with Neuroendocrine Agents
  • 5.2.1.Thyroid hormones
  • 5.2.2.Estrogen
  • 5.2.3.Other neuroendocrine agents
  • 5.3.Other Agents
  • 5.3.1.Lithium
  • 5.3.2.GABA-ergic agents
  • Contents note continued: 5.3.3.Folates and s-adenosylmethionine (SAMe)
  • 5.3.4.Anticonvulsants
  • 5.3.5.Miscellaneous other agents
  • Summary and Conclusion of Part I
  • pt. II Next-Step Treatment Strategies
  • 6.Polypharmacy Strategies for Treatment-Resistant Depression
  • 6.1.Adjunctive Treatment with Monoaminergic Agents
  • 6.1.1.Pindolol
  • 6.1.2.5HT2 and α-2 adrenergic-receptor antagonists
  • 6.1.3.Tricyclic antidepressants
  • 6.1.4.Selective 5HT1A agonists
  • 6.1.5.Other antidepressants
  • 6.1.6.Atypical antipsychotic agents
  • 6.1.7.Dopaminergic agents
  • 6.1.8.Other monoaminergic agents
  • 6.2.Adjunctive Treatment with Neuroendocrine Agents
  • 6.2.1.Thyroid hormones
  • 6.2.2.Androgens
  • 6.2.3.Estrogens
  • 6.2.4.Steroids and steroid synthesis inhibitors
  • 6.2.5.Melatonin
  • 6.3.Other Agents
  • 6.3.1.Lithium
  • 6.3.2.ω-3 fatty acids
  • 6.3.3.Modafinil
  • 6.3.4.Glutamatergic agents
  • 6.3.5.Anticonvulsants
  • 6.3.6.Inositol
  • Contents note continued: 6.3.7.Folates, s-adenosyl methionine (SAMe) and B-vitamins
  • 6.3.8.Cholinergic agents
  • 6.3.9.Miscellaneous other agents
  • 7.Monotherapy Strategies for Resistant Depression
  • 7.1.Increasing the Dose of Antidepressants
  • 7.2.Switching Antidepressants Due to Lack of Efficacy
  • 7.2.1.Switching from a TCA to an SSRI or MAOI and vice versa
  • 7.2.2.Switching to a TCA or an MAOI following the failure of multiple antidepressants
  • 7.2.3.Switching from one SSRI to another, or to a non-SSRI antidepressant
  • 7.2.4.Other switch strategies
  • 8.Non-pharmacologic Approaches for Resistant Depression
  • 8.1.Device-Based Therapies
  • 8.1.1.Electroconvulsive therapy
  • 8.1.2.Vagus nerve stimulation
  • 8.1.3.Transcranial magnetic stimulation
  • 8.1.4.Deep brain stimulation
  • 8.1.5.Transcranial direct current stimulation (tDCS)
  • 8.1.6.Bright light therapy
  • 8.1.7.Acupuncture
  • 8.2.Psychotherapy
  • 8.3.Exercise
  • 8.4.Yoga and Meditation
  • Contents note continued: Summary and Conclusion of Part II
  • pt. III Maintaining Treatment Gains
  • 9.Pharmacotherapy of Relapse/​Recurrence Prevention and Treatment
  • 9.1.Antidepressant Continuation and Maintenance Therapy Studies
  • 9.1.1.Tricyclic antidepressants (TCAs)
  • 9.1.2.Monoamine oxidase inhibitors (MAOIs)
  • 9.1.3.Selective serotonin reuptake inhibitors (SSRIs)
  • 9.1.4.Newer antidepressants
  • 9.1.5.Summary of continuation and maintenance trials
  • 9.2.Special Topics in the Pharmacotherapy of Relapse Prevention
  • 9.2.1.Long-term efficacy differences among antidepressants
  • 9.2.2.Optimal duration of long-term therapy
  • 9.2.3.Long-term dosing and risk of relapse
  • 9.2.4.Continuing adjunctive agents during long-term therapy
  • 9.2.5.Instituting antidepressants among non-medicated remitters
  • 9.2.6.Timing of symptom improvement and risk of relapse
  • 9.2.7.Treatment-resistance and risk of relapse
  • 9.3.Treatment of Depressive Relapse/​Recurrence
  • Contents note continued: 10.Pharmacologic Strategies to Enhance Antidepressant Tolerability
  • 10.1.Adjunctive Therapy
  • 10.1.1.Sexual dysfunction
  • 10.1.2.Fatigue and hypersomnia
  • 10.1.3.Insomnia, anxiety, and "activation"
  • 10.1.4.Akathisia and bruxism
  • 10.1.5.Gastrointestinal symptoms
  • 10.1.6.Weight gain
  • 10.1.7.Anticholinergic and other side effects
  • 10.1.8.Cognitive side effects
  • 10.2.Switching Antidepressants Due to Intolerance
  • Summary and Conclusion of Part III
  • pt. IV Future Directions in Treatment Development
  • 11.Agents Operating on Non-monoaminergic Neurotransmitter Systems
  • 11.1.GABA-ergic Treatments
  • 11.1.1.Benzodiazepines
  • 11.1.1.1.Clinical evidence
  • 11.1.1.2.Treatment limitations
  • 11.1.1.3.Neuropharmacology of GABA-A receptors
  • 11.1.1.4.Conclusion
  • 11.1.2.Barbiturates
