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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_5203_Библиотеки_им_академика_М_И_Перельмана.pdf
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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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327

Chapter 3
The Basic Principles andPrecautions
ofDrug Therapy
QunWang, XuefengWang, LiJiang, andHongZhang
3.1 The Basic Principles ofAntiepileptic Drug Selection
Epilepsy is a chronic brain disease. Epidemiological surveys have shown that the
prevalence of epilepsy is 7%, and there are approximately 50 million patients worldwide. Although there are a variety of treatment modalities available, medications are
still the main method for controlling epileptic seizures. To achieve the desired results,
it is important to follow some rules that researchers have summarized in practice.
3.1.1 When toStart Medication
Deciding when to start medication is one of the rst questions that medical professionals need to answer. Considering that epilepsy is not only a chronic brain disease
but also a potentially fatal disease, as epidemiological surveys have shown that the
Q. Wang
Department of Neurology, Beijing Tiantan Hospital, Capital Medical University,
Beijing, China
X. Wang
Department of Neurology, The First Afliated Hospital of Chongqing Medical University,
Chongqing, China
L. Jiang (
Department of Neurology, Children’s Hospital of Chongqing Medical University, National
Clinical Research Center for Child Health and Disorders, Chongqing, China
e-mail: ljiang@hospital.cqmu.edu.cn
H. Zhang
Department of Neurology, Shengjing Hospital of China Medical University, Shenyang, China
Ltd. 2025
X. Wang, L. Zhou (eds.), Pharmacological Treatment of Epileptic Seizures,
https://doi.org/10.1007/978-981-96-8520-2_3
*)
329© The Author(s), under exclusive license to Springer Nature Singapore Pte

330
Q. Wang et al.
mortality rate of patients with epilepsy is 2–3 times that of the general population
[1], experts argue that once the diagnosis of epilepsy is established, treatment needs
to be started. International organizations have three different views on the diagnosis
of epilepsy. In 1981, the International League against Epilepsy and the World Health
Organization suggested that the presence of epilepsy should not be determined until
a second seizure. However, in 2005, the International League against Epilepsy proposed that the rst noninduced seizure is diagnosable as epilepsy; for the diagnosis
of epilepsy in this case, several important conditions have been established, such as
the need to determine whether the epilepsy patient’s brain has a susceptibility to
recurrent seizures. The determination of this susceptibility includes a family history
of epilepsy, a clear epileptoid discharge on the electroencephalogram (EEG), and
the existence of factors that have been proven to cause recurrent seizures, such as
delayed epilepsy after a head injury, epilepsy left over from encephalitis, and lateonset epilepsy caused by cerebrovascular disease [2]. The 2014 criteria required that
the probability of recurrence within 10years be greater than 60% [3]. However, a
large number of studies have suggested that starting treatment after the rst or second episode has no effect on the outcome of the patient’s treatment [4]. Based on
these studies, we argue that (1) when there are ILAE seizure susceptibility preconditions, treatment can be started after the rst seizure, and (2) if the collected data
are not sufcient to support the above preconditions, waiting for the patient to have
a second seizure may be more benecial to the patient. Existing antiepileptic drugs
are mostly for the control of seizures and have no antiepileptic effects; therefore, for
patients who only have one attack for more than six months to several years, the
pros and cons of starting treatment or no treatment should be explained clearly to
the patients and their relatives, and the patients or their families should decide
whether to use drugs. If patients or their families seek the advice of doctors, experts
believe that drug treatment is safer [4, 5].
3.1.2 How toChoose Anti-Seizure Medication
When deciding on treatment, choosing the right medication is a matter to consider.
At present, there are dozens of antiseizure drugs on the market, so there are conditions and a basis for drug selection. Before the advent of evidence-based medicine,
traditional drug therapy advocated drug selection according to the epilepsy seizure
type, but this view has been questioned by evidence-based medical research. A large
number of evidence-based medical research results did not validate this method of
drug selection, so although this method of drug selection is still widely used in clinical practice, drug selection based on the seizure type is declining in popularity. It is
no longer the only condition for the selection of antiepileptic drugs [6–9]. The
experts believe that (1) in addition to special types of seizures, such as absence seizures, there is little difference in the efcacy of different antiepileptic drugs. (2) The
selection of antiepileptic drugs needs to take into consideration the “three elements”
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