Stahl's Essential Psychopharmacology
Höfundur:
Stephen M. Stahl (Útgáfa: 5)
Kaup valmöguleikar
Long established as the preeminent source in its field, the eagerly anticipated fifth edition of Dr Stahl's essential textbook of psychopharmacology is here! With its use of icons and figures that form Dr Stahl's unique 'visual language', the book is the single most readable source of information on disease and drug mechanisms for all students and mental health professionals seeking to understand and utilize current therapeutics, and to anticipate the future for novel medications.
Every aspect of the book has been updated, with the clarity of explanation that only Dr Stahl can bring. The new edition includes over 500 new or refreshed figures, an intuitive color scheme, fourteen new uses for older drugs and eighteen brand new drugs, coverage of Parkinson's Disease Psychosis, behavioural symptoms of dementia, and mixed features in major depressive episodes, and expanded information on the medical uses of cannabis and hallucinogen assisted psychotherapy.
Nánar um bókina
- Cambridge University Press
- 9781108981217
- 9781108838573
- ePub
- 5
- Stephen M. Stahl
- English
- 2021-07-29
- 10
- 2
- 2
Kaflar
- Cover
- Half title
- Additional material
- Title page
- Imprints page
- Contents
- Preface to the Fifth Edition
- What’s New in the Fifth Edition?
- What Has Not Changed in the Fifth Edition?
- How has the Essential Psychopharmacology family of books and educational services grown?
- Expansion of Essential Psychopharmacology Books
- Online OptionsEssential Psychopharmacology Online
- The NEI Website, www.neiglobal.com
- CME Information
- Release/expiration dates
- Learning objectives
- Accreditation and credit designation statements
- Optional posttests and CME credit instructions
- Peer review
- Disclosures
- Author
- Content Editor
- Editorial Staff
- Peer Reviewers
- Donna M. Wilcock, PhD
- Disclosure of Off-Label Use
- Cultural and Linguistic Competency
- Support
- 1 Chemical Neurotransmission
- Anatomical versus Chemical Basis of Neurotransmission
- General Structure of a Neuron
- Principles of Chemical Neurotransmission
- Neurotransmitters
- Neurotransmission: Classic, Retrograde, and Volume
- Excitation—Secretion Coupling
- Signal Transduction Cascades
- Overview
- Forming a Second Messenger
- Beyond the Second Messenger to Phosphoprotein Messengers
- Beyond the Second Messenger to a Phosphoprotein Cascade Triggering Gene Expression
- How Neurotransmission Triggers Gene Expression
- Molecular Mechanism of Gene Expression
- Epigenetics
- What Are the Molecular Mechanisms of Epigenetics?
- How Epigenetics Maintains or Changes the Status Quo
- A Brief Word about RNA
- Alternative Splicing
- RNA Interference
- Summary
- 2 Transporters, Receptors, and Enzymes as Targets of Psychopharmacological Drug Action
- Neurotransmitter Transporters as Targets of Drug Action
- Classification and Structure
- Monoamine Transporters (SLC6 Gene Family) as Targets of Psychotropic Drugs
- Other Neurotransmitter Transporters (SLC6 and SLC1 Gene Families) as Targets of Psychotropic Drugs
- Where Are the Transporters for Histamine and Neuropeptides?
