Epilepsy is a clinical syndrome caused by highly synchronized abnormal discharge of brain neurons caused by various reasons.

Episodic, transient, repetitive, stereotyped

Sensory, motor, conscious, mental, behavioral, autonomic nervous system dysfunction, or both

Clinically, a patient may suffer from one or several forms of epileptic seizures during each attack or attack process.

Symptomatic epilepsy/secondary epilepsy

Idiopathic epilepsy/primary epilepsy

cryptogenic epilepsy

partial seizure

generalized seizure

partial seizure

generalized seizure

Is it epilepsy?

Which seizure type or epilepsy syndrome

Cause

Degree of damage

quality of life assessment

A complete and detailed medical history

Electroencephalogram [EEG]

neuroimaging tests

Fainting

Pseudo-epileptic seizures (hysterical-like seizures)

narcolepsy

basilar migraine

transient ischemic attack

hypoglycemia

Control attacks and reduce the number of attacks

Long-term treatment without obvious adverse reactions

Maintain/restore their original physiological, psychological and social functional status

Are you taking any medication?

Correct choice of medicine?

Medication usage?

Closely monitor adverse reactions

Use monotherapy whenever possible

Reasonable combination therapy

Principles for adding, subtracting, discontinuing, and changing medications

Traditional definition: Consciousness has not fully recovered between consecutive seizures and relapses frequently, or epileptic seizures last for more than 30 minutes and do not stop on their own.

Current opinion: If a generalized myotonic-clonic seizure lasts for more than 5 minutes, the diagnosis should be considered and emergency treatment with AEDs is required.

status generalized seizure

status partial seizures

Purpose

General measures

Stop the attack as soon as possible

After terminating the attack

Chapter 15 Epilepsy Overview Epilepsy is a clinical syndrome caused by highly synchronized abnormal discharge of brain neurons caused by various reasons. It is characterized by episodic, transient, repetitive and stereotyped nature. The location of abnormally discharged neurons is different and the areas affected by abnormal discharge Differences in scope lead to different seizure patterns in patients, which can manifest as sensory, motor, consciousness, mental, behavioral, autonomic nervous system dysfunction or It’s both. Clinically, each attack or the process of each attack is called a seizure. A patient may have one or several forms of seizures. A type of disease attack. In epilepsy, a group of specific epilepsy phenomena with similar symptoms and signs are collectively called epilepsy. syndrome. 【Epidemiology】 Epilepsy is a common disease of the nervous system. Epidemiological data show that the annual incidence rate of epilepsy is (50-70)/100,000; the prevalence rate is approximately 5%o; the mortality rate is (1.3~3.6)/100,000, which is 2~3 times that of the general population. There are currently more than 9 million patients with epilepsy in our country, and each There are 650,000 to 700,000 new cases of epilepsy every year, and about 30% are refractory epilepsy. There are at least 2 million patients with refractory epilepsy in my country. above. 【Cause】 Epilepsy is not an independent disease, but a group of diseases or syndromes. The causes of epilepsy are very complex. Depending on the etiology, epilepsy Can be divided into three major categories: 1. Symptomatic epilepsy Defined structural damage or dysfunction of the central nervous system Caused by: brain trauma, cerebrovascular disease, brain tumors, central nervous system infection, parasites, genetic metabolic diseases, cortical development disorders, neurological disorders Degenerative diseases of the nervous system, drugs and poisons, etc. 2. Idiopathic epilepsy The cause is unknown, and no structural damage to the brain has been found that could cause epileptic seizures. Injury or functional abnormality may be closely related to genetic factors. It often starts at a certain age and has characteristic clinical and electroencephalographic manifestations. For example: benign childhood epilepsy with central melting area spikes, familial epilepsy, etc. 3. The clinical manifestations of cryptogenic epilepsy suggest symptomatic epilepsy, but existing examination methods cannot A clear cause is found. It accounts for approximately 60% to 70% of all epilepsy diseases. [Factors affecting seizures] 1. Age-idiopathic epilepsy is closely related to age. For example, infantile epilepsy begins within 1 year of age, and childhood absence disease peaks in At 6 to 7 years old, myometrial epilepsy begins around puberty. The common causes of epilepsy are also different in different age groups: perinatal injuries, Congenital diseases and metabolic disorders, etc.: 2 to 12 years old: mostly acute infections, idiopathic epilepsy, perinatal injuries and febrile shock, etc.: 12 to 18 years old Most of them are idiopathic epilepsy, facial trauma, vascular malformation and perinatal injuries; those aged 18 to 35 mostly suffer from facial trauma, brain tumors and idiopathic epilepsy. Diseases: 35 to 65 years old are mostly caused by brain tumors, facial trauma, cerebrovascular diseases and metabolic disorders; after 65 years old are mostly caused by cerebrovascular diseases and brain tumors tumors, complications of Alzheimer’s disease, etc. 2. Genetic factors can affect the susceptibility to epilepsy: for example, more than 40% of siblings of children with absence seizures develop it between the ages of 5 and 16. Abnormal EEG of 3 Hz spike-slow waves, but only 1/4 have absence seizures. The prevalence rate among close relatives of symptomatic epilepsy patients is 15%o, which is higher than the general population. Through the crowd. There are reports of a high consistent rate of absence and generalized ankylosing syndrome in children with monozygotic twins 3. Sleep epilepsy attacks are closely related to the sleep-wake cycle: generalized tonic-convulsive seizures often occur after waking up in the morning; infantile epilepsy attacks 349

350 Chapter 15 Epilepsy Li's syndrome often attacks after waking up and before going to bed; benign childhood epilepsy with central melting area spikes often attacks during sleep. 4. Changes in the internal environment, endocrine disorders, electrolyte imbalance, and metabolic abnormalities, etc. can affect the threshold value of neuron discharge and lead to disease onset. do. For example, a few patients only have epilepsy during menstruation or early pregnancy, which is menstrual epilepsy and pregnancy epilepsy; fatigue, lack of sleep, muscle hunger, and constipation Secrets, drinking, flashing lights, emotional impulses and transient metabolic disorders can all lead to disease attacks 【Pathogenesis】 The pathogenesis of epilepsy is very complex, and its entire mechanism has not yet been fully understood, but some important links in the pathogenesis have been explored. 1. The onset of pathological discharge and abnormal neuron discharge are the electrophysiological basis of epilepsy. Normally, neurons spontaneously generate There is rhythmic electrical activity, but at a lower frequency. The membrane potential of the neuron in the lesion is different from that of the normal neuron. It occurs after each action potential. Paroxysmal depolarization shift (PDS) is present, and high-amplitude and high-frequency spike discharges are produced at the same time. Neuronal heterogeneity Frequent discharge may lead to abnormalities in ion channel proteins and neurotransmitters or modulators due to various causes, resulting in changes in ion channel structure and function. Caused by abnormal movement of ions across membranes. In the pathogenesis of epilepsy, two concepts need to be distinguished for the origin of abnormal neuron discharge: ① Epilepsy focus (lesion): the origin of epilepsy The pathological basis of the operation refers to the abnormal brain tissue morphology or structure that can directly or indirectly lead to pathological discharges or epileptic seizures. CT or MRI usually Lesions can be displayed, and some need to be discovered under a microscope; ② Seizure focus: one or several brightest spots on the EEG Obvious pathological discharge site, which may be caused by local cortical neuron reduction and gliosis due to focus extrusion, local ischemia, etc. Research shows that it is not the pathological focus of epilepsy that directly causes epilepsy, but the causative focus. Caused by a single lesion (such as tumor, vascular malformation, etc.) The causative lesions are mostly located at the edge of the lesion, and the causative lesions caused by extensive epileptic lesions (such as medial sclerosis of the lobe and traumatic phlegm marks, etc.) are often included in the lesion. Within the focus, sometimes in the ipsilateral or contralateral brain area far away from the epileptic focus 2. Spread of pathological discharge. Abnormal high-frequency discharges repeatedly induce peripheral and distant symptoms through synaptic connections and posttetanic facilitation. Neurons fire synchronously, causing continuous propagation of abnormal potentials. When abnormal discharge is limited to a certain area of ​​the cerebral cortex, it manifests as partial Partial seizures; if the abnormal discharge is conducted for a long time in the local feedback loop, it will show a partial seizure status; if the abnormal discharge passes through the electrical The field effect and conduction pathway spread to other areas on the same side or even to one hemisphere, manifesting as a Jackson seizure; if the abnormal discharge not only affects the same side, The lateral hemisphere can also spread to the contralateral cerebral hemisphere at the same time, manifesting as a secondary generalized seizure; if the initial part of the abnormal discharge is in the thalamus and upper When the ascending activation system only extends to the brainstem reticular formation, it manifests as an absence seizure; if the abnormal discharge projects widely to both cerebral cortex When the reticulospinal tract is inhibited, a generalized tonic-burst seizure occurs. 3． The mechanism for the termination of pathological discharges is not yet fully understood. The possible mechanism is the active inhibition of various layers of the brain, that is, epilepsy. During a disease attack, a huge postsynaptic potential is generated within the lesion, which activates a negative feedback mechanism and leaves the cell membrane in a state of excessive depolarization for a long time. state, thereby inhibiting the spread of abnormal discharges, reducing the transmission impulse from epileptic lesions, and promoting the termination of ictal discharges. 【pathology】 The causes of epilepsy are complex, and the pathological changes are also diverse. We usually divide the pathological changes of epilepsy into two categories, namely those that cause epilepsy. The pathological changes caused by epileptic seizures (i.e., the causes of epileptic seizures) and the pathological changes caused by epileptic seizures (i.e., the consequences of epileptic seizures) are important for clarifying the The pathogenesis of the disease and seeking surgical treatment are of great significance Due to medical ethics restrictions, most of the current pathological research on the disease comes from the group of surgically resected lesions in patients with refractory epilepsy. Tissue, among this type of patients, hippocampal sclerosis (HS) is somewhat representative. Hippocampal sclerosis also known as Ammon's horn sclerosis Ammon horn sclerosis (AHS) or mes i al temporal sclerosis (MTS), which can be caused by recurrent epilepsy The result of the seizure may also be the cause of recurrent epilepsy, and is closely related to the success or failure of epilepsy treatment. Visual observation of hippocampal sclerosis The hippocampus is shrunken and hard; histologically, bilateral hippocampal sclerosis lesions are often asymmetrical, and obvious hippocampal sclerosis is often found on one side. There is only mild neuronal loss in the hippocampus on the other side; in addition, structures such as the parahippocampal gyrus, amygdala, and uncus may also be affected. under the mirror Typical manifestations are neuron loss and gliosis, and neuron loss is more obvious in epilepsy vulnerable areas, such as CA 1 area and CA 3 area and door area. Mossy fiber sprouting is another important pathological manifestation in patients with hippocampal sclerosis. granule cell axon