  • 11.1.3.Other GABA-ergic agents
  • 11.2.Glycine and Glutamate-Based Treatments
  • 11.2.1.Neuropharmacology
  • 11.2.2.NMDA-active agents
  • Contents note continued: 11.2.3.Other glutamatergic agents
  • 11.2.4.Glycinergic agents
  • 11.3.Agents with Combined GABA-ergic and Glutamatergic Activity
  • 11.3.1.Anticonvulsants
  • 11.4.Other Anticonvulsants
  • 11.5.Neurokinin-Receptor Antagonists
  • 11.5.1.Neuropharmacology
  • 11.5.2.Clinical evidence
  • 11.6.Nicotinic Receptor-Based Treatments
  • 11.6.1.Neuropharmacology
  • 11.6.2.Nicotinic-receptor agonists
  • 11.6.3.Cholinesterase inhibitors
  • 11.6.4.Nicotinic-receptor antagonists
  • 11.7.Cannabinoids and Endocannabinoids
  • 11.8.Opioidergic Therapies
  • 11.8.1.Opioid-receptor antagonists
  • 11.8.2.Opioid-receptor agonists
  • 11.8.3.Mixed agonists/​antagonists
  • 11.9.Other Neurotransmitter Systems
  • 12.Neuroendocrine-Based Agents
  • 12.1.Hypothalamic-Pituitary-Gonadal Axis (HPG)
  • 12.1.1.Estrogen
  • 12.1.2.Progesterone
  • 12.1.3.Androgens
  • 12.1.4.Dehydroepiandrosterone (DHEA)
  • 12.1.5.Other gonadotropic agents
  • 12.2.Hypothalamic-Pituitary-Adrenal Axis (HPA)
  • Contents note continued: 12.2.1.Corticosteroids
  • 12.2.2.Steroid synthesis inhibitors
  • 12.2.3.Steroid- and CRF-receptor antagonists
  • 12.3.Hypothalamic-Pituitary-Thyroid Axis (HPT)
  • 12.4.Melatonin and Melatonergic Agents
  • 12.5.Other Hormones
  • 13.Metabolic-Based and Other Agents
  • 13.1.Metabolic-Based Agents
  • 13.1.1.Elements of the "one carbon cycle"
  • 13.1.1.1.S-adenosylmethionine (SAMe)
  • 13.1.1.2.Folates and other B-vitamins
  • 13.1.2.Agents acting on neuronal "second messenger" systems
  • 13.1.2.1.Anatomy of the "second messenger" system
  • 13.1.2.2.Phosphodiesterase inhibitors
  • 13.1.2.3.Inositol
  • 13.1.2.4.Other agents
  • 13.1.3.Essential fatty acids
  • 13.1.3.1.Overview
  • 13.1.3.2.Clinical studies
  • 13.1.4.Carnitine
  • 13.1.5.Minerals, trace elements, and vitamins (non-B vitamins)
  • 13.2.Agents with Unknown Mechanism of Action
  • 13.2.1.Herbal remedies
  • 13.2.1.1.Hypericum perforatum
  • 13.2.1.2.Ginseng
  • 13.2.1.3.Kava kava
  • Contents note continued: 13.2.1.4.Valerian root and Ginkgo bilboa
  • 13.2.2.Modafinil
  • 13.2.3.Pivagabine
  • 14.Biological Predictors, Moderators, and Mediators of Efficacy
  • 14.1.Definition and Significance of Mediators of Outcome
  • 14.2.Genetic Markers
  • 14.2.1.Studies involving SSRI therapy
  • 14.2.1.1.Genes coding for TPH and 5HTT
  • 14.2.1.2.Genes coding for 5HT-receptors
  • 14.2.1.3.Genes coding for NET or NE-receptors
  • 14.2.1.4.Genes coding for MAO and COMT
  • 14.2.1.5.Genes coding for other proteins
  • 14.2.2.Studies involving therapy with other antidepressants
  • 14.2.3.Studies comparing antidepressants
  • 14.3.Neurophysiology
  • 14.3.1.Brain functioning and metabolism
  • 14.3.1.1.Positron emission tomography
  • 14.3.1.2.Functional magnetic resonance imaging
  • 14.3.1.3.Magnetic resonance spectroscopy
  • 14.3.2.Electroencephalography
  • 14.3.2.1.Traditional electroencephalography
  • 14.3.2.2.Quantitative electroencephalography
  • Contents note continued: 14.3.2.3.Loudness Dependence of Auditory Evoked Potentials (LDAEP)
  • 14.3.3.Brain functional asymmetry (dichotic listening)
  • 14.4.Molecular Biology
  • 14.4.1.Receptor and transporter kinetics
  • 14.4.2.Intracellular signal transduction
  • 14.4.3.Inflammatory markers
  • Summary and Conclusion of Part IV
  • Appendix A
  • Appendix B
  • Appendix C
  • Appendix D
  • Bibliography
  • Chapter 1
  • Chapter 2
  • Chapter 3
  • Chapter 4
  • Chapter 5
  • Chapter 6
  • Chapter 7
  • Chapter 8
  • Chapter 9
  • Chapter 10
  • Chapter 11
  • Chapter 12
  • Chapter 13
  • Chapter 14.
Notes
  • Formerly CIP.
  • Includes bibliographical references and index.
Language
  • English
ISBN
  • 9789814287586 (hbk.)
  • 981428758X (hbk.)
Dewey Number
  • 616.8527061
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