- Vesicular Transporters: Subtypes and Function
- Vesicular Transporters (SLC18 Gene Family) as Targets of Psychotropic Drugs
- G-Protein-Linked Receptors
- Structure and Function
- G-Protein-Linked Receptors as Targets of Psychotropic Drugs
- No Agonist
- Agonists
- Antagonists
- Partial Agonists
- Light and Dark as an Analogy for Partial Agonists
- Inverse Agonists
- Enzymes as Sites of Psychopharmacological Drug Action
- Cytochrome P450 Drug Metabolizing Enzymes as Targets of Psychotropic Drugs
- Summary
- 3 Ion Channels as Targets of Psychopharmacological Drug Action
- Ligand-Gated Ion Channels as Targets of Psychopharmacological Drug Action
- Ligand-Gated Ion Channels, Ionotropic Receptors, and Ion-Channel-Linked Receptors
- Ligand-Gated Ion Channels: Structure and Function
- Pentameric Subtypes
- Tetrameric Subtypes
- The Agonist Spectrum
- Different States of Ligand-Gated Ion Channels
- Allosteric Modulation: PAMs and NAMs
- Voltage-Sensitive Ion Channels as Targets of Psychopharmacological Drug Action
- Structure and Function
- VSSCs (Voltage-Sensitive Sodium Channels)
- VSCCs (Voltage-Sensitive Calcium Channels)
- Ion Channels and Neurotransmission
- Summary
- 4 Psychosis, Schizophrenia, and the Neurotransmitter Networks Dopamine, Serotonin, and Glutamate
- Symptoms of Psychosis
- The Three Major Hypotheses of Psychosis and Their Neurotransmitter Networks
- The Classic Dopamine Hypothesis of Psychosis and Schizophrenia
- The Dopamine Neurotransmitter Network
- Synthesis and Inactivation of Dopamine in Dopaminergic Neurons
- Dopamine Receptors
- Classic Dopamine Pathways and Key Brain Regions
- Tuberoinfundibular Dopamine Pathway
- Thalamic Dopamine Pathway
- Nigrostriatal Dopamine Pathway
- The Mesolimbic Dopamine Pathway
- The Classic Dopamine Hypothesis of the Positive Symptoms of Psychosis: Mesolimbic HyperDopaminergia
- New Developments in the Dopamine Hypothesis of Positive Symptoms of Psychosis in Schizophrenia
- Corollary to the Classic Dopamine Hypothesis of Schizophrenia: Mesocortical HypoDopaminergia and the Cognitive, Negative, and Affective Symptoms of Schizophrenia
- The Glutamate Hypothesis of Psychosis and Schizophrenia
- The Glutamate Neurotransmitter Network
- Glutamate Synthesis
- Synthesis of Glutamate Cotransmitters Glycine and D-Serine
- Glutamate Receptors
- Key Glutamate Pathways in the Brain
- The NMDA Glutamate Hypofunction Hypothesis of Psychosis: Faulty NMDA Neurotransmission at Glutamate Synapses on GABA Interneurons in Prefrontal Cortex
- Linking the NMDA Glutamate Hypofunction Hypothesis of Psychosis to the Dopamine Hypothesis of Psychosis
- The Serotonin Hypothesis of Psychosis and Schizophrenia
- The Serotonin Neurotransmitter Network
- Serotonin Synthesis and Termination of Action
- 5HT Receptors: Overview
- Presynaptic Receptors: Serotonin Regulating Serotonin
- Presynaptic 5HT1A Receptors
- Presynaptic 5HT2B receptors
- Presynaptic 5HT1B/D Receptors
- Postsynaptic Serotonin Regulates Other Neurotransmitters in Downstream Brain Circuits
- Constructing the 5HT Network
- 5HT1A Receptors
- 5HT1B Receptors
- 5HT2A Receptors
- 5HT2C Receptors
- 5HT3 Receptors
- 5HT6 Receptors
- 5HT7 Receptors
- The Serotonin Hyperfunction Hypothesis of Psychosis
- Linking the Psychosis Hypothesis of Serotonin Hyperfunction at 5HT2A Receptors to the Dopamine Hypothesis of Psychosis
- Summary and Conclusions Regarding Dopamine, NMDA, and Serotonin Neurotransmission in Psychosis
- Schizophrenia as the Prototypical Psychotic Disorder
- Beyond the Positive and Negative Symptoms of Schizophrenia
- What is the Cause of Schizophrenia?
- Genetics and Schizophrenia
- Schizophrenia: Problems with Neurodevelopment, Neurodegeneration, or Both?