351 Chapter 15 Epilepsy They are mossy fibers, which normally only project to the portal area and CA 3 area. Repeated epileptic seizures trigger the sprouting of mossy fibers and enter the dentate gyrus. The molecular layer (mainly the dendrites of granule cells) and CA 1 area form local abnormal neural circuits, leading to epileptic seizures Abnormalities in the structure of the dentate gyrus can also be found in patients with hippocampal sclerosis. The most common is disperse of dentate granulosa cells. granular cells), which shows that the width of granular cells in the dentate gyrus is significantly wider than that of the normal control, and the boundaries between the granular layer and the molecular layer are blurred. This may be due to The normal migration of granule cells is disrupted by epileptic seizures or as a result of epilepsy-induced neurogenesis. In addition, many scholars reported that Abnormal neurons are found in the hippocampal hilus of patients with epilepsy, accompanied by abnormalities in the cytoskeletal structure. For patients without hippocampal sclerosis, it remains to be seen whether neuropathological changes in the hippocampus such as neuron loss must occur after repeated epileptic seizures. Inconclusive. Some foreign scholars collected household examination specimens from epilepsy patients and found that patients with long-term and recurrent epilepsy do not necessarily have neuronal abnormalities. Lost. With the rapid development of basic disciplines such as molecular biology, the ultrastructural damage to cells and molecular diseases caused by epileptic seizures have The management mechanism will gradually become clear Section 1 Classification of epilepsy The classification of epilepsy is very complex: the classification of epilepsy attacks refers to the classification based on the clinical manifestations and electroencephalogram characteristics of epilepsy attacks; Syndrome classification refers to comprehensive factors such as the etiology, pathogenesis, clinical manifestations, disease evolution, and treatment effects of epilepsy. Classification. The most widely used ones currently are the International League Against Epilepsy (I LAE) 1981 classification of epileptic seizures and the 1989 classification of epilepsy syndromes. (Table 15-1, Table 15-2). Table 15-1 International League Against Epilepsy (I LAE, 1981) classification of epileptic seizures 1. Partial seizures 1.1 Motor seizures: focal motor, rotational, Jackson, postural, articulatory Sensory seizures: special senses (oh, vision, taste, hearing) Somatic sensation (pain, temperature, touch, movement, position sense) dizziness Autonomic attacks (palpitation, polydipsia, feeling of urination, etc.) Psychotic symptomatic episodes: speech impairment, memory impairment, cognitive impairment, emotional changes, delusions, structural hallucinations 1.2 complex partial seizures Disorder of consciousness after a simple partial seizure: starting from a simple partial seizure and followed by disorder of consciousness or spontaneous ADHD Disorder of consciousness from the beginning: including only disorder of consciousness or automatism Partial seizures followed by generalized seizures 1.3 Simple partial seizure followed by generalized seizure complex partial seizures secondary to generalized seizures Simple partial seizures followed by complex partial seizures and then generalized seizures 2. Generalized seizure 2.1 Absence seizures typical absence seizure Atypical absence seizures: one or more components such as transient tonicity, seizures, or autonomic nervous system symptoms tonic seizure 2.2 paroxysmal seizure 2.3 2.4 tonic seizure 2.5 myogenital attack atonic seizure 2.6 3. Unclassifiable seizures

352 Chapter 15 Epilepsy International League Against Epilepsy (I LAE, 1989) Classification of epilepsy and epilepsy syndromes Table 15-2 1. Site-related (focal, localized and partial) epilepsy and Symptomatic or secondary epilepsy and epilepsy syndromes 2.3 epilepsy syndrome No specific cause 1.1 Idiopathic epilepsy (age-related) Early-onset myogenic encephalopathy Benign childhood epilepsy with central-granular spikes Early-onset infantile epileptic encephalopathy with burst suppression (Oh tahara Benign childhood epilepsy with paroxysmal discharges in the occipital lobe syndrome) Other symptomatic generalized epilepsy-specific syndromes primary reading epilepsy symptomatic epilepsy Epilepsy syndrome with special triggering method 1.2 lobe epilepsy Specific epilepsy syndromes in other disease states frontal lobe epilepsy 3. Epilepsy or epilepsy syndrome that cannot be determined to be partial or comprehensive 3.1 Both generalized and partial seizures parietal epilepsy Occipital lobe epilepsy neonatal seizure Severe myocardial epilepsy of infancy Chronic progressive partial epilepsy state in children cryptogenic epilepsy 1.3 Epilepsy with persistent spikes and waves occurring during slow wave sleep Epilepsy is presumed to be symptomatic, but the cause has not yet been found Acquired epileptic aphasia (Landau-Kleffner syndrome 2. Generalized epilepsy and epilepsy syndrome Other unspecified epilepsy 2.1 Idiopathic epilepsy (age-related) Unable to determine generalized or partial epilepsy 3.2 benign familial neonatal panic Including all clinical and EEG cannot be attributed to the whole body or localization benign neonatal shock Cases of generalized ankylosing spondylitis with clear diagnosis, as follows Persistent spike-wave complex epilepsy in slow-wave sleep Cases of multiple sleep attacks cannot be clearly defined as systemic or focal type. Benign infantile myeloid epilepsy childhood absence disease 4. Special syndrome adolescent absence disorder 4.1 Febrile panic and other generalized idiopathic epilepsy Juvenile myeloid epilepsy 4.2 Isolated attack or isolated lean state, induced by special activities Generalized tonic epilepsy on awakening 4.3 Other generalized idiopathic epilepsy Occurs only in episodes of acute metabolic or toxic conditions Epilepsy induced by special activities Cryptogenic and/or symptomatic epilepsy 2.2 West syndrome Lennox-Gas taut syndrome Myometrium Li - ataxia epilepsy myotonic distraction epilepsy In 2001, I LAE proposed new classifications of epileptic seizures and epilepsy syndromes, see Table 15-3 and Table 15-4. Table 15-3 2001 I LAE classification of epileptic seizures 1. Self-limiting seizures 1.2 Partial seizures generalized seizure Attacks with primary sensory symptoms 1.1 Tonic-tonic seizures Episodes with experiential sensory symptoms focal paroxysmal seizure tonic seizure With asymmetric tonic seizures (supplementary motor area seizures) paroxysmal seizure Episodes with classic automatisms typical absence seizure atypical absence seizures Attacks with hyperkinetic automatisms myogenital absence seizure with focal negative myometrium Myocardial seizure with inhibitory motor seizures laughing fit Oculofacial myometrium attack Atonic seizures Hemiplegia attack partial secondary generalized seizures Negative myometrium attack focal epilepsy reflex seizure syndrome atonic seizure 2. Sustained epileptic seizures Pain Li (referring to the baby's pain in Li) 2.1 Generalized status epilepticus Reflex seizures in generalized epilepsy syndrome

354 Chapter 15 Epilepsy 1. Classification of epilepsy The clinical manifestations of epilepsy are rich and diverse, but they all have the following common characteristics: ① Paroxysmal, that is, symptoms occur suddenly, last for a period of time, and then quickly Recovery is rapid, and the intermittent period is normal; ② Transient, that is, the duration of the attack is very short, usually seconds or minutes, except for status epilepticus. Rarely more than half an hour; Repetitive, that is, after the first attack, there will be a second or more attacks at different intervals; ④ Stereotyped Sexuality means that the clinical manifestations of each attack are almost the same. 1. Partial seizure refers to abnormal discharge originating from local neurons in the cerebral hemisphere, including simple partial seizures. There are three types of seizures: partial, complex partial, and partial secondary generalized seizures. The former is localized discharge and unconsciousness disorder, and the latter two discharges expand from a local area. It spreads to both sides of the brain and causes disturbance of consciousness. (1) Simple partial seizure: The attack duration is short, usually no more than 1 minute, and the onset and end of the attack are even. Sudden, unconscious disorder. Can be divided into the following four types: 1) Partial motor seizures: manifested by involuntary twitching of a certain part of the body, mostly seen on one side of the eye, face, mouth, hands or toes, and also It can affect one side of the face or limbs, and the lesions are mostly in the precentral gyrus and nearby areas. The following attack forms are common: ①Jackson attack: abnormal movement The movement starts from the local area and moves along the motor area of ​​the cerebral cortex. The clinical manifestations are extracted from the fingers, wrist, forearm, elbow, shoulder, mouth corner, and face one by one. It develops gradually and is called Jackson's attack; patients with severe partial motor seizures may have short-lived seizures (eliminating within half an hour to 36 hours). Limb paralysis is called Todd's palsy. ② Rotational seizure: manifested by the sudden deviation of the eyes to one side, followed by the involuntary rotation of the head in the same direction. It is accompanied by body torsion, but rarely exceeds 180°. Excessive rotation in some patients can cause falls and secondary generalized seizures. ③ Posture Seizure: manifested by abduction of the upper limb on the side of the seizure, flexion of the elbow, twisting the head to the same side, and staring at the same side. ④ Articulatory seizures: table The present condition is involuntary repetition of the single sounds or words before the attack, and occasionally there may be language suppression. 2) Partial sensory seizures: Somatosensory seizures often present with numbness and pins and needles on one side of the limb, mostly in the corners of the mouth, tongue, and hands. Fingers or toes, the lesions are mostly in the central postcentral somatosensory area: special sensory attacks can be manifested as visual (such as flashes of light or black light, etc.), auditory Sex, sensation and taste; dizziness attacks are manifested by falling, floating or horizontal/vertical movement sensations, etc. 3) Autonomic attack: Pallor, flushing of face and body, excessive sweating, piloerection, mydriasis, vomiting, abdominal pain, bowel sounds, polydipsia and Feeling of need to urinate, etc. The lesions are mostly located in the insula, thalamus and surrounding areas (limbic system), and can easily spread and cause disturbance of consciousness, leading to complex partial seizures. a part of. 4) Psychotic attacks: can manifest as various types of memory disorders (such as déjà vu, unfamiliarity, obsessive thinking, rapid recall of the past) things, emotional disorders (nameless fear, depression, euphoria, anger), delusions (visual objects become larger or smaller, sounds become stronger or weaker), complex hallucinations Jue et al. The lesions are located in the limbic system. Although psychotic attacks can occur alone, they are often the precursor to complex partial attacks and can also develop into generalized attacks. Ankylosing - attacks of stranguria. (2) Complex partial seizure (CP S): accounting for more than 50% of adult epileptic seizures, also known as psychiatric seizures In dynamic seizures, the lesions are mostly in the granular lobe, so it is also called granular lobe epilepsy. It can also be found in the frontal lobe, cortex and other parts of the body. Due to origin, diffusion pathways and Different speeds lead to large differences in clinical manifestations, which are mainly divided into the following types 1) Only disorder of consciousness: Generally, it manifests as blurred consciousness. Loss of consciousness is less common. Because the attack may be psychotic or mental Sensory components are present, and disturbances of consciousness are often masked and appear similar to absence. Adult "absences" are almost without exception complex partial seizures However, attention should be paid to identifying absence seizures in children 2) Manifested as disturbance of consciousness and automatism: Classic complex partial seizures can start with an aura, which is the onset of consciousness during a sick attack. The patient retains consciousness before the loss. Abnormal sensations in the upper abdomen are the most common. Emotions (fear) and cognition (déjà vu) may also occur. Consciousness) and sensory (hallucinations) symptoms, followed by confusion, freezing, and cessation of movement. Attacks usually last 1 to 3 minutes. Automatism refers to a condition with certain coordination and confusion that occurs during or after an epileptic attack. Adaptive unconscious activities. Automatism occurs on the basis of disturbance of consciousness and is accompanied by amnesia. Automatism can manifest itself as repeated mouth licking, Mouth, chewing, chewing, teething or swallowing (oral or gastrointestinal automatism); or repeatedly rubbing hands, picking noodles, constantly dressing, undressing, unbuttoning, and groping for clothes. Syndrome (hand-foot automatism); it may also manifest as wandering, running, opening and closing doors without purpose, riding in cars, or getting on boats; it may also manifest as talking to oneself, shouting, Singing (verbal automatism) or mechanically repeating original actions. Automatism is not unique to complex partial seizures and may occur in other seizures (such as amnesia).

