Symptomatic epilepsy syndrome

Introduction to symptomatic epilepsy syndrome Symptomatic epilepsy syndrome refers to epilepsy with a clear cause. After embryogenesis, structural changes or metabolic abnormalities of the brain cause epilepsy due to various reasons. It can be limited or diffuse, or it can be static or progressive. In addition to various types of seizures, there are various symptoms of the primary disease. Therefore, this type of epilepsy is often called clinical epilepsy or acquired epilepsy. In addition, some epilepsy is symptomatic epilepsy, but it is difficult to find the exact cause. For this type of epilepsy, we call it cryptogenic epilepsy, which is still the category of secondary epilepsy. basic knowledge The proportion of sickness: 0.04%-0.07% Susceptible people: no specific population Mode of infection: non-infectious Complications: disturbance of consciousness

Symptoms of symptomatic epilepsy syndrome

Localized or diffuse brain disease (35%):

(1) Congenital anomalies: various causes of embryonic development lead to brain penetrating malformations, microcephaly, congenital hydrocephalus, corpus callosum deficiency and cerebral cortex hypoplasia, perinatal fetal brain injury.

(2) Acquired brain injury: Some clinical events such as epilepsy after brain trauma are 20%, 10% to 50% after craniocerebral surgery, 4% to 20% after stroke, and 30 after intracranial infection. % to 80%, acute alcoholism is 24%.

(3) birth injury: the incidence of neonatal epilepsy is about 1%, combined with birth trauma at the time of delivery with cerebral hemorrhage or cerebral hypoxia damage, neonatal with congenital malformation or birth injury, the incidence of epilepsy up to 25%.

(4) Inflammation: including central nervous system bacteria, viruses, fungi, parasites, spirochete infections and AIDS neurological complications.

(5) cerebrovascular diseases: such as cerebral arteriovenous malformations, cerebral infarction and cerebral hemorrhage.

(6) Intracranial tumor: primary tumor such as glioma, meningioma epilepsy incidence rate of about 10%, brain metastases about 30%.

(7) Inherited metabolic diseases: such as tuberous sclerosis, brain-face hemangiomatosis, Tay-Sachs disease, phenylketonuria and the like.

(8) Degenerative diseases of the nervous system: such as Alzheimer's disease, Pick disease, etc., about one-third of patients have seizures.

Systemic disease (25%):

(1) Hypoxic encephalopathy: such as sudden cardiac arrest, CO poisoning, asphyxia, N2O anesthesia, anesthesia accidents and respiratory failure can cause myoclonic seizures or systemic episodes.

(2) Metabolic encephalopathy such as hypoglycemia most often leads to epilepsy, other metabolic and endocrine disorders such as hyperglycemia, hypocalcemia, hyponatremia, and uremia, dialysis encephalopathy, hepatic encephalopathy and thyrotoxicosis Hypertension can cause seizures.

(3) Cardiovascular diseases: such as cardiac arrest, hypertensive encephalopathy, etc.

(4) febrile seizures: thermal episodes of infants and young children can cause hippocampal neuron loss and gliosis, which is called Ammon horn sclerosis. Autopsy found that the incidence of hippocampal sclerosis was 9% to 10%. Shi Da 30%; heat episodes cause hippocampal sclerosis is a secondary seizure of temporal lobe epilepsy, and become an important cause of refractory epilepsy.

(5) eclampsia.

(6) Poisoning: such as alcohol, ether, chloroform, camphor, isoniazid, carboazole and other drugs and lead, bismuth and other heavy metal poisoning.

Cryptogenic epilepsy (15%):

More common, clinical manifestations suggest symptomatic epilepsy, but did not find a clear cause, can start at a particular age, no specific clinical and EEG performance.

Status-related seizures (5%):

Attacks are related to special conditions, such as high fever, hypoxia, endocrine changes, electrolyte imbalance, drug overdose, long-term drinking withdrawal, sleep deprivation and excessive drinking, etc., normal people can also appear, although the nature of seizures is seizures, but related to removal The state does not occur anymore, so no epilepsy is diagnosed.

60% to 80% of patients with epilepsy have an initial age before the age of 20, and the etiology of each age group is different (Table 2).

