Ketamine for Treatment-Resistant Depression: Neurobiology and Applications

Description

Ketamine for Treatment-Resistant Depression: Neurobiology and Applications provides a simple, evidence-based overview for neuropsychiatrists and translational researchers on this medication, its mechanisms of actions, eligibility of patients for treatment, and the preparation and implementation of ketamine clinics. Front Cover Ketamine for Treatment-Resistant Depression Ketamine forTreatment-Resistant Depression: Neurobiology and Applications Copyright Contents Contributors 1 - Ketamine, Clio, and the hippocratic triangle—fragments of the history of ketamine Introduction A note on methodology The origin of the term dissociative anesthesia A note on the history of dissociation From Phencyclidine and ketamine to model psychosis Dumb me, dumb me! Final reflections References 2 - Ketamine's potential mechanism of action for rapid antidepressive effects – a focus on neuroplasticity Background Ketamine restores molecular neuroplastic molecules to induce rapid antidepressant effects Glutamate, glutamine, and γ-aminobutyric acid availability and cycling Enhanced activation of the α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor Increased mechanistic target of rapamycin signaling pathway activation Brain-derived neurotrophic factor VGF Eukaryotic elongation factor 2 p70 ribosomal S6 kinase Glycogen synthase kinase 3 Limitations to mechanistic target of rapamycin involvement in ketamine's mechanism of action Inhibition of MAPK/ErK microRNA expression Divergence of mechanisms for ketamine's rapid effects versus sustained effects Limitations to the molecular neuroplasticity mechanism and recent findings Conclusion References 3 - Treatment resistant depression Defining treatment-resistant depression Staging models Comparing staging models Prevalence Diagnosis and differential diagnosis Etiopathology Treatment strategies Switching antidepressants Combination and adjunctive therapies Atypical antipsychotics Lithium Thyroid hormone (T3) Pindolol Anxiolytics Psychostimulants and stimulantlike drugs Dopaminergic agents Anticonvulsants Anti-inflammatory agents Sex steroids Nicotinic antagonists Muscarinic cholinergic receptor antagonists Opioids Nutraceuticals Neuromodulation Electroconvulsive therapy Magnetic seizure therapy Repetitive transcranial magnetic stimulation Theta burst stimulation Deep brain stimulation Vagus nerve stimulation Trigeminal nerve stimulation Transcranial direct current stimulation Psychotherapy Psychedelics Psilocybin Lysergic acid diethylamide 3,4-Methylenedioxymethamphetamine Ayahuasca N-methyl-d-aspartate receptor antagonists: ketamine and esketamine Conclusion References 4 - Suicide in psychiatric disorders: rates, risk factors, and therapeutics Introduction Suicidal risks in the general population Risk factors Suicidal risks in psychiatric disorders Risk factors for suicidal behavior Therapeutics Challenges for studies of suicide prevention Antidepressants Lithium Anticonvulsants Antipsychotics Anxiolytics and sedatives Ketamine Psychotherapy and other interventions Conclusions References 5 - Overview of ketamine for major depression: efficacy and effectiveness Historical background The antidepressant properties of ketamine: evidence from animal studies Open-label and nonrandomized studies on the antidepressant potential of ketamine Ketamine for suicidality Evidence from randomized controlled trials Role of ketamine in electroconvulsive therapy for depression Possible mechanisms for the rapid antidepressant effects of ketamine Predictors of treatment response to ketamine Limitations and caveats References 6 - How to implement a ketamine clinic Background Administrative approval Initiation of the clinic Patient evaluation The clinical setting for ketamine Treatment protocol Ketamine infusion frequency—acute and maintenance therapies Sustainability of the infusion service Conclusion References 7 - Development of new rapid-action treatments in mood disorders Introduction Molecular targets for rapid-action treatments CLOCK genes Glutamatergic transmission Cholinergic transmission Overview of underdevelopment rapid-action treatments Esketamine Rapastinel Scopolamine Conclusions References Further reading 8 - Closing remarks Introduction State of the art and current challenges Limitations of knowledge Challenges in knowledge translation Conclusion References Index A B C D E F G H I K L M N O P Q R S T V Y Z Back Cover