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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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Q. Wang et al.

Chapter 2
Antiseizure Medications
WeiJing, MeizhenSun, andChaoYan
2.1 Commonly Used Antiseizure Medications
2.1.1 First-Generation Antiseizure Medications (ASMs)
2.1.1.1 Carbamazepine
Drug Characteristics
[Chemical name] 5H-Dibenzo[b,f]azepine-5-formamide
[Chemical structure formula]
W. Jing (*)
Shanxi Bethune Hospital, Shanxi Academy of Medical Sciences, Third Hospital of Shanxi
Medical University, Tongji Shanxi Hospital, Taiyuan, Shanxi, China
M. Sun
Department of Neurology, The First Hospital of Shanxi Medical University,
Taiyuan, Shanxi, China
C. Yan
Nanjing University, School of Life Sciences, Department of Physiology,
Nanjing, Jiangsu, China
Ltd. 2025
X. Wang, L. Zhou (eds.), Pharmacological Treatment of Epileptic Seizures,
https://doi.org/10.1007/978-981-96-8520-2_2
59© The Author(s), under exclusive license to Springer Nature Singapore Pte
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