355 Chapter 15 Epilepsy Seizures) or postictal disturbances of consciousness may also occur. The mechanism for the emergence of automatism may be that the advanced control function is released and the original automatic Release of behavior. The severity and duration of the disorder of consciousness and the relative integrity of lower-level brain functions meet the conditions for the emergence of automatic behavior. Complex partial seizure automatism is most common in bed. 3) Manifested as disturbance of consciousness and motor symptoms: Complex partial seizures can manifest as disturbance of consciousness and various motor symptoms from the beginning. Symptoms, especially occurring during sleep, may be related to the rapid spread of discharge. Motor symptoms may be focal or asymmetrical rigidity, bursts, and variations Sexual muscle tension movements, various special postures (such as fencing-like movements), etc., can also be a combination of different motor symptoms or appear one after another, and are related to discharge. It is related to the source location and the area affected by the diffusion process. (3) Partial seizures followed by generalized seizures: Simple partial seizures can develop into complex partial seizures. Simple or complex partial seizures Seizures can be generalized into generalized tonic seizures. 2. Generalized seizure. The initial symptomatology and electroencephalogram suggest that the seizure originates from both sides of the brain. Loss of consciousness early in the attack (1) Generalized tonic-clonic seizure (GTC S): loss of consciousness, bilateral tonic seizure followed by seizures This is the main clinical feature of this type of attack. It can evolve from partial seizures, or it can manifest as generalized tonic-flare attacks at the beginning of the disease. do. Loss of consciousness and falls occur early, and subsequent attacks are divided into three phases: 1) Tonic phase: It manifests as continuous contraction of skeletal muscles throughout the body. Eye muscle contraction causes pulling of the eyes, upward turning of the eyeballs, or staring: contraction of the masticatory muscles The mouth shrinks and opens, and then closes violently, which can bite the tip of the tongue; the laryngeal and respiratory muscles contract tonicly, causing the patient to scream and stop breathing; neck The tonic contraction of the neck and trunk muscles causes the neck and trunk to flex first and then to expand; the upper limbs rotate from being lifted up and then rotated to adducted and pronated, and the lower limbs first flex and then expand. Straighten violently and continue for 10 to 20 seconds before entering the formation phase. 2) The burst phase: the muscles alternately contract and relax, twitching alternately, the burst frequency gradually slows down, and the relaxation time gradually slows down. Extended, this period can last 30 to 60 seconds or longer. After a violent burst, the attack stopped and entered the late stage of the attack. Both the above two issues can be issued Life bites, accompanied by respiratory arrest, increased blood pressure, increased heart rate, dilated pupils, loss of light reflex, and increased saliva and other secretions Bab in ski sign can be positive. 3) Late stage of the attack: There are still short bursts in this stage, mainly on the facial muscles and masseter muscles, resulting in trismus and bite injuries. Whole body in this issue Urinary incontinence can occur when the muscles relax, the sphincter relaxes, and urine flows out on its own. Breathing recovered first, and then pupils, blood pressure, and heart rate gradually returned to normal. Muscle tone relaxes and consciousness gradually returns. It takes about 5 to 15 minutes from onset to recovery of consciousness. After waking up, patients often feel headache, body aches, Drowsiness, and some patients are confused. At this time, forcibly restraining the patient may cause injury or self-injury. Typical EEG changes of GTC S are, tonic The phase begins with a gradually increasing spike-wave rhythm of 10 beats/second, and then the frequency continues to decrease and the amplitude continues to increase. During the phase of the queuing phase, diffuse slow waves are accompanied by intermittent Intermittent spike waves show obvious EEG suppression in the later stages of the epidemic. The longer the onset time, the more obvious the suppression. (2) Tonic seizure: more common in children with diffuse brain damage, with more seizures during sleep. manifested as ankylosing The tonic contraction of skeletal muscles throughout the body is similar to the tonic phase in paroxysmal seizures, often accompanied by obvious autonomic nervous system symptoms, such as pale complexion, etc. You may fall violently while standing during an attack. The attack lasts from a few seconds to tens of seconds. The typical ictal EEG is fulminant polyspike. (3) Clonic seizure: almost all occur in infants and young children, characterized by repeated clonic tics accompanied by loss of consciousness. No ankylosing phase. Tics that are bilaterally symmetrical or dominated by one limb, with variable amplitude, frequency and distribution, are characteristic of infantile seizures and last for 1 minute. to several minutes. E EG lacks specificity, and fast activity, slow waves, and irregular spike-slow waves can be seen. (4) Absence seizure: divided into typical and atypical absence seizures, clinical manifestations, EEG background activity and seizure period Changes and prognosis are quite different. 1) Typical absence seizures: onset in childhood and stop before puberty. The characteristic manifestation is sudden and brief (5 to 10 seconds) consciousness. Loss and interruption of ongoing actions, eyes staring blankly, and responding to calls, which may be accompanied by simple automatic actions, such as wiping the nose, chewing, swallowing, etc. Or it may be accompanied by loss of tone, such as falling something in the hand or having a slight seizure. Generally, there will be no fall. There is no memory of the attack afterwards. The attack may occur several to several times a day. A hundred times. You wake up immediately after the attack, without obvious discomfort, and can continue your previous activities. Can't recall after waking up. During the attack, EEG was bilaterally symmetrical at 3 Hz. Spinal-slow complex wave (Figure 15-1. G 2) Atypical absences: The onset and termination of absences are slower than typical absences. In addition to loss of consciousness, they are often accompanied by decreased muscle tone and occasionally muscle contractions. E EG shows slower (2.0-2.5 Hz) irregular spike-slow waves or sharp-slow waves, and abnormal background activity. More common in patients with diffuse brain damage

356 Chapter 15 Epilepsy S mw::7~ ? AM?? Figure 15-1 EEG manifestations of typical absence seizures During the attack, each EEG lead showed bilaterally symmetrical 3 Hz spike-slow complex waves. In children, the prognosis is poor. (5) Myo cl onic seizure: manifests as rapid, brief, electric shock-like muscle contractions, which can occur throughout the body or be limited to It often occurs in a certain muscle group or a certain limb and can be induced by stimulation such as sound and light. It can occur at any age and is common in idiopathic diseases with a good prognosis. Patients with epilepsy, such as benign myocardial epilepsy in infants; also seen in rare hereditary neurodegenerative diseases and diffuse brain damage. attack period Typical EEG changes are spiny-slow waves. (6) A tonic seizure: caused by loss of postural tone. Sudden loss of muscle tone in part or the whole body causes drooping Neck (nodding), mouth opening, limb drooping (falling while holding an object) or loss of tension, falling or falling to pieces, lasting from a few seconds to 1 minute, if the duration is shorter The disturbance of consciousness may not be obvious, and the person wakes up and stands up immediately after the attack. E EG shows polyspiny-slow wave or low potential activity In 2001, I LAE proposed several new clinically proven types of epilepsy attacks: 1. Giotic epilepsy. In 1971, Gascon and Lom Bros. proposed the diagnostic criteria for giggly epilepsy: unprovoked, stereotyped, Recurrent episodes of giggles are often accompanied by other symptoms of epilepsy. There are disease-like discharges of EEG during and between ictal periods. No other disease can explain this. Paroxysmal giggles. Laughter is the main feature of this type of attack. Crying can also be the main clinical manifestation. Drug resistance can also occur, such as combined attacks. Treatment may be effective 2. Persistent aura, I LAE regards persistent aura as a subtype of epilepsy in the new epilepsy classification, and also regards it as partial sensory Synonyms for epilepsy. From a clinical point of view, it can be divided into 4 subtypes: somatosensory (such as dysesthesia affecting the trunk, head and limbs) etc.); special senses (such as vision, hearing, hearing, balance and taste); obvious persistent aura of autonomic nervous system symptoms; manifested as psychosis persistent symptoms. 2. Classification of epilepsy or epilepsy syndrome An epileptic seizure refers to the entire process of a seizure, while epilepsy or epilepsy syndrome is a general term for a group of diseases or syndromes. 1. Site-related epilepsy (1) Age-related idiopathic epilepsy 1) Benign childhood epilepsy with centro temporal spike: 3~13 The disease starts at the age of 9 and peaks at 9 to 10 years old. It is more common in boys and some patients have genetic predispositions. The attack is characterized by brief movements of one side of the face or mouth.