Pathogenesis

1. Normal people can induce seizures due to electrical stimulation or chemical stimulation, suggesting that normal brains have an anatomical-physiological basis for seizures, which are susceptible to various stimuli, and certain frequencies and intensity current stimuli can cause pathogenic discharges in the brain (seizure discharge) ), after the stimulation stops, the discharge continues, resulting in a generalized tonic attack; after the stimulation is weakened, only a short post-discharge occurs. If the stimulation is repeated regularly (or even once a day), the post-discharge interval and diffusion range gradually increase until Causes systemic seizures, even without any stimulation, spontaneously appears to cause seizures. The characteristic change of epilepsy is that many neurons in the restricted area of the brain are synchronously activated for 50-100ms, and then inhibited, and EEG has a high amplitude negative. The phase-wavelet discharge, followed by a slow wave, can cause a partial partial seizure with repeated synchronous discharge of the neurons in the localized area for a few seconds. The discharge can spread through the brain for several seconds to several minutes, and a complex partial or systemic attack can occur.

2. Electrophysiological and neurochemical abnormalities In recent years, the advancement and wide application of neuroimaging techniques, especially the development of epilepsy functional neurosurgery, have been able to detect neurobiochemical changes in patients with symptomatic epilepsy and epilepsy syndrome, excessive neuron Excitability can lead to abnormal discharge, and intracerebral cortex hyperexcitability in an animal model of epilepsy with intracellular electrodes is found. Continuous depolarization and hyperpolarization occur after neuronal action potential outbreaks, producing excitatory postsynaptic potential (EPSP) and depolarization. Drift (DS), the intracellular Ca2 and Na increased, extracellular K increased, Ca2 decreased, a large number of DS appeared, and spread to peripheral neurons several times faster than normal conduction, biochemical studies found that hippocampus and temporal lobe nerve Meta-depolarization can release a large number of excitatory amino acids (EAA) and other neurotransmitters. After activation of NMDA receptors, a large amount of Ca2 influx leads to further enhancement of excitatory synapses. Extracellular K increase in epileptic lesions can reduce inhibition. Amino acid (IAA) release, reducing presynaptic inhibitory GABA receptor function, making excitatory discharge easy to project to the surrounding and distant regions, epileptic focus from isolated discharge At the time of seizure, the post-DS inhibition disappearance was replaced by the depolarization potential, and the neurons in the adjacent region and the synaptic junction were activated, and the discharge was through the cortical local circuit, the long combined pathway (including the corpus callosum) and the subcortical Pathway spread, focal episodes can spread locally or throughout the brain, and some rapidly turn into systemic seizures. The development of idiopathic generalized seizures may be achieved through a broad network of thalamic cortical circuits.

3. Seizures may be associated with decreased synaptic inhibition of intracranial inhibitory neurotransmitters such as gamma aminobutyric acid (GABA), excitatory transmitters such as N-methyl-D-aspartate (NMDA) receptor-mediated valleys. Related to the enhancement of the amino acid reaction, inhibitory transmitters include monoamines (dopamine, norepinephrine, serotonin) and amino acids (GABA, glycine).

GABA exists only in the CNS, has a wide distribution in the brain, and has the highest content of substantia nigra and globus pallidus. It is an important inhibitory transmitter of CNS. Epileptic priming transmitters include acetylcholine and amino acids (glutamate, aspartic acid, Taurine), CNS synaptic neurotransmitter receptors and ion channels play important roles in information transmission. For example, glutamate has three receptors: kainic acid (KA) receptor, which makes glutamate And N-methyl-D-aspartate (NMDA) receptors, accumulation of glutamate during seizures, acting on NMDA receptors and ion channels, causing excessive synaptic excitation, leading to seizures In one case, endogenous neuronal burst discharges are usually voltage-dependent calcium current enhancement. Some focal epilepsy is mainly due to the loss of inhibitory interneurons. Hippocampal sclerosis may result in epilepsy due to abnormal return of excitatory connections between surviving neurons. Atheistic seizures may be due to increased voltage-dependent calcium currents in the thalamic neurons, and cortical diffuse synchronous spine-slow wave activity occurs. Antiepileptic drugs act on the above mechanisms, such as phenytoin, carbamazepine, phenobarbital and propylidene. Acid is blocked by voltage The sodium channel of lysate reduces high-frequency repetitive discharge and does not affect single action potential; phenobarbital and benzodiazepine enhance GABA-mediated inhibition, and ethosuxamide blocks low-threshold transient calcium current in neurons, and non-urethane decreases Excitatory neurotransmitters, lamotrigine reduces glutamate release and affects voltage-dependent sodium channels, stabilizing neuronal membranes, and so on.

4. Pathological morphological abnormalities and epileptic foci using cortical electrode exploration of cortical epileptic lesions, found varying degrees of gliosis, gray matter ectopic, microglioma or capillary hemangioma, electron microscopy can be seen epileptic neurites The electron density of the contact gap increased, and the vesicle emission marked by synaptic transmission activity increased significantly. Immunohistochemistry confirmed that there were a large number of activated astrocytes around the epileptogenic focus, which changed the ion concentration around the neurons, making the excitability easy to spread to the surrounding.