- Neurodevelopment and Schizophrenia
- Neurodegeneration and Schizophrenia
- Other Psychotic Illnesses
- Mood-Related Psychosis, Psychotic Depression, Psychotic Mania
- Parkinson’s Disease Psychosis
- Dementia-Related Psychosis
- Summary
- 5 Targeting Dopamine and Serotonin Receptors for Psychosis, Mood, and Beyond: So-Called “Antipsychotics”
- Targeting Mesolimbic/Mesostriatal Dopamine D2 Receptors Causes Antipsychotic Actions
- Targeting Dopamine D2 Receptors in Mesolimbic/Mesostriatal and Mesocortical Pathways Causes Secondary Negative Symptoms
- Secondary Negative Symptoms Due to Targeting Mesolimbic Dopamine D2 Receptors
- Secondary Negative Symptoms Due to Targeting Mesocortical Dopamine D2 Receptors
- Targeting Tuberoinfundibular Dopamine D2 Receptors Causes Elevation of Prolactin
- Targeting Nigrostriatal Dopamine D2 Receptors Causes Motor Side Effects
- Drug-Induced Parkinsonism
- Drug-Induced Acute Dystonia
- Akathisia
- Neuroleptic Malignant Syndrome
- Tardive Dyskinesia
- Pathophysiology
- Treatment
- Drugs Targeting Dopamine D2 Receptors: So-Called First Generation or Conventional “Antipsychotics”
- Drugs Targeting Serotonin 2A Receptors with or without Simultaneously Targeting Dopamine D2 Receptors
- 5HT2A Receptor Regulation of Dopamine Release in Three Downstream Pathways
- How Do 5HT2A Antagonist Actions Reduce Hyperprolactinemia?
- Drugs Targeting Serotonin 1A Receptors and DOPAMINE D2 Receptors as Partial Agonists
- D2 Partial Agonism
- How Does D2 Partial Agonism Cause Fewer Motor Side Effects than D2 Antagonism?
- How Does D2 Partial Agonist Action Reduce Hyperprolactinemia?
- 5HT1A Partial Agonism
- Links between Receptor Binding Properties of Drugs Used to Treat Psychosis and Other Therapeutic Actions and Side Effects
- Mania
- Antidepressant Actions in Bipolar and Unipolar Depression
- Anxiolytic Actions
- Agitation in Dementia
- Sedative Hypnotic and Sedating Actions
- Cardiometabolic Actions
- Pharmacological Properties of Selected Individual First-Generation D2 Antagonists
- Chlorpromazine
- Fluphenazine
- Haloperidol
- Sulpiride
- Amisulpride
- An Overview of the Pharmacological Properties of Individual 5HT2A/D2 Antagonists and D2/5HT1A Partial Agonists: The Pines (Peens), Many Dones and a Rone, Two Pips and a Rip
- The Pines (Peens)
- Clozapine
- Olanzapine
- Quetiapine
- Different Drug at Different Doses?
- Asenapine
- Zotepine
- Many Dones and a Rone
- Risperidone
- Paliperidone
- Ziprasidone
- Iloperidone
- Lurasidone
- Lumateperone
- Two Pips and a Rip
- Aripiprazole
- Brexpiprazole
- Cariprazine
- Selective 5HT2A Antagonist
- Pimavanserin
- The Others
- Sertindole
- Perospirone
- Blonanserin
- Future Treatments for Schizophrenia
- Roluperidone (MIN-101)
- D3 Antagonists
- Trace Amine Receptor Agonists and SEP-363856
- Cholinergic Agonists
- A Few Other Ideas
- Summary
- 6 Mood Disorders and the Neurotransmitter Networks Norepinephrine and γ-Aminobutyric Acid (GABA)
- Description of Mood Disorders
- Mood Spectrum
- Distinguishing Unipolar Depression from Bipolar Depression
- Mixed Features: Are Mood Disorders Progressive?
- Neurobiology of Mood Disorders
- Neurotransmitters
- Norepinephrine
- GABA (γ-Aminobutyric Acid)
- GABAA Receptor Subtypes
- The Monoamine Hypothesis of Depression
- The Monoamine Receptor Hypothesis and Neurotrophic Factors
- Beyond Monoamines: The Neuroplasticity and Neuroprogression Hypothesis of Depression
- Symptoms and Circuits in Mood Disorders
- Symptom-Based Treatment Selections
- Summary
- 7 Treatments for Mood Disorders: So-Called “Antidepressants” and “Mood Stabilizers”
- Definitions of Clinical Effects of Treatment in Depression
- How Well Do Classic Monoamine Reuptake Blockers Work in Unipolar Depression?