357 Chapter 15 Epilepsy Dynamic attacks are often accompanied by somatosensory symptoms, often occur at night, and the attacks tend to generalize. The frequency of attacks is sparse, once a month or several months, and rarely short-lived. Those who have frequent attacks during the period. E EG manifests itself as high-amplitude spike-slow waves in the central-grain area on the basis of normal background activity. Often activated by sleep, with expansion A tendency to wander or wander (move from one side to another). Treatment with carbamazepine or sodium valproate is effective, but it is currently believed that carbamazepine may induce cerebral The electrogram shows epileptic electrical status during sleep (ESE S phenomenon), which is not conducive to the recovery of the patient's brain electricity. Most patients recover spontaneously during adolescence 2) Benign childhood epilepsy with occipital paroxysms: age of onset From 1 to 14 years old, the attack begins with visual symptoms and vomiting, followed by eye muscle spasms and hemilateral spasms, and may also be combined with generalized ankylosing and convulsions. Seizures and automatisms. E EG shows paroxysmal high-amplitude spikes-slow waves or sharp waves in one or both sides of the occipital region, which appear in a repetitive rhythmic pattern and only appear when the eyes are closed. See you sometimes. Carbamazepine or sodium valproate can be used for treatment. 3) Primary reading epilepsy: induced by reading, without spontaneous seizures, with clinical manifestations of mandibular pulling during reading, often accompanied by hand movements. Cancer of the arm, if you continue reading, you will have a generalized tonic-convulsive attack. (2) Symptomatic epilepsy 1) Temporal lobe epilepsy: manifests as simple partial seizures, complex partial seizures, and secondary generalized seizures or a combination of these seizure patterns. It often starts in childhood or adolescence, 40% have a history of febrile shock, and some patients have a positive family history. According to the The origin of seizures can be divided into hippocampal-amygdala seizures and lateral granular lobe seizures. Seizure types that are highly suggestive of lobar epilepsy include: manifestations of autonomic nervous system and/or simple partial attacks of psychiatric symptoms, sensory, auditory (including delusions) symptoms (such as rising gas in the upper abdomen); in the digestive system Systemic automatisms are complex partial seizures with prominent manifestations, such as swallowing, hearing at the mouth, etc. Typical seizure duration is longer than 1 minute, and seizures occur frequently Goto Taki, unable to recall afterwards, gradually recovered. E EG is common in unilateral or bilateral leaflet spikes, and may also be caused by other abnormalities (including non-flavonoid anomalies). Normal) or no abnormality. 2) Frontal lobe epilepsy: It can occur at any age and manifests as simple or complex partial seizures, often with secondary seizures. Generalized sexual seizures. The seizures are short in duration and stereotyped in form, usually manifesting as tonic or postural seizures and complex automatisms in both lower limbs. Status epilepticus is prone to occur. It may occur only during sleep at night. During the ictal phase, EEG manifests as fulminant fast rhythm, slow rhythm, and fulminant spike, sharp wave, or spike-slow complex 3) Parietal lobe epilepsy: It can occur at any age. Often begins with a simple partial sensory attack, followed by Have a generalized seizure. Visual hallucinations or self-cognitive impairment (such as hemi-neglect) are rare. Ictal EEG appears to be localized or widespread Spike wave. 4) Occipital lobe epilepsy: Mainly characterized by simple partial seizures accompanied by visual symptoms, which may or may not continue. Generalized seizures. Often accompanied by migraines. A basic visual attack may be a brief flash of vision that may be negative. Visual symptoms (blind spots, black images) can also be positive visual symptoms (flashes, phosphenes), or can also manifest as illusions (optical illusions, visual disturbances in the size of objects). changes) and complex visual hallucinations (colorful and complex scenes) 5) Chronic progressive partial persistent epilepsy in children (Ko jew niko w syndrome): It can occur at any age and usually manifests It is a simple motor partial seizure with a fixed location, and in the later stage, a muscle complex on the same side as the seizure appears. E EG background activity is normal, with localized pattern abnormality (spike or slow wave). The cause can often be found, including tumors, mitochondrial encephalomyopathy, and vascular disease, unless the cause of the disease has progressed. In addition, epilepsy syndromes themselves are generally not progressive. 6) Epilepsy syndromes with special precipitating methods: Precipitated seizures refer to epilepsy that is precipitated by environmental or intrinsic factors that are always present before the seizure. Seizures can be triggered by non-specific factors (insomnia, alcohol withdrawal, or hyperventilation) or by special sensations or perceptions (reflex epilepsy), which can occur suddenly Call triggering (startle epilepsy) (3) Cryptogenetic: From the types of epileptic seizures, clinical characteristics, and common locations, it is inferred that it is secondary epilepsy, but the cause is unknown. 2. Generalized epilepsy and epilepsy syndrome (1) Age-related idiopathic epilepsy 1) Benign neonatal familial convulsions: autosomal dominant inheritance. 2~ after birth Onset occurs within 3 days, manifesting as seizures or apnea, with no characteristic changes in E and EG. About 14% of patients will later develop epilepsy. 2) Benign neonatal convulsions: onset around 5 days after birth, manifested by frequent and short bursts of convulsions Or apnea attack, E EG has sharp waves and 8 waves appearing alternately. The attacks do not recur, and psychomotor development is not affected.

358 Chapter 15 Epilepsy 3) Benign myocl onic epilepsy in infancy: Onset between 1 and 2 years old, mostly in males, characterized by shortness of breath Temporary outbreak of generalized myocardial infarction, E EG can show paroxysmal spike-slow complex waves 4) Childhood absence epilepsy: The peak incidence is between 6 and 7 years old. It is more common in girls and has an obvious genetic tendency. Spike-slow wave, normal background activity, hyperventilation can easily induce pathological discharges or even attacks. Sodium valproate and lamotrigine have good therapeutic effects and prognosis Good condition, most acne heals, a few cases develop GTC S after puberty, but a few still have absence seizures. 5) Juvenile absence epilepsy (juvenile absence epilepsy): onset in adolescence, no difference between men and women, the frequency of seizures is less than that of childhood epilepsy In epilepsy, more than 80% of patients experience generalized tonic-convulsive seizures. E EG shows extensive spike-slow complex, and the prognosis is good. 6) Juvenile myocardial epilepsy: It usually occurs between the ages of 8 and 18 and manifests as twitching of the limbs. They are often combined with generalized tonic-convulsive seizures and absence seizures, often photosensitivity, and respond well to antiepileptic drugs, but they often relapse after drug withdrawal. 7) Epilepsy with generalized tonic-cl onic seizure on awakening: common in 10-20 years old, onset in the morning when waking up in the morning or when resting in the evening, manifesting as generalized tonic-tonic seizures, which may be accompanied by absence or myotonic seizures (2) Cryptogeni cor symptomatic: It is speculated that it is symptomatic, but the medical history and existing detection methods have not confirmed it. The cause can be discovered. 1) West syndrome: also known as baby syndrome, onset within 1 year after birth, with a peak incidence between 7 months and 7 months, and is more common in boys. Muscle Lee Sexual seizures, mental retardation and EEG hyperarrhythmia (hyps arrhythmia) are the characteristic triad of this disease and are typical manifestations of myocardial seizures. There is rapid nodding pain, the upper limbs are abducted, the lower limbs and trunk are flexed, and the lower limbs may sometimes be straightened. Symptoms are common and the prognosis is generally poor. morning Periodic use of ACT H or corticosteroids is more effective. Before the age of 5, 60% to 70% of seizures stop, and 40% transform into other types of seizures such as Lennox-Gas taut syndrome or tonic seizures 2) Lennox-Gas taut syndrome: It usually occurs between the ages of 1 and 8, and a few appear in adolescence. Tonic seizures, atonic seizures, myotonic seizures Various seizure types such as seizures, atypical absence seizures, and generalized tonic-convulsive seizures coexist, and mental development is retarded. EEG shows spinous-slow relapse. Multiple waves (1 to 2.5 Hz) and a fast rhythm of 10 Hz during sleep are the three major characteristics of this syndrome, and status epilepticus is prone to occur. Treatment optional The prognosis of most children with sodium valproate, promethazine, and lamotrigine is poor 3) Myo cl onic-a static seizures (epilepsy with myo cl onic-a static seizures) is also called myo cl onic-a static seizures: Onset occurs between the ages of 2 and 5, with more boys than girls. The first attack is mostly generalized tonic-convergent seizures. After several months, myotonic seizures and absences occur. Attacks and falls several times a day, lasting 1 to 3 years. E EG manifests as a slow wave rhythm of 4 to 7 Hz in the early stage, and later becomes regular or irregular. Regular bilateral synchronous 2 to 3 Hz spike-slow complexes and/or polyspiny-slow complexes, with uncertain course and prognosis. 4) Epilepsy with myo cl onic absences (epilepsy with myo cl onic absences): onset around 7 years old, more common in boys, characteristics Sexual manifestations include absence of consciousness accompanied by severe bilateral rhythmic beating. E EG shows bilateral synchronous, symmetrical, rhythmic 3 Hz spine-slow complexes Waves are similar to absence seizures, but the treatment effect is poor and there is mental retardation. (3) Symptomatic or secondary 1) No specific cause: ① Early myocl onic encephalopathy: onset before 3 months after birth In the early stage, it is a non-continuous single myocardial seizure (generalized or partial), and then it is a weird partial attack, a large number of myocardial traction or tonic seizures. plum. E EG indicates suppression of explosive activity, which can progress to high-level dysrhythmia, severe illness, and death within the first year. ②With outbreak suppression Early infantile epileptic encephalopathy suppression-burst: also known as Ohtawara syndrome, Occurring within a few months after birth, it is often a tonic seizure, and partial attacks may occur. Myotonic seizures are rare. While awake and sleeping Periodic burst suppression waveforms were seen in both E and EG. The prognosis is poor, and severe psychomotor retardation and refractory attacks may occur, often between 4 and 6 years old. Progressed to West syndrome at 6 months of age. Other symptomatic generalized epilepsy. 2) Special syndrome: Epileptic seizures can be complicated by many diseases, including diseases with epileptic seizures as their manifestation or main feature, including Malformations (somniac agenesis syndrome, gyral hypoplasia, etc.) and diseases confirmed or suspected to be inborn errors of metabolism (phenylketonuria, Ceroid lipofuscinosis, etc.). 3. Epilepsy or epilepsy syndrome that cannot be determined to be partial or comprehensive (1) Both generalized and partial seizures