Symptomatic epilepsy syndrome prevention

Prevention of epilepsy is very important. Prevention of epilepsy is not only related to the medical field, but also related to the whole society. Prevention of epilepsy should focus on three levels: one is to focus on the cause and prevent the occurrence of epilepsy; the second is to control the seizure; the third is to reduce epilepsy. The physical, psychological and social adverse effects of the patient.

Early prevention and early diagnosis of symptomatic epilepsy syndrome, early treatment is also very important. For those with genetic factors, the importance of genetic counseling should be emphasized. The family survey should be conducted in detail to understand the parents, siblings and close relatives. Whether there are seizures and their seizure characteristics, for some serious hereditary diseases that can cause mental retardation and epilepsy, prenatal diagnosis or neonatal screening should be carried out to decide to terminate pregnancy or early treatment.

Symptomatic epilepsy syndrome complications Complications

General concomitant disturbances and convulsions.

Symptoms of symptomatic epilepsy syndrome Common symptoms Cerebellar ataxia dysarthria dysfunction dysfunction tremor neonatal epilepsy persistent state frontal lobe epilepsy cingulate gyrus myoclonus frontal lobe epilepsy movement intelligently deficient neurological deafness

The clinical manifestations of common symptomatic epilepsy syndrome are described below.

1. Infantile spasm is an infantile epilepsy caused by different causes, often accompanied by mental retardation, first reported by West (1841), also known as West syndrome, the cause of this disease is unclear, special Sexual infantile spasms are autosomal recessive.

Most children have a disease before the age of 1 year, the peak is 4 to 7 months, more common in male infants, usually characterized by characteristic paralysis, mental retardation and high amplitude amplitude loss EEG triad, is flexion, stretch, lightning Sample or nod, often a combination of multiple types, the disease is divided into two types of symptoms and idiopathic, symptomatic more than a history of brain damage or a clear cause, showing mental motor development retardation, visible neurological signs or neuroimaging Abnormal; idiopathic is rare, no history of brain damage, clear cause, neurological signs or neuroimaging signs.

Infant snoring EEG features (Figure 1), each lead is irregular, not synchronized with high amplitude slow waves, accompanied by irregular spikes, spikes, spines slow waves, multiple spikes, high degree of disordered EEG The picture changes.

2. Lennox-Gastaut syndrome (LGS), also known as minor motor seizures, is a child with refractory epilepsy syndrome, with certain types of seizures, often accompanied by mental retardation and typical EEG Changed to characteristics, accounting for 4.2% to 10.8% of children with epilepsy, Gibbs et al (1939) first described the EEG characteristics of LGS, compared with the typical absence of seizures 3 times / s spine wave synthesis (SSW), LGS is less than 2.5 times / s Spinal slow wave synthesis, called petit mal variant (PMV), suggests that patients with slow SSW have severe uncontrollable seizures. Lennox and Gastaut discuss the relationship between symptomology and EEG in detail. Lennox-Gastaut syndrome.

The causes of symptomatic LGS include prenatal, perinatal and postpartum factors, congenital brain development and metabolic abnormalities, infections, trauma, etc., 10% to 20% of cases have had infantile spasms before LGS.

Usually 4 months to 11 years old, more common before 4 years old, 1 to 2 years old, male to female ratio of 1.4:1 to 3.3:1, often accompanied by mental retardation, 60% of children have a history of encephalopathy, the child at the same time Two or more episodes are important features of LGS, common tonic seizures and atypical absence seizures, as well as tonic seizures, myoclonic seizures, GTCS and simple partial seizures, frequent episodes, and often epileptic seizures.

20% to 60% of children with LGS have mental retardation at the time of onset, 75% to 90% have mental retardation after several years of onset, and mental retardation is related to the onset of the disease. Half of the children have behavioral abnormalities, manifested as ADHD or aggressive, and destroyed. Sexual behavior, half of the children with neurological and imaging examinations were normal, and the rest may be associated with cerebral palsy, abnormal speech and other neurological deficits.

EEG background activity is abnormal at the time of attack, there is <3Hz spine slow wave, often visible multi-causal abnormality, usually EEG background activity is abnormal when awake, 1 ~ 2.5 times / s spine wave synthesis (SSW) is a prominent feature, often common synchronously, One side is also quite common, with a few being focally distributed and the forehead being the most significant.