- Redefining “Mood Stabilizers”: A Labile Label
- Drugs for Unipolar Depression
- Selective Serotonin Reuptake Inhibitors (SSRIs)
- What the Six SSRIs Have in Common
- Unique Properties of Each SSRI: The Not-So-Selective Serotonin Reuptake Inhibitors
- Fluoxetine: An SSRI with 5HT2C Antagonist Properties
- Sertraline: An SSRI with Dopamine Transporter (DAT) Inhibition and σ1 Binding
- Paroxetine: An SSRI with Muscarinic Anticholinergic and Norepinephrine Transporter (NET) Inhibitory Actions
- Fluvoxamine: An SSRI with σ1 Receptor Binding Properties
- Citalopram: An SSRI with a “Good” and a “Bad” Enantiomer
- Escitalopram: The Quintessential SSRI
- Serotonin Partial Agonist Reuptake Inhibitors (SPARIs)
- Serotonin–Norepinephrine Reuptake Inhibitors (SNRIs)
- NET Inhibition Increases Dopamine in the Prefrontal Cortex
- Venlafaxine
- Desvenlafaxine
- Duloxetine
- Milnacipran
- Levomilnacipran
- Norepinephrine–Dopamine Reuptake Inhibitors (NDRIs): Bupropion
- Agomelatine
- Mirtazapine
- Alpha-2 Antagonist Action
- 5HT3 Antagonist Action
- Serotonin Antagonist/Reuptake Inhibitors (SARIs)
- Different Drug at Different Doses and at Different Delivery Rates?
- Vortioxetine
- SERT Inhibition and 5HT1A Agonism
- SERT Inhibition and 5HT1B/D Presynaptic Antagonism
- 5HT1B Partial Agonism/Antagonism at Heteroreceptors
- SERT Inhibition and 5HT3 Antagonism
- SERT Inhibition and 5HT7 Antagonism
- Neuroactive Steroids
- Treatment Resistance in Unipolar Depression
- Choosing Treatment for Treatment Resistance in Depression on the Basis of Genetic Testing
- Augmenting Strategies for Unipolar Depression
- Serotonin/Dopamine Antagonists/Partial Agonists as Augmenting Agents for Treatment-Resistant Unipolar Depression
- Olanzapine–Fluoxetine Combination
- Quetiapine
- Aripiprazole
- Brexpiprazole
- Cariprazine
- Ketamine
- Esketamine
- Other Drug Combinations for Treatment-Resistant Depression
- Lithium
- Buspirone
- Thyroid Hormones
- Triple-Action Combo: SSRI/SNRI + NDRI
- California Rocket Fuel: SNRI plus Mirtazapine
- Arousal Combos
- Second-Line Monotherapies Used for Treatment-Resistant Depression
- Tricyclic Antidepressants
- Monoamine Oxidase Inhibitors (MAOIs)
- MAO Subtypes
- The Dietary Tyramine Interaction
- Drug–Drug Interactions for MAOIs
- Drugs for Bipolar Disorder Spectrum
- Serotonin/Dopamine Blockers: Not Just for Psychosis and Psychotic Mania
- Putative Pharmacological Mechanism of Serotonin/Dopamine Antagonists/Partial Agonists in Mania
- Serotonin/Dopamine Antagonists/Partial Agonists across the Depression Spectrum: Bipolar Depression, Depression with Mixed Features, and as Adjuncts to SSRIs/SNRIs in Unipolar Major Depression
- Olanzapine–Fluoxetine
- Quetiapine
- Lurasidone
- Cariprazine
- Lithium, the Classic “Antimanic” and “Mood Stabilizer”
- Anticonvulsants as “Mood Stabilizers”
- Anticonvulsants with Proven Efficacy in Bipolar Disorder Valproic Acid (Valproate, Sodium Valproate)
- Carbamazepine
- Lamotrigine
- Anticonvulsants with Uncertain or Doubtful Efficacy in Bipolar Disorder
- Oxcarbazepine/Eslicarbazepine
- Topiramate
- Gabapentin and Pregabalin
- Calcium Channel Blockers (L-Type)
- Riluzole
- Combinations are the Standard for Treating Bipolar Disorder
- Future Treatments for Mood Disorders
- Dextromethorphan–Bupropion and Dextromethorphan–Quinidine
- Dextromethadone
- Hallucinogen-Assisted Psychotherapy
- 3,4-Methylene-dioxymethamphetamine (MDMA)
- Psilocybin
- Summary
- 8 Anxiety, Trauma, and Treatment
- Symptom Dimensions in Anxiety Disorders
- When Is Anxiety an Anxiety Disorder?