359 Chapter 15 Epilepsy 1) Neonatal epilepsy (neonatal seizures): It is more common in immature children, and its clinical manifestations are often ignored. 2) Severe myocl onic epilepsy in infancy: also known as Dravet syndrome. 1 year after birth Internal onset, the initial manifestations are convulsions all over the body or one side, and later there will be frequent myocardial convulsions starting from the local area, and some patients have focal Seizures or atypical absences, psychomotor development retardation and other neurological deficits starting from the age of 2 years 3) Epilepsy with continuous spike-waves during slow-wave sleep It is a combination of various seizure types and usually has a benign course, but neuropsychiatric disorders are often present. 4) Landau-Kleffner syndrome: also known as acquired epileptic aphasia, onset age is 3 to 8 years old, more males than females, onset in the hidden circle, manifestations It is a speech-auditory agnosia and a rapid decrease in spontaneous speech. This disease is rare. The condition and electroencephalogram can be relieved before the age of 15. (2) Unable to determine as comprehensive or partial epilepsy: including all clinical and EEG findings that cannot be classified as comprehensive or partial. Diagnosed cases, such as many cases of grand sleep attacks. 4. Special syndromes, including febrile convulsions, isolated attacks or isolated epileptic states, and those occurring in acute metabolic or poisoning situations (ethanol, drug intoxication, nonketotic hyperglycemic coma) episodes Several clinically proven epilepsy diseases and epilepsy syndromes newly proposed by I LAE in 2001 1. Familial lobar epilepsy is inherited in an autosomal dominant manner, with a penetrance of 60%. It mostly occurs in adolescents or early adulthood, with an average age of onset. 24 years old. Some patients have febrile panic or a family history of febrile panic. The clinical manifestations are mostly partial seizures originating from the granular lobe. MRI is mostly normal, some Diffuse punctate T hyperintensity was observed: linkage analysis found no linkage with known lobar sites in lobar epilepsy or febrile convulsions. Carbamazepine is optional Treatment with phenytoin and sodium propionate has a good prognosis. Care should be taken to differentiate it from mesial lobar epilepsy. The average age of onset of the latter is 9 years old, and 6% have febrile disease. A history of shock, rarely a family history, focal disease-like discharges are common in E and EG, and MRI shows high T signal in the hippocampus, which is usually difficult to treat. 2. Familial partial epilepsy with different lesions has autosomal dominant inheritance. Linkage analysis confirmed that it is related to the long arm of chromosome 2 and chromosome 22. It is related to the chromosome q 11 to q 12 region, with a penetrance of 62% and an average age of onset of 13 years (2 months to 43 years). Clinical features vary across families Members' partial epilepsy originates from different cortices, with the frontal and granular lobes being the most commonly affected areas. Almost all patients present with simple or complex symptoms. Partial seizures. 50% to 60% of patients with EEG have interictal pathological discharges, which are more likely to be recorded during sleep. Physical examination of the nervous system and Imaging examinations were all negative. 85% to 96% respond well to traditional antiepileptic drugs. Different from previously reported familial partial epilepsy Some of the epilepsy cases in the latter family members all originate from the same cortical areas. 3. Early migratory partial seizures in infants, onset age 13 days to 7 months, early manifestations of motor and autonomic neurosis Symptoms include apnea, hairpins, and facial flushing. Later attacks are diverse and can change from one attack type to another. Clinical manifestations Presently, strabismus in both eyes is accompanied by eye muscle lesions, eye and face discoloration, limb acne, chewing movements, etc. Secondary generalized attacks may also occur, and muscle lesions are rare. Between attacks, the baby is listless, has diarrhea, is lethargic, and cannot swallow. 4. Myogenic status of non-progressive encephalopathy. The average age of onset is 12 months, and most patients have encephalopathy and neurological dysfunction. These are more or less typical partial motor seizures, myocardial absences, and thick myocardial seizures, which manifest as distant seizures on the face and/or limbs. Muscle bursts initially occur in different muscles and are wandering and asynchronous, followed by muscle bursts with different frequencies but consistent rhythms. Li movement is more prominent when there is obvious absence of consciousness. Absence and muscle matrix Li disappear during slow wave sleep. 5. In the 1989 international classification of startle epilepsy, it was regarded as a symptom of epilepsy with special triggers. In this international classification, it will be As an epileptic syndrome, it is included in reflex epilepsy. A sudden, unexpected attack, usually caused by some kind of sound, manifested as startling Jumping, followed by short-term, asymmetrical rigidity, often with falls, but also with seizures, frequent attacks, lasting less than 30 seconds. Most suffer from The patient is only sensitive to one kind of stimulation and may have short-term tolerance to repeated stimulation. Carbamazepine can improve unilateral signs and localized neurological impairment Lamotrigine and clonazepam are also partially effective as adjuvant treatments for the seizures of patients with injuries and localized electroencephalogram abnormalities, and can control epilepsy in the long term Attacks are more difficult, and there are reports that surgery can control startle attacks accompanied by hemiparesis. Section 2. Diagnosis of epilepsy Epilepsy is a disease caused by multiple causes. Its diagnosis needs to follow a three-step principle: first, determine whether the episodic symptoms are epileptic seizures; Next, what type of epilepsy or disease syndrome; finally, what is the cause of the attack?

360 Chapter 15 Epilepsy [Medical history and physical examination] A complete and detailed medical history is of great significance for the diagnosis, classification and differential diagnosis of epilepsy. Because the patient's attack was large Most patients have impaired consciousness and it is difficult to describe the attack, so relatives or witnesses of the patient should be questioned in detail. Medical history should include age of onset, onset of The detailed process of the operation, the development of the disease, the triggers of the attack, whether there are auras, the frequency of attacks and the treatment process: the past history should include the mother’s pregnancy Whether there are any abnormalities and pregnancy medication history, whether there are any abnormalities during the perinatal period, and whether you have suffered from any important diseases in the past, such as facial trauma, encephalitis, meningitis, Heart disease or liver or kidney disease; family history should include any family history of epileptic seizures or related disorders (such as migraines). detailed Thorough consultation and physical examination of the body and nervous system are required. 【Auxiliary inspection】 1. Electroencephalogram (E EG) is the most important auxiliary examination method for diagnosing epilepsy. E EG is of great value in the diagnosis of episodic symptoms value, which helps to clarify the diagnosis and classification of epilepsy and identify special syndromes. Theoretically, any type of epileptic seizure can be recorded using EEG to ictal or interictal disease-like discharges, but in actual work due to technical and operational limitations, conventional scalp EEG can only record 49.5% of patients have pathological discharge. Repeating three times can increase the positive rate to 52%. Induction methods such as hyperventilation and flash stimulation can also be used. To further increase the positive rate of EEG, there are still some patients with epilepsy whose EEG examinations are always normal. Occasionally, some normal people also Disease-like discharges can be recorded, so epilepsy cannot be determined solely based on abnormal or normal brain electrical activity. The 24-hour long-term EEG monitoring and video-EEG (video-EEG) that have been widely used in recent years make it more likely to detect disease-like discharges. In order to improve the accuracy, the latter can simultaneously monitor and record the patient's seizure status and corresponding EEG changes, and clarify the relationship between seizure symptoms and EEG changes. relation. 2. Neuroimaging examinations, including CT and MRI, can confirm Brain structural abnormalities or lesions, diagnosis and analysis of epilepsy and epilepsy syndrome Similar facial features are helpful, and sometimes the cause of the disease can be diagnosed, such as intrafacial tumors, gray hair, etc. heterotopia, etc. MRI is more sensitive, especially the coronal and hippocampal volumes Measurement can better display hippocampal lesions (Figure 15-2). international antiepileptic The Neuroimaging Committee of the Disease Alliance proposed the following situation in 1997 Neuroimaging examination should be performed: ① Any age, medical history or EEG It is suggested that it is a partial seizure; ② The type cannot be classified under 1 year old or in adults. attacks or obvious generalized attacks; ③ neurological or neuropsychological syndrome Obviously there is localized damage; ④ First-line anti-epileptic drugs cannot control epilepsy. seizures; antiepileptic drugs cannot control seizures or seizure patterns change. and those who may have progressive disease. Functional imaging tests such as SPEC T, PET, etc. can reflect local metabolic changes in the brain from different angles. Figure 15-2 Coronal MRI shows left hippocampal sclerosis ation, assisting in the localization of epilepsy lesions. 【Differential Diagnosis】 1. Syn cope refers to a short-term overall decrease in cerebral blood perfusion, instantaneous loss of consciousness and falls caused by ischemia and hypoxia. There are many Obvious triggers, such as standing for a long time, severe pain, bleeding, emotional excitement, severe cold, etc., can cause the intrathoracic pressure to increase sharply, such as coughing, crying, laughing, exerting force, etc. Nausea, defecation and urination can also be induced. There are often auras such as nausea, dizziness, weakness, shaking face, heaviness in the abdomen, or darkening of the eyes. and epilepsy The onset is relatively slow, with symptoms such as paleness, sweating, sometimes irregular pulse, and occasionally twitching and urinary incontinence. few patients Rigidity and spasms of the limbs may occur, but they are different from disease attacks. They usually occur after 10 seconds of loss of consciousness and last for a short period of time. degree is weak. Simple syncope occurs in the upright or sitting position, and also occurs in the recumbent position, which usually indicates a disease attack. Loss of consciousness caused by fainting Loss rarely exceeds 15 seconds, and is characterized by rapid recovery of consciousness and complete awakening, without confusion of consciousness after the attack, unless the cerebral ischemia time is too long. 2. Pseudo epileptic seizures, also known as cancer-like seizures, are a non-epileptic seizure disorder. The disease is an abnormal brain function caused by a psychological disorder rather than a disorder of brain electrical hormones. There may be confusion of movement, sensation, and consciousness similar to epileptic seizures shape, difficult to distinguish. The key to identification is the absence of corresponding pathological discharges on the EEG during seizures and the ineffective anti-epileptic treatment (Table 15-5). But should Note that 10% of patients with pseudoepileptic seizures may have real diseases at the same time, and 10% to 20% of patients with epilepsy are accompanied by pseudoseizures.