The main clinical types are as follows:

(1) tonic seizures: generally tonic axial (tonic axial), showing head, nodding and body straight, sometimes difficult to distinguish from West syndrome, transient episodes without loss of consciousness, recurrent episodes of conscious disorder, multiple sleep In particular, stage II sleep, EEG with bilateral moderate to high amplitude 10 to 25 times / s fast rhythm outbreak, anterior lead, especially slow wave sleep (NREM), short duration, sometimes clinical discharge Low-level background activity or general spine-wave integrated discharge is often seen before the burst discharge.

(2) Atypical absence seizures: seen in half of the patients, showing gaze or eyeball upturn, the ongoing activity is interrupted, compared with the typical absence episode, the seizure is not sudden, the stopping process is slow, the consciousness is not completely lost, and the autonomic disorder may be associated with Autonomic abnormalities lasted for a few seconds to more than ten seconds. At the time of onset, EEG showed irregularities ranging from 2 to 2.5 times per s of spine wave synthesis, which was often difficult to distinguish from the interspinning period.

(3) Disorder of tension: more common in infants, sudden disappearance of muscle tension can not maintain body posture, so that patients suddenly fall and trauma, instant attacks can be unconscious, severe loss of consciousness, lasting for a few seconds, EEG can see spikes, sharp Wave, slow wave or spine slow wave synthesis.

(4) clonic seizures: manifested systemic or partial myoclonic tics, no tonic attack, may be associated with loss of consciousness, seizures mostly in the NREM phase, EEG is generally 10 times / s activity, mixed with spine slow wave integrated discharge.

(5) Sustained state of atypical absence seizures: seizures persist, consciousness is turbid, there may be tension, and short-term systemic myoclonic seizures, also known as small seizure persistence, seen in 14% to 50% of LGS patients.

3. Juvenile cerebrosideosis disease, also known as juvenile (type III) Gaucher disease, is autosomal recessive glucocerebrosidosis (glucoserebrosidosis), it has been found that children with this disease exist lq2131 Alleles 1448 nucleotide alleles, children mostly develop within 10 years old, nervous system shows chronic progressive mental retardation, cerebellar ataxia, seizures such as myoclonic epilepsy, extrapyramidal symptoms such as hand and foot Movement, tremors and dystonia.

EEG showed diffuse 6 to 10 Hz reversing spine slow wave and rhythmic sharp wave, 6 ~ 10 Hz light stimulation can induce myoclonic seizures.

4. Juvenile familial schizophrenia (familial amaurotic idiocy) is an autosomal recessive inheritance. Most children have a Jewish genetic background, which is the amino acid of the long arm of the chromosome 15 (15q23-q24). Hexosidase A deficiency, the child is 4 to 10 years old, the first symptoms are progressive vision loss and optic atrophy, various types of seizures such as absence seizures, myoclonic seizures or general tonic-clonic seizures, etc. Disorders, dysarthria and mental decline.

Early EEG showed a paroxysmal high-wavelength slow-wave burst with diffuse slow-wave background, with multi-phase spikes and low-wavelength slow-wave activity in the late stage.

5. Cherry erythema-myoclonus syndrome Cherry-red spot-myoclonus syndrome is an autosomal recessive inheritance. It has been confirmed that there is a 10q23 gene mutation in patients with neuronic acid deposition, resulting in - Defects in N-acetylneuraminase causes impaired function of the nervous system due to lysosomal storage.

More than 8 to 15 years old, visible progressive vision loss, crystal opacity, fundus examination can be seen cherry red spots, cerebellar ataxia and peripheral neuropathy, etc., after several years of onset of myoclonus, multiple myoclonus and intentionality Intention myoclonus.

EEG showed diffuse 10-20 Hz positive phase spikes, 10-20 Hz simultaneous discharge during myoclonic seizures, urine increased sialic acid oligosaccharide, lysozyme in peripheral blood leukocytes and lymphocytes Body storage, skin fibroblast culture showed obvious sialic acid deficiency, pathological examination showed liver Ketffer cells, intestinal muscle plexus neurons and brain neurons storage.

6. Progressive myoclonus epilepesy (PME) is an autosomal recessive inheritance, including the following three types:

(1) Lafora small body myoclonic epilepsy: also known as Lafora disease, is a rare autosomal recessive genetic disease, 6 to 19 years old (average 14 years old) onset, mostly with tonic-clonic seizures, followed by irregularities Myoclonic seizures, flashing, noisy and contact stimuli can induce mild limb twitching, gross myoclonic or focal seizures, early onset of mental decline, rapid progression, cerebellar ataxia in late stages of the disease months or years later , cones of tendons and involuntary movements, extrapyramidal signs.

