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- •Preface
- •Acknowledgments
- •Contents
- •Contributors
- •1.4.3.1 Electrical Stimulation Kindling Model
- •1.4.2 Acute Epilepsy Models
- •1.4.2.1 Maximal Electroshock Seizure Model
- •1.4.2.3 Acute Pentylenetetrazol-Induced Seizure Model
- •1.4.2.4 Local Penicillin Model
- •1.4.3 Chronic Epilepsy Models
- •1.4.3.2 Kindling Model
- •1.4.3.3 Optogenetic Kindling Model
- •1.4.4 Poststatus Epilepticus Models
- •1.4.5 Genetic Models
- •1.4.5.1 Rodent Animal Models
- •Absence Seizure Models
- •1.4.5.2 Nonrodent Animal Models
- •Baboon Photosensitive Epilepsy Model
- •1.4.6.1 Posttraumatic Epilepsy Models
- •Fluid Percussion Injury Model
- •Controlled Cortical Impact Model
- •Impact Acceleration Model
- •1.4.6.2 Poststroke Epilepsy Models
- •1.4.6.3 Postinfection Epilepsy Models
- •1.5.1 Voltage-Gated Ion Channel Modulation Mechanism
- •1.5.1.1 Blocking Voltage-Gated Sodium Channels
- •1.5.1.2 Blocking Voltage-Gated Calcium Channels
- •1.5.1.3 Voltage-Gated Potassium Channel Enhancement
- •1.5.2 Blocking Excitatory Neurotransmission
- •1.5.4 Improving Neuronal GABAergic Inhibitory Function
- •1.5.4.3 Carbonic Anhydrase Inhibitors
- •1.5.5 Other Mechanisms
- •1.5.6 Conclusion
- •References
- •2.1 Commonly Used Antiseizure Medications
- •2.1.1 First-Generation Antiseizure Medications (ASMs)
- •2.1.1.1 Carbamazepine
- •Drug Characteristics
- •2.1.1.2 Clonazepam
- •Drug Characteristics
- •Other Studies
- •2.1.1.3 Ethosuximide
- •Drug Characteristics
- •Other Studies
- •2.1.1.4 Phenobarbital
- •Drug Characterization
- •2.1.1.5 Primidone
- •Drug Characteristics
- •2.1.1.6 Valproic Acid
- •Drug Characteristics
- •Mental Illness
- •Migraine Prevention
- •Ischemic Stroke
- •Tumors
- •Others
- •Hepatic Impairment
- •Hyperammonemia (HA)
- •Dyskinesia
- •Others
- •Summary
- •2.1.1.7 Phenytoin Sodium
- •Drug Characteristics
- •Other Research
- •2.1.1.8 Nitrazepam
- •Drug Characteristics
- •Other Studies
- •2.1.2 Second-Generation Antiseizure Drugs
- •2.1.2.1 Lamotrigine
- •General Characteristics
- •Historical Evolution
- •Adverse Effects
- •Cutaneous Adverse Effects
- •Hematological Adverse Effects
- •Cardiovascular Adverse Effects
- •Miscellaneous
- •Fundamental Research
- •2.1.2.2 Levetiracetam
- •Drug Characteristics
- •Preclinical Research
- •2.1.2.3 Topiramate
- •Topiramate-Related Adverse Reactions
- •2.1.2.4 Gabapentin
- •Drug Characteristics
- •Preclinical Research
- •2.1.2.5 Pregabalin
- •Drug Characteristics
- •2.1.2.6 Clobazam
- •Drug Characteristics
- •2.1.2.7 Felbamate
- •Drug Characteristics
- •Evidence-Based Medical Research Regarding Felbamate
- •Other Studies Involving Felbamate
- •2.1.2.8 Vigabatrin
- •Drug Characteristics
- •Historical Evolution
- •Evidence-Based Medical Research
- •Side Effects
- •Basic Research
- •Other Research
- •2.1.2.9 Zonisamide
- •Drug Characteristics
- •2.1.3 Third-Generation Antiseizure Medications
- •2.1.3.1 Lacosamide
- •Medicinal Features
- •Recent Fundamental Research
- •Adverse Effects
- •Serum Concentrations
- •2.1.3.2 Perampanel