361 Chapter 15 Epilepsy Table 15-5 Differentiation between epileptic seizures and pseudoepileptic seizures Features pseudoepileptic seizure epileptic seizure There are mental triggers and someone is present Occasion of attack in any circumstances Sudden stereotypic attack Seizures come in various forms, with strong self-expression, such as locking Attack characteristics eyes, crying, twitching of hands and feet, hyperventilation, etc. eye position The upper face is raised and the eyeballs are moved upward or to one side. Eyes and face tightly closed, eyeballs moving randomly Complexion and mucous membranes hair Paleness or redness pupil Diffusion and loss of light reflection Normal, light reflex exists against passive movement cannot Can may have none Fall, tongue bite, urinary incontinence Duration and termination method It will stop automatically after about 1~2 minutes. It can last for several hours and requires comfort and hints. pyramidal tract sign (one) Bab in ski symptoms ( ) It can cause loss of consciousness and collapse, and is easily misdiagnosed as epilepsy. According to sudden onset of inability to 3. Narcolepsy The tetrad of suppressed sleep, sleep paralysis, hypnagogic hallucinations, and collapsing syndrome can be distinguished 4. Basilar artery type migraine should be distinguished from absence seizures due to disturbance of consciousness, but it occurs slowly and is mild, often before loss of consciousness. Dream-like feeling; migraine is bilateral, often accompanied by dizziness, ataxia, blurred vision in both eyes or eye movement disorders, and EEG may show spikes in the occipital area 5. Transient ischemic attack (TIA). TIA is more common in the elderly and often suffers from arteriosclerosis, coronary heart disease, hypertension, diabetes and other diseases. History, clinical symptoms are mostly deficit symptoms (loss of sensation or reduced limb paralysis), irregular limb twitching, and no rotation of the head and neck. Symptoms often last from 15 minutes to several hours, and there are no obvious pathological discharges on the electroencephalogram; epilepsy can occur at any age, mostly in teenagers, and the aforementioned risks The risk factors are not prominent, and the symptoms are mostly irritating symptoms (abnormal sensation, limb twitching). The attack duration is usually several minutes and rarely exceeds half an hour. Sometimes, there are many pathological discharges on the electroencephalogram. 6. Hypoglycemia. When the blood sugar level is lower than 2 mmol/L, local epileptic twitching or limb tonic attacks may occur, accompanied by loss of consciousness. It is common in patients with pancreatic beta cell tumors or type 2 diabetes who have been taking antidiabetic drugs for a long time. The medical history is helpful for diagnosis. Section 3 Treatment of Epilepsy At present, the treatment of epilepsy is still based on drug treatment. Drug treatment should achieve three purposes: control seizures or minimize the number of seizures. number; long-term treatment has no obvious adverse reactions: patients can maintain or restore their original physical, psychological and social functional status. In recent years, anti-epileptic The advancement of anti-epileptic drugs (A EDs) treatment, the development of pharmacokinetic monitoring technology, and the emergence of new A EDs are all due to Provides conditions for effective treatment of epilepsy 【medical treatement】 1. General principles of drug treatment (1) Determine whether to take medication: The probability of epilepsy occurring once or several times in a person's life is as high as 5%, and 39% of patients with epilepsy experience spontaneous remission. tendency, so not every patient needs medication. Generally speaking, for those who have more than two attacks within six months, once the diagnosis is clear, they should be treated with Anti-epileptic drugs; for those who have the first seizure or have seizures more than half a year apart, they can be informed of the possible adverse reactions of anti-epileptic drugs and the possible consequences of no treatment. In this case, patients and their families should patiently choose to use or not use anti-epileptic drugs according to their wishes. (2) Correct selection of drugs: Choose drugs according to the type of epilepsy attack, type of epilepsy and epilepsy syndrome. 70% to 80% of newly diagnosed epilepsy Patients with epilepsy can control epileptic seizures by taking an anti-epileptic drug, so the choice of drug for initial treatment is very critical and can increase the number of patients with epilepsy. The possibility of successful treatment; if the drug is improperly selected, not only will the treatment be ineffective, but it will also lead to aggravation of epilepsy attacks. In 2006, a large number of evidence-based medicine After summarizing scientific data, the International League Against Epilepsy has launched treatment guidelines for different seizure types of epilepsy, which can be used as clinical reference (Table 15-6). This guideline is very strict in screening clinical data. Many epilepsy seizure types cannot be identified due to lack of qualified research data. For line medication, in actual work, it is necessary to select drugs based on clinical experience and individual patient observation. According to current clinical medication habits, some For drug selection for epilepsy syndrome, please refer to Table 15-7.

(3) Usage of drugs: The method of drug use depends on the drug metabolism characteristics, principle of action and occurrence patterns of adverse reactions, etc., and therefore varies. Very big. From the perspective of pharmacokinetics, there are three ways of relationship between dose and blood drug concentration. The representative drugs are phenytoin and valproic acid. Sodium and carbamazepine. It can be seen from Figure 15-3 that when the conventional dose of phenytoin is ineffective, increasing the dose can easily lead to poisoning, so be very careful: acrylic acid The treatment range is large, and a regular dose can be given at the beginning: carbamazepine gradually accelerates its metabolism due to its self-induction effect, and its half-life is shortened. Gradually increase the dose and reach the regular dose in about 1 week. The dosage of lamotrigine and toxopate should be gradually increased until the therapeutic dose is reached in about 1 month, otherwise it is easy to Skin rash, central nervous system adverse reactions, etc. may occur. The daily dose can be divided into divided doses based on the half-life of the drug. half-life senior daily 1 to 2 times, such as phenytoin, phenobarbital, etc.; drugs with short half-life should be taken 3 times a day. Pharmacokinetics and Dosing of Antiepileptic Drugs See Table 15-8. (4) Closely observe adverse reactions: Most anti-epileptic drugs have varying degrees of adverse reactions, and you should be careful before using anti-epileptic drugs. Check liver and kidney function and routine hematuria. After taking the drug, you need to monitor routine blood and urine every month, and monitor liver and kidney function every quarter for at least half a year. Adverse reactions include specificity, dose-related, chronic and teratogenic (Table 15-9). Dose-related adverse reactions are the most common, usually It occurs at the beginning or during the increment of medication and is related to blood drug concentration. Most common adverse reactions are transient and can be seen by slowly reducing the dosage. Significantly reduced. Most anti-epileptic drugs are alkaline and can reduce gastrointestinal reactions when taken after meals. Taking larger doses before bed can reduce daytime Sedative effect.

(5) Monotherapy as much as possible: The basic principle of anti-epileptic drug treatment is monotherapy as much as possible. About 70% to 80% of patients with epilepsy Seizures can be controlled by monotherapy. Monotherapy should start with a low dose and be slowly titrated to achieve maximum seizure control. If there are no adverse reactions or the adverse reactions are very mild, it is the lowest effective dose: if the epileptic seizure cannot be effectively controlled, it meets partial control and does not Adverse reactions occur. Monitor blood drug concentration to guide medication and reduce blindness during medication. (6) Reasonable combination therapy; although monotherapy has obvious advantages, about 20% of patients still cannot cure the disease after two monotherapy treatments. To control seizures, reasonable combination therapy should be considered at this time. The so-called rational multi-drug combination therapy is to “minimize the increase in adverse reactions.” Under the premise, obtain maximum seizure control.” Reasonable combination therapy can be considered in the following situations: ① There are multiple types of attacks; ② For adverse drug reactions, such as phenytoin sodium treatment If absence seizures occur when treating partial seizures, in addition to using broad-spectrum antiepileptic drugs, clonazepam can also be used to treat absences caused by phenytoin. Attack: ③According to the special situation of the patient, such as patients with menstrual epilepsy, acetazolamide can be added before and after menstruation to improve clinical efficacy; 4 pairs Some patients who are ineffective on single drug therapy can be treated with a combination of drugs. Attention should be paid to combined use of drugs: ① It is not advisable to combine drugs with the same chemical structure, such as phenobarbital and proton, clonazepam and diazepam; ② Try to avoid the combination of drugs with the same side effects. For example, phenytoin can cause liver and kidney damage, and valproic acid can cause idiopathic allergic liver necrosis. Therefore, when using combined drugs in patients with impaired liver function, attention should be paid to the adverse reactions of these two drugs; ③ When using drugs together, attention should be paid to the correlation between drugs. Interactions, such as the induction of liver enzymes by one drug can accelerate the metabolism of another drug, and the competitive binding of drugs and proteins can also change the metabolism of another drug. The free concentration in the blood at which a drug exerts its primary pharmacological effect. (7) Principles for increasing or decreasing drugs, discontinuing drugs, and changing drugs: ① Increase or decrease drugs; the increase of drugs can be appropriately fast, but the decrease of drugs must be slow, and must be increased or decreased one by one to facilitate the treatment. It is necessary to accurately evaluate the efficacy and toxic side effects; ②A EDs must be taken for a long time after the attack is controlled. Unless serious adverse reactions occur, it should not be taken at any time. Decrease or discontinue the drug intentionally to avoid inducing status epilepticus: ③Change the drug: If a first-line drug has reached the maximum tolerated dose and still cannot be controlled To control seizures, another first-line or second-line drug can be added. After the seizure is controlled or the maximum tolerated dose is reached, the original drug can be gradually reduced and switched to When switching to a single drug, there should be a transition period of 5 to 7 days during the dressing change; ④ Withdrawal: The principle of slow and gradual dose reduction should be followed. Generally speaking, comprehensive ankylosis After 4 to 5 years of complete control of seizures, tonic seizures, and convulsive seizures, and half a year after the absence seizures have stopped, discontinuation of medication can be considered, but the medication should be discontinued before There is a slow tapering process, and generally patients who have been symptom-free for no less than 1 to 1.5 years can stop taking the drug. People with automatisms may need to take long-term medication. 2. Commonly used anti-epileptic drugs (1) Traditional A EDs