EEG was normal at the beginning of the disease, and there were non-specific short bursts of multiple spikes. The background activity was normal and sleep was not induced. After the cerebellum, pyramidal and extrapyramidal signs, the EEG showed typical changes, and the background activity was slow and arrhythmia. There are a wide variety of spikes or spikes, and characteristic photosensitive discharges can be seen in the late stage. Special apolyglycan bodies can be seen in the axillary sweat glands or liver biopsy. It is an ellipsoidal basophilic basophilic deposit composed of polyglucan.

(2) myoclonic epilepsy with ragged-red fibers (MERRF): or MERRF syndrome, is a mitochondrial disease caused by maternal genetic mitochondrial DNA mutations, more common in 5 to 15 years old Children, usually after 10 years of age or later, have a clear family history, characterized by myoclonic epilepsy, with tonic-clonic seizures, cerebellar ataxia, mental decline, dementia and myopathy Dwarf, neurological deafness, optic atrophy, foot deformity such as arched foot, sputum reflex disappearance, deep sensory disturbance and endocrine disorders.

EEG background activity is normal, bilateral slow spine waves and extensive spine waves, diffuse delta wave outburst, light stimulation sensitivity, diffuse brain atrophy, white matter damage, basal calcification and low density lesions can be seen by CT and MRI. Muscle biopsy can be seen as a broken or scalp-like red fiber, which helps to confirm the diagnosis.

(3) Unverricht-Lundborg syndrome: This syndrome is autosomal recessive. The child is 6 to 18 years old and the disease progresses rapidly. The average course of disease is 2 to 10 years. The first symptom is myoclonic twitching, and the consciousness is awake. Spontaneous action myoclonus occurs, irregular, not synchronized, sensitive to light stimulation, etc., can be combined with tonic-clonic seizures, cerebellar ataxia, dysarthria and dementia.

EEG abnormalities can precede clinical symptoms, showing bilateral synchronous spine slow wave and multi-spine slow wave outbreak, progressive scattered background rhythm, light stimulation can appear bilateral 4 ~ 6Hz violent spikes and renaturation spikes, The visual evoked potential is highly abnormal, the brain CT examination is normal, and the GABA content in the cerebrospinal fluid is reduced.

Examination of symptomatic epilepsy syndrome

1. Blood, urine, routine examination of stool and blood sugar, electrolyte (calcium, phosphorus) determination.

2. Cerebrospinal fluid examination of central nervous system infections such as viral encephalitis, increased pressure, increased white blood cells, increased protein, bacterial and bacterial infections, sugar and chloride decreased, cerebral parasitic diseases may have eosinophilia, central nervous system In syphilis, the antibody to Treponema pallidum is positive, and intracranial tumors may have increased intracranial pressure and increased protein.

3. Amino acid analysis of serum or cerebrospinal fluid can reveal possible amino acid metabolism abnormalities.

4. Neurophysiological examination of traditional EEG recordings, including scalp electrodes and special electrodes, such as sphenoidal electrodes, snuff electrodes, foramen oval electrodes and intracranial electrodes, intracranial electrodes including subdural electrodes and deep brain electrodes The subdural electrode, including the wire electrode and the gate electrode, is placed in the brain that may be the area of the epilepsy, and can often determine the epileptic focus and the area of epilepsy, and can use electrical stimulation to determine the boundaries of motion, sensation, and language, called functional localization. Figure, it is very helpful to plan the scope of surgical resection.

Although the traditional EEG recording method can determine the epileptic foci and epilepsy area, it is often impossible to link the electroencephalogram seizures with the clinical symptoms. Therefore, using CCTV or TV images and EEG recording simultaneously For long-term surveillance, it is often possible to record multiple habitual seizures, distinguish between false epilepsy and determine the relationship between the onset of seizures and clinical symptoms.

The newly developed magnetoencephalogram (MEG) provides a more accurate positioning of the deep brain epilepsy discharge source (dipolesource).

5. Neuroimaging CT and MRI greatly improved the diagnosis of epilepsy structural abnormalities, 50% to 70% of symptomatic epilepsy (symptomatic epilepsy) can be seen on CT or MRI pathological changes.

CT and MRI see static structural abnormalities, which cannot be correctly estimated for brain dysfunction caused by epilepsy. Currently, brain function tests have been applied in clinical practice, including positron emission tomography (PET), single photon. Single photon emission tomography (SPECT) and magnetic resonance spectroscopy (MRS), PET can measure the metabolism of sugar and oxygen in the brain, cerebral blood flow