- Overlapping Symptoms of Major Depression and Anxiety Disorders
- Overlapping Symptoms of Different Anxiety Disorders
- The Amygdala and the Neurobiology of Fear
- Cortico-Striato-Thalamo-Cortical (CSTC) Loops and the Neurobiology of Worry
- Benzodiazepines as Drugs for Anxiety
- Alpha-2-Delta Ligands as Anxiolytics
- Serotonin and Anxiety
- Noradrenergic Hyperactivity in Anxiety
- Fear Conditioning versus Fear Extinction
- Novel Approaches to the Treatment of Anxiety Disorders
- Fear Extinction
- Therapeutic Facilitation of Fear Extinction
- Blocking Fear Conditioning and Fear Memories
- Treatments for Anxiety Disorder Subtypes
- Generalized Anxiety Disorder
- Panic Disorder
- Social Anxiety Disorder
- PTSD
- Summary
- 9 Chronic Pain and Its Treatment
- What is Pain?
- “Normal” Pain and the Activation of Nociceptive Nerve Fibers
- Nociceptive Pathway to the Spinal Cord
- Nociceptive Pathway from the Spinal Cord to the Brain
- Neuropathic Pain
- Peripheral Mechanisms in Neuropathic Pain
- Central Mechanisms in Neuropathic Pain
- The Spectrum of Mood and Anxiety Disorders with Pain Disorders
- Fibromyalgia
- Decreased Gray Matter in Chronic Pain Syndromes?
- Descending Spinal Synapses in the Dorsal Horn and the Treatment of Chronic Pain
- Targeting Sensitized Circuits in Chronic Pain Conditions
- Targeting Ancillary Symptoms in Fibromyalgia
- Summary
- 10 Disorders of Sleep and Wakefulness and Their Treatment: Neurotransmitter Networks for Histamine and Orexin
- Neurobiology of Sleep and Wakefulness
- The Arousal Spectrum
- Histamine
- Orexins/Hypocretins
- Pathways of Arousal and Sleep for the Sleep/Wake Cycle
- Ultradian Cycles
- Neurotransmitters and the Ultradian Sleep Cycle
- Why Do We Sleep? Can’t I Sleep When I Die?
- Insomnia
- What Is Insomnia?
- Diagnosis and Comorbidities
- Treating Insomnia: Drugs with Hypnotic Actions
- Benzodiazepines (GABAA Positive Allosteric Modulators)
- Z Drugs (GABAA Positive Allosteric Modulators)
- Dual Orexin Receptor Antagonists (DORAs)
- Serotonergic Hypnotics
- Histamine 1 Antagonists as Hypnotics
- Anticonvulsants as Hypnotics
- Hypnotic Actions and Pharmacokinetics: Your Sleep Is at the Mercy of Your Drug Levels!
- Behavioral Treatments of Insomnia
- Excessive Daytime Sleepiness
- What Is Sleepiness?
- Causes of Hypersomnia
- Circadian Rhythm Disorders
- Circadian Treatments
- Melatonergic Hypnotics
- Wake-Promoting Agents and Treatment of Excessive Daytime Sleepiness
- Caffeine
- Amphetamine and Methylphenidate
- Modafinil/Armodafinil
- Mechanism of Action
- Narcolepsy
- Obstructive Sleep Apnea
- Shift Work Disorder
- Solriamfetol, a Wake-Promoting NDRI
- Pitolisant, H3 Presynaptic Antagonist
- Sodium Oxybate and Narcolepsy/Cataplexy
- Summary
- 11 Attention Deficit Hyperactivity Disorder and Its Treatment
- Symptoms and Circuits: ADHD as a Disorder of the Prefrontal Cortex
- ADHD as a Disorder of Inefficient “Tuning” of the Prefrontal Cortex by Dopamine and Norepinephrine
- Neurodevelopment and ADHD
- Treatments for ADHD
- Which Symptoms Should Be Treated First?
- Stimulant Treatment of ADHD
- General Principles
- Methylphenidate
- Amphetamine
- The Mysterious DAT
- Slow-Release Versus Fast-Release Stimulants
- Noradrenergic Treatment of ADHD
- Atomoxetine
- Alpha-2A-Adrenergic Agonists
- Future Treatments for ADHD
- Summary
- 12 Dementia: Causes, Symptomatic Treatments, and the Neurotransmitter Network Acetylcholine
- Dementia: Diagnosis and Causes
- What Is Dementia?
- What Is Mild Cognitive Impairment (MCI)?