366 Chapter 15 Epilepsy 1) Phenytoin (phenytoin, PH T): It is effective for GTC S and partial seizures, but can aggravate absence and myopathic attacks. gastrointestinal tract It is slowly absorbed and the metabolic enzymes are saturable. After saturation, a smaller dose will be added to reach the toxic dose. It is difficult for children to detect toxic side effects. Infants and young children It is not suitable for children and children. The adult dose is 200 mg/d. Be careful when increasing the dosage. It has a long half-life. After reaching steady state, adults can take it once a day, and children can take it once a day. Take 2 times. 2) Carbamazepine (C BZ): It is the drug of choice for partial seizures and is more effective than other drugs for complex partial seizures. A EDs also have a good effect on secondary GTC S, but can aggravate absence and myotic stretch attacks. due to autoinduction of liver enzymes The half-life is 20 to 30 hours when first used, and the conventional therapeutic dose is 10 to 20 mg/(kg·d). The clearance rate is low at the beginning of medication. The dose should be 2 to 3 mg/(kg·d), and gradually increased to the therapeutic dose after one week. After 3 to 4 weeks of treatment, the half-life is 8 to 12 hours and needs to be increased Increase dosage to maintain efficacy. 3) Valproate (val proate, VP A): It is a broad-spectrum A EDs, which is a generalized seizure, especially GTC S combined with typical absence seizures. The drug of choice is also used for partial seizures. It is quickly absorbed from the gastrointestinal tract, inhibits the oxidation, binding, and epoxidation functions of the liver, and binds to plasma proteins. Highly potent, it has complex interactions with other A EDs. The half-life is short, and the half-clearance period is 8 to 9 hours during combined treatment. The usual dosage is People: 600-1800 mg/d, children: 10-40 mg/(kg·d). 4) Phenobarbital (PB): often used as the drug of choice for pediatric epilepsy, it has a broad spectrum, fast onset of action, and is effective against GTC S. It is also used for simple and complex partial seizures, and has a preventive effect on febrile panic. The half-life is as long as 37 to 99 hours and can be used for acute brain damage. Harm combined with epilepsy or status epilepticus. Conventional dosage is 60-90 mg/d for adults and 2-5 mg/(kg·d) for children. 5) Primidone (PMD): It is metabolized by the liver into phenobarbital and phenethylmalonamide, which have anti-disease effects. Indications are GTC S. and simple and complex partial seizures. 6) Ethosuximide (ethos ux imi de, ES X): only used for simple absence seizures. Absorbed quickly, about 25% is excreted unchanged by the kidneys. Other A EDs rarely interact and hardly bind to plasma proteins 7) Clonazepam (clo naze pam, C NZ): acts directly on the GABA receptor subunit and has a rapid onset of action, but it is prone to drug resistance. drop. As an auxiliary drug, small doses can often achieve good results. For adults, try 1 mg/d. If necessary, gradually increase the dosage: for children, try 0.5 mg/d. (2) New A EDs 1) To pira mate (T PM): a natural monosaccharide-dextrose thiolate, used for refractory partial seizures and secondary GTC S Additional or monotherapy drugs also have certain effects on Lennox-Gas taut syndrome and infantile pain syndrome. Semi-clearance period 20 to 30 days Hour. The conventional dose is 75 to 200 mg/d for adults and 3 to 6 mg/(kg·d) for children. It should start with a small dose and gradually increase to the therapeutic dose within 3 to 4 weeks. therapeutic dose. It has good long-term efficacy, no obvious drug resistance, and can also be used as monotherapy in high doses. Carbamazepine and phenytoin may decrease the Plasma concentrations, thiolate may also reduce the efficacy of phenytoin and oral contraceptives 2) Lamotrigine (LTG): It is an add-on or monotherapy drug for partial seizures and GTC S. It is also used for Lennox Treatment of gas taut syndrome, absence seizures, and myogenic seizures. Completely absorbed from the gastrointestinal tract and metabolized by the liver. The half-life is 14 to 50 hours. Combined use of sodium valproate can extend the time by 70 to 100 hours. The starting dose for adults is 25 mg/d, and then the dose is slowly increased to a maintenance dose of 100 to 300 mg/d; The starting dose for children is 2 mg/(kg·d), and the maintenance dose is 5-15 mg/(kg·d); when combined with sodium valproate, the dose is reduced to half or lower, starting from children. The initial dose is 0.2 mg/(kg·d), and the maintenance dose is 2 to 5 mg/(kg·d). Gradually increase to the therapeutic dose over 4 to 8 weeks. 3) Gabapentin (GBP): used for the adjuvant treatment of partial epileptic seizures and GTC S in adults over 12 years old. It is not metabolized by the liver and excreted unchanged by the kidneys. The starting dose is 100 mg, 3 times/day, and the maintenance dose is 900-1800 mg/d, taken in 3 divided doses. 4) Felba mate (FB M): effective for partial seizures and Lennox-Gas taut syndrome, and can be used as a monotherapy. The starting dose is 400 mg/d, and the maintenance dose is 1800-3600 mg/d. 90% is excreted unchanged through the kidneys. 5) Oxcarbazepine (ox car baz e pine, 0 XC): It is a 10-keto derivative of carbamazepine. The indications are the same as carbamazepine. Intended for use as add-on or monotherapy for partial seizures and secondary generalized seizures. But it has a slight hepatic enzyme induction effect and no drug metabolism itself. Inducible effects and minimal pharmacokinetic interactions. Not converted to carbamazepine or carbamazepine epoxide in the body, to carbamazepine Two-thirds of patients with allergies tolerate oxcarbazepine. Adult initial dose 300 mg/d, increase by 300 mg daily, monotherapy dose 600～1200 mg/d. Oxcarbazepine 300 mg is equivalent to carbamazepine 200 mg, so the dosage should be increased by 50% when replacing. 6) Vigabatrin (VG B): used for partial seizures, secondary GTC S and Lennox-Gas taut syndrome, for infants

367 Chapter 15 Epilepsy It is effective against plum disease and can also be used as a single drug treatment. Mainly excreted by the kidneys, it irreversibly inhibits GABA transaminase and enhances GABAergic neurons. effect. The starting dose is 500 mg/d, increasing by 500 mg every week, and the maintenance dose is 2~3 g/d, taken in 2 divided doses. 7) Tia gabi ne (T GB): as an adjuvant treatment for refractory complex partial seizures. Rapid absorption from the gastrointestinal tract, reaching 1 hour peak concentration. It has a half-life of 4 to 13 hours and has no hepatic enzyme induction or inhibitory effects, but can be induced by phenytoin, carbamazepine and phenobarbital. The lifespan is shortened to 3 hours. The starting dose is 4 mg/d, and the general dosage is 10 to 15 mg/d. 8) Zonisamide (ZNS): It has obvious effects on GTC S and partial seizures, and can also treat secondary generalized seizures, Atonic seizures, West syndrome, Lennox-Gas taut syndrome, atypical absence seizures and myogenic seizures. Because it is distributed in Europe and the United States Nowadays, some patients develop kidney stones, so it is used less often. 9) Levetiracetam (levetiracetam, LEV): This is a derivative of the same type of piracetam. The mechanism of action is still unclear. It is currently believed to have specific Heterobinding to synaptic vesicle protein SV 2 A. It is effective for partial seizures with or without secondary GTC S, myogenic seizures, etc. Oral absorption Rapidly, with a half-life of 6 to 8 hours. Well tolerated, no serious adverse reactions 10) Pregabalin (pre gabal in): This drug is a gamma-aminobutyric acid analogue. Its structure and effect are similar to gabapentin. It has anti-epileptic properties. Activity, but the anti-epileptic mechanism of this drug is still unclear. Mainly used for auxiliary treatment of partial seizures in epilepsy. [Drug-refractory epilepsy] Different epilepsy attacks and epilepsy syndromes have different clinical characteristics and prognosis. Even for patients with the same epilepsy syndrome, the prognosis is There are differences too. Overall, about 1/3 of epilepsy patients undergo monotherapy for a period of time, and even a small number of patients recover without treatment. Long-term relief can be obtained. About 1/3 of the patients can effectively control their attacks with single drug or reasonable combination of multiple drugs. Obtain satisfactory curative effect. Therefore, about 70% of epilepsy patients have a good prognosis. Multiple studies have confirmed that despite appropriate drug treatment, In addition, about 30% of patients still have protracted epilepsy attacks, which is called intractable epilepsy; epilepsy that is difficult to control The onset of the disease causes serious damage to the patient's health, and its mortality rate is significantly higher than that of the normal population. There is currently no treatment for refractory epilepsy Unified definition, the domestic definition of refractory epilepsy is "frequent epileptic seizures at least 4 times a month, appropriate AEDs People with central nervous system diseases or space-occupying lesions in the face." A common feature of refractory epilepsy is a certain degree of drug resistance to AEDs with different mechanisms of action. This kind of epilepsy The development of drug resistance may involve multiple mechanisms and multiple factors. Currently, there are two hypotheses that are increasingly popular regarding the mechanism of drug refractory Attention, one is the target hypothesis, which is that the drug effect changes the target, causing the sensitivity to A EDs to decrease. is low, which may be the basis for the formation of drug resistance in epilepsy; the other is the multi-drug transporter hypothesis (multi drug transporters), which believes that due to innate Or acquired reasons lead to the overexpression of multidrug transporters, which increases the active pumping of A EDs through the blood-brain barrier, resulting in drug The drug cannot effectively reach the treatment point, and the local A EDs cannot reach the effective therapeutic concentration, thus leading to the intractability of epilepsy. Generally speaking, those with multiple seizure types or complex partial seizures have a worse prognosis than those with other types of seizures. therapeutic drugs Good response to drugs, especially those who are effective to the first A EDs, is an important indicator of good prognosis. Early diagnosis and treatment of patients with poor response to A EDs Indicates that epilepsy is not easy to control. From an etiological perspective, idiopathic epilepsy has a good prognosis, and symptomatic epilepsy and latent epilepsy have a cause or potential cause. The overall prognosis of epilepsy is poor, and the rate of refractory disease is significantly higher. Because refractory epilepsy may cause mental and physical impairment in patients Damage and bringing about a series of psychological and social problems have become the focus of epilepsy treatment, prevention and research. Intractable epilepsy should be treated early If identified, more aggressive treatment measures should be adopted as early as possible, but it is necessary to recognize that errors in diagnosis, improper drug selection, insufficient dosage, and compliance The so-called "iatrogenic refractory epilepsy" caused by poor factors. 【Surgical treatment】 Patients have undergone long-term formal monotherapy, or have used two AEDs successively to reach the maximum tolerated dose, and have undergone a formal combination. If treatment is still ineffective, surgery may be considered. As mentioned before, 20% to 30% of patients with epilepsy have difficulty controlling their seizures with various AEDs. For patients who have been treated for more than 2 years, whose blood drug concentration is within the normal range, who still have more than 4 attacks per month, and who are resistant to AEDs, they should be considered refractory to treatment. Sexual madness. Appropriate surgical treatment should be used to alleviate the patient's seizures and provide the opportunity for the patient to gain complete seizure control. Indications for surgery: Most of the patients with ideal results are partial seizures, mainly refractory complex partial seizures originating from one side of the lobe. If the lesion is close to the cerebral cortex, can be reached by surgery, and will not cause serious neurological deficits after resection, the curative effect will be better. Head