- •Other Studies
- •2.1.3.3 Brivaracetam
- •Evidence-Based Medical Research
- •Drug Characteristics
- •Historical Development
- •Evidence-Based Medical Research
- •Basic Research
- •Other Research
- •2.1.3.5 Tiagabine (TGB)
- •Drug Characteristics
- •Historical Development
- •Evidence-Based Medical Research
- •Side Effects
- •Basic Research
- •Other Research
- •2.2 New Antiseizure Medications under Study
- •2.2.1 Cannabidiol
- •2.2.1.1 Drug Characteristics
- •References
- •3.1.4 Discontinue Anti-Seizure Medications
- •3.3.6 Pharmacokinetic Changes
- •3.4.1.1 Physiological Stage
- •3.4.1.2 Hypothalamic-Pituitary-Ovarian Axis
- •3.4.1.3 Menstrual Cycle
- •3.5.1 Introduction
- •3.5.5 Conclusions
- •3.6 Acute Symptomatic Epileptic Seizures
- •3.6.2 Historical Evolution
- •3.6.4 Epidemiological Investigation
- •3.6.5 Clinical Manifestations
- •3.6.6 Predictor
- •3.7.4.2 Serotonin Transferrin
- •3.7.4.3 Night Monitoring
- •3.7.4.4 Others
- •References
- •4.1.1.1 Focal Onset Seizures
- •4.1.1.2 Generalized-Onset Seizures
- •Generalized-Onset Tonic, Clonic, or Atonic Seizures
- •Generalized-Onset Myoclonic Seizures
- •Myoclonic-Atonic Seizures
- •Epileptic Spasms
- •Absence Seizures
- •4.2.3.1 Pretreatment Assessment
- •4.2.3.4 First-Line Anti-seizure Medications
- •4.3.1.2 Epidemiology
- •4.3.1.5 Drug Selection
- •4.3.2.2 Epidemiology
- •4.3.3.1 Epidemiology
- •4.3.3.2 Pathophysiological Mechanism
- •4.3.4.2 Pathologic Typing
- •Historical Evolution
- •Molecular Pathological Characterization
- •4.3.4.4 Pathogenic Mechanisms
- •Glial Cell Dysfunction
- •Extrasynaptic Mechanisms
- •4.3.4.5 Treatment
- •Other Medications
- •4.3.5.1 Epidemiological Information.
- •4.3.5.2 Pathogenesis
- •4.3.5.3 Clinical Manifestations
- •4.3.5.4 Anti-seizure Medications
- •4.3.6.1 Rasmussen Encephalitis
- •4.3.6.2 Anti-GAD65-Associated Epilepsy
- •4.3.6.3 Paraneoplastic Antibody-Associated Epilepsy
- •4.3.7.1 Hypoxic-Ischemic Encephalopathy
- •Pathogenic Mechanisms
- •Treatment
- •4.3.7.2 Metabolic Encephalopathy
- •Hepatic Encephalopathy
- •4.3.7.3 Uremic Encephalopathy
- •Pathogenic Mechanisms
- •Treatment
- •4.3.7.4 Pulmonary Encephalopathy
- •Pathogenic Mechanisms
- •Treatment
- •4.3.7.5 Autoimmune-Related Encephalopathy
- •Hashimoto’s Encephalopathy
- •Pathogenic Mechanisms
- •Treatment
- •Lupus Encephalopathy
- •Pathogenic Mechanisms
- •Treatment
- •4.3.7.6 Toxic Encephalopathy
- •Carbon Monoxide Poisoning
- •Pathogenic Mechanisms
- •Treatment
- •Chronic Alcoholic Encephalopathy
- •Pathogenic Mechanisms
- •Treatment
- •4.3.7.7 Heroin-Induced Spongiform Leukoencephalopathy
- •Pathogenic Mechanisms
- •Treatment
- •4.3.7.8 Radiation Encephalopathy
- •Pathogenic Mechanisms
- •Treatment
- •4.3.8.1 Epidemiology
- •4.3.8.3 Anti-seizure Medication Selection
- •4.4.1.1 Historical Evolution
- •4.4.1.2 Epidemiology
- •4.4.1.5 Treatment
- •4.4.1.6 Prognosis
- •4.4.2.1 Historical Evolution
- •4.4.2.2 Epidemiological Investigation
- •Other Manifestations
- •4.4.2.6 Treatment
- •References

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