- Four Major Causes of Dementia
- Alzheimer Disease (AD)
- Vascular Dementia
- Lewy Body Dementias (LBD)
- Frontotemporal Dementia
- Mixed Dementia
- Pursuit of Disease-Modifying Therapies by Targeting Aß in Alzheimer Disease
- The Amyloid Cascade Hypothesis
- Current Status of the Amyloid Cascade Hypothesis and Treatments Targeting Aß
- Diagnosing Alzheimer Disease Before It Is Too Late
- Presymptomatic Stage 1
- MCI Stage 2
- Dementia Stage 3
- Overview of Symptomatic Treatments for Dementia
- Targeting Acetylcholine for the Symptomatic Treatment of Memory and Cognition in Alzheimer Disease
- Acetylcholine: Synthesis, Metabolism, Receptors, and Pathways
- Symptomatic Treatment of Memory and Cognition in Alzheimer Disease by Inhibiting Acetylcholinesterase
- Donepezil
- Rivastigmine
- Galantamine
- Targeting Glutamate for the Symptomatic Treatment of Memory and Cognition in Alzheimer Disease
- Memantine
- Targeting the Behavioral Symptoms of Dementia
- Defining Agitation and Psychosis in Alzheimer Disease
- Pharmacological Treatment of Psychosis and Agitation in Dementia
- Targeting Serotonin for the Symptomatic Treatment of Dementia-Related Psychosis
- Neuronal Networks of Agitation in Alzheimer Disease
- Targeting Multimodal Neurotransmitters (Norepinephrine, Serotonin, and Dopamine) for the Symptomatic Treatment of Agitation in Alzheimer Disease
- Targeting Glutamate for the Symptomatic Treatment of Agitation in Alzheimer Disease
- Treating Depression in Dementia
- Pseudobulbar Affect (Pathological Laughing and Crying)
- Apathy
- Other Treatments for the Behavioral Symptoms of Dementia
- Summary
- 13 Impulsivity, Compulsivity, and Addiction
- What Are Impulsivity and Compulsivity?
- Neurocircuitry and the Impulsive–Compulsive Disorders
- The Dopamine Theory of Addiction: The Mesolimbic Dopamine Circuit as the Final Common Pathway of Reward
- Substance Addictions
- Stimulants
- Atypical Stimulants
- Treatment of Stimulant Addiction
- Nicotine
- Treatment of Nicotine Addiction
- Alcohol
- Treatment of Alcoholism
- Sedative Hypnotics
- Gamma-Hydroxybutyrate (GHB)
- Opiates or Opioids?
- Endogenous Opioid Neurotransmitter System
- Opioid Addiction
- Treatment of Opioid Addiction
- Cannabis
- Hallucinogens
- Empathogens
- Dissociatives
- Abuse Your Way to Abstinence?
- Drink Your Way to Sobriety
- Inject Your Way to Heroin Abstinence
- Smoke Your Way to Quitting
- “Therapeutic” Dissociation, Hallucinations, and Empathy?
- Ketamine-Assisted Psychotherapy
- Psilocybin-Assisted Psychotherapy
- MDMA-Assisted Psychotherapy
- Behavioral Addictions
- Binge Eating Disorder
- Other Behavioral Addictions
- Obsessive–Compulsive and Related Disorders
- Impulse Control Disorders
- Summary
- Suggested Reading and Selected References
- General References: Specialty Textbooks
- General References:Textbooks in the Stahl’s Essential Psychopharmacology Series
- Chapters 1–3 (Basic Neuroscience): Textbooks
- Chapters 4 (Psychosis, Schizophrenia, and the Neurotransmitter Networks Dopamine, Serotonin, and Glutamate) and 5 (Targeting Dopamine and Serotonin Receptors for Psychosis, Mood, and Beyond: So-called “Antipsychotics”)
- Chapters 6 (Mood Disorders) and 7 (Treatment of Mood Disorders), including Norepinephrine and GABA
- Chapter 8 (Anxiety and Trauma)
- PTSD
- Chapter 9 (Pain)
- Chapter 10 (Sleep/Wake Disorders and Their Treatment Including Histamine and Orexin)
- Chapter 11 (Attention Deficit Hyperactivity Disorder)
- Chapter 12 (Dementia) and Acetylcholine
- Chapter 13 (Impulsivity, Compulsivity, and Addiction)
- Index