Chapter 15 Epilepsy 368 Previously, it was believed that resection of epilepsy lesions must meet specific conditions. The basic points are: ① The location of epilepsy lesions must be clear; ② The resection of lesions should be relatively localized. Limitation; ③ There is no risk of serious functional disability after surgery. Surgical treatment of epilepsy involves multiple links and requires a combination of neuroelectrophysiology and neurology before surgery. Through comprehensive preoperative evaluation using multiple testing methods such as imaging, nuclear medicine, and neuropsychology, and comprehensive localization of the pathogenic source area, epilepsy is a The key to the success of surgical treatment. Commonly used methods include: ① Anterior lobe resection and selective amygdala and hippocampectomy; ② Extralobular cortical resection; ③ Epilepsy Lesion resection: 4 cerebral hemisphere resections: 5 body dissections; multiple subleptomeningeal transection. In addition, there is Vagus God Transstimulation, chronic cerebellar electrical stimulation, stereotactic brain damage, etc., are theoretically effective in treating various refractory epilepsy diseases. Section 4 Status Epilepsy Status epilepticus (SE), also known as epileptic state, is traditionally defined as “continuous epileptic seizures”. The consciousness has not fully recovered and relapsed frequently, or the epileptic seizure lasted for more than 30 minutes and did not stop on its own.” The current view is that if the patient If a patient has a generalized tonic seizure that lasts for more than 5 minutes, neuronal damage may occur. For patients with GTC S, if the seizure lasts for more than 5 minutes, If the time exceeds 5 minutes, the diagnosis of status epilepticus should be considered and AEDs must be used for emergency treatment. Epilepsy is a common medical emergency. If not Prompt treatment may lead to permanent brain damage, disability and mortality due to high fever, circulatory failure, electrolyte imbalance or neuronal excitotoxic damage. All are very high. Status epilepticus can occur in any type of epilepsy, among which generalized tonic-convulsive seizures are the most common and most harmful. The most common causes of status epilepticus are inappropriate discontinuation of AEDs or acute encephalopathy, stroke, encephalitis, trauma, tumors, and medications. Caused by drug poisoning, etc., the cause is unknown in individual patients. Irregular treatment of A EDs, infection, mental factors, excessive fatigue, pregnancy and childbirth, and alcohol consumption are all Can be induced. 【Classification】 Recent studies have confirmed that the onset time of a single panic attack in non-status epilepticus generally does not exceed 2 minutes, so it is recommended to start with 30 minutes. Minutes are not a very appropriate time limit for diagnosis. From a clinical perspective, behavioral and electroscan activities lasting 10 minutes are a more realistic time limit. International standards, and this is also the time point required to start intravenous administration. Depending on the initial localization of the attack, it can involve a certain part of one cerebral hemisphere, Or if both cerebral hemispheres are affected at the same time, it is further divided into generalized status epileptic us and partial seizure status. Partial status epileptic us. 1. Generalized status ictal status (1) Generalized tonic-tonic status epilepticus: It is the most common and most dangerous clinical status epilepticus, manifesting as tonic-tonic seizures. Recurrent, disturbance of consciousness accompanied by high fever, metabolic acidosis, hypoglycemia, shock, electrolyte imbalance (hypokalemia, hypocalcemia) and myoglobin Urine, etc., may cause multiple organ failure such as brain, heart, liver, lungs, etc., and changes in autonomic nervous system and vital signs. (2) Tonic status: more common in children with Lennox-Gas taut syndrome, manifesting varying degrees of consciousness disorder (Xiangmi comparison) less), with tonic seizures or other types of seizures, such as muscle spasms, atypical absences, atonic seizures, etc., E EG appears slowly and persists Spiny-slow or sharp-slow wave discharge (3) Paroxysmal seizure status: When the paroxysmal seizure persists for a long time, confusion and even intoxication may occur (4) Status epilepticus: Status epilepticus is rare in patients with idiopathic myogenous epilepsy, and it is an advanced stage of severe organic encephalopathy. For example, subacute sclerosing panencephalitis and familial progressive myeloid epilepsy are more common. EEG in idiopathic patients shows a close connection with myometrium Systemic polyspike waves have a better prognosis; secondary EEG usually shows non-rhythmic repetitive spike waves and has a poor prognosis. (5) Absence seizure status: mainly manifested by a decrease in the level of consciousness, or even only a decrease in reactivity and academic performance; E EG Sustained spike-slow wave discharges with slow frequency (<3 Hz) are seen. Mostly caused by improper treatment or discontinuation of medication 2. Status partial seizures (1) Simple partial seizure status: The clinical manifestations are characterized by repeated localized continuous drawings of the face or body, or persistent dislocation of the body. It is characterized by local abnormal sensation, clear consciousness during the attack, and localized discharges in corresponding brain areas on EEG. The evolution of the disease depends on the nature of the disease, and some Some cryptogenic patients may no longer relapse after cure. Some non-progressive organic lesions may be accompanied by ipsilateral myometres in the later stages. Rasmussen Comprehensive Symptoms (partial continuous epilepsy) occur in the early stages of myocardial seizures and other forms of seizures, accompanied by progressive diffuse neurological damage.

369 Chapter 15 Epilepsy (2) Status limbic epilepsy: often manifests as disturbance of consciousness and mental symptoms, also known as psychomotor epileptic state, commonly seen in Lobular epilepsy must be distinguished from mental abnormalities caused by other causes. (3) Hemiparesis with hemiparesis: mostly occurs in young children, showing hemiplegia on one side, accompanied by transient or permanent changes in the same side of the limb after the attack. Body paralysis. In addition, there is also a tendency to classify status epilepticus into status epilepticus according to the presence or absence of panic attacks. (convulsive status epileptic us, C SE) and non-convulsive status epileptic us (NC SE) 【treat】 The goals of treatment of status epilepticus are to maintain stable vital signs and provide cardiopulmonary function support and to terminate persistent epilepsy. Seizures, reduce the damage to brain neurons caused by epileptic seizures; find and eradicate the causes and incentives as much as possible; deal with complications. 1. General measures (1) Symptomatic treatment: Keep the respiratory tract open, inhale oxygen, perform tracheal intubation or incision if necessary, and perform ECG, blood pressure, and blood tests on the patient as much as possible. Monitoring of respiration and EEG, regular blood gas analysis and full biochemical examination; finding and treating the causes of status epilepticus; Those with clenched teeth should have braces placed. (2) Establish intravenous channel: maintain intravenous injection of normal saline. It is worth noting that glucose solution can precipitate some anti-epileptic drugs. Especially phenytoin (3) Actively prevent and treat complications: cerebral edema can be treated with rapid intravenous infusion of 125 to 250 ml of 20% mannitol; antibiotics can be used preventively to control the infection. Infection; high fever can be given physical cooling; metabolic disorders such as hypoglycemia, hyponatremia, hypocalcemia, hyperosmolar state and hepatic encephalopathy can be corrected, and acidosis can be corrected poison, and provide nutritional support treatment. 2. Drug Selection The ideal anti-status epilepticus drug should have the following characteristics: 1. It can be administered intravenously; 2. It can enter the human brain quickly, Preventing epileptic seizures: ③ No unacceptable adverse reactions, and it exists in the brain for a long enough time to prevent another seizure. Control the persistence of epilepsy Selection should be based on the specific status epilepticus types and their pharmacokinetic characteristics and ease of use (1) Diazepam treatment: First, intravenously inject 10 to 20 mg of diazepam, not exceeding 2 mg per minute. If effective, then 60 to 100 mg Dixitin was dissolved in 5% glucose saline and infused slowly intravenously within 12 hours. The first dose for children is 0.25 to 0.5 mg/kg. Generally no more than 10 mg. Diazepam may occasionally inhibit breathing, so the injection needs to be stopped and respiratory stimulants added if necessary. (2) Diazepam plus phenytoin: first use 10 to 20 mg of diazepam intravenously to achieve therapeutic effect, then use 0.3 to 0.6 g of phenytoin sodium Add 500 ml of normal saline for intravenous infusion at a rate not exceeding 50 mg/min. If blood pressure drops or arrhythmia occurs during medication, it is necessary to reduce the dose Slow down the intravenous infusion rate or stop the drug. (3) Phenytoin: Some patients can also use phenytoin alone. The dosage and method are the same as above. (4) 10% chloral hydrate: 20 to 30 ml plus an equal amount of vegetable oil for retention enema, once every 8 to 12 hours, suitable for liver insufficiency or liver dysfunction Those who should use phenobarbiturates. (5) Paraaldehyde: 8~10 ml (0.3 ml/kg for children) diluted with vegetable oil and retained for enema. Can cause severe cough, do not use if you have respiratory problems After the above treatment and seizure control, phenobarbital 0.1 to 0.2 g intramuscular injection can be considered, twice a day to consolidate and maintain the curative effect. same Nasogastric antiepileptic drugs were administered at this time, and phenobarbital was gradually discontinued after reaching a steady-state concentration. Those who fail to respond to the above methods should be treated as refractory status epilepticus. reason. After the seizure has stopped, the cause of the epileptic state needs to be actively searched for and dealt with. Corresponding treatment should also be given to coexisting complications. 3. Intractable status epilepticus. Refractory status epilepticus refers to persistent epileptic seizures, which are resistant to the initial first-line drugs diazepam and chloroquine. Nitrile, phenobarbital, phenytoin, etc. are ineffective and the symptoms last for more than 1 hour. Status epilepticus is an emergency, and the prognosis depends not only on the cause but It is also related to the time of successful treatment. If the attack lasts for more than 1 hour, the stability of the internal environment will be destroyed, which will cause many problems in the central nervous system. Irreversible damage, therefore the first priority in the treatment of refractory epilepsy is to quickly terminate the seizure. The following drugs can be used: (1) Amobarbital: It is the standard therapy for the treatment of refractory status epilepticus and is almost always effective. Adults: 0.25~0.5 g each time, Children aged 1 to 4 years old take 0.1 g each time, and children older than 4 years old take 0.2 g each time. Dilute with water for injection and inject slowly intravenously, no more than 1 minute per minute. 100 mg. Hypotension, respiratory depression, and delayed resuscitation are its main adverse reactions, so tracheal intubation and mechanical ventilation are often required during use. Qi to ensure the stability of vital signs

(2) Midazolam: Due to its rapid onset of action, pharmacological effects appear in 1 to 5 minutes. Anti-epileptic effects appear in 5 to 15 minutes. How to use it It has less inhibitory effect on blood pressure and respiration than traditional drugs. In recent years, it has widely replaced amobarbital and has become the treatment for refractory epilepsy. Trends in standard treatments for disease states. The usual dosage is 0.15-0.2 mg/kg intravenously for the first dose, and then 0.06-0.6 mg/(kg·h) intravenously. maintain. Newborns can receive continuous intravenous infusion at 0.1 to 0.4 mg/(kg·h). (3) Propofol: It is a non-barbiturate short-acting intravenous anesthetic that can significantly enhance the release of GABAergic neurotransmitters. Terminates epileptic seizures and pathological discharges on EEG within seconds, with an average onset of effect of 2.6 minutes. The recommended dose is 1 to 2 mg/kg intravenously, followed by Maintain with continuous intravenous infusion of 2 to 10 mg/(kg·h). The blood drug concentration required to control an attack is 2.5 ug/ml. Sudden discontinuation can aggravate the attack. There will be no rebound of epileptic seizures if the dose is tapered. Possible adverse effects of propofol include induction of seizures, but these are uncommon and occur at lower doses than recommended. At the recommended dose, other central nervous system excitement symptoms may also occur, such as myotonia, opisthotonus, and choreoathetosis. children quiet Note: Adverse reactions such as rhabdomyolysis, refractory hypoxemia, acidosis, and heart failure may occur if the recommended dose exceeds 24 hours. (4) Lidocaine: It is effective for neonatal epileptic states that are ineffective in phenobarbital treatment. The first loading dose to terminate the seizure is 1~ 3 mg/kg, most patients still need intravenous maintenance administration after the seizure has stopped. Although there are few toxic and side effects in controlling epileptic seizures, However, during the application of lidocaine, attention should still be paid to its common adverse reactions: such as irritability, delirium, mental abnormality, arrhythmia and excessive Allergic reactions, etc. Use with caution in patients with heart block and bradycardia. (5) Ketamine, thiopental sodium, etc. can also be used for treatment. (Hong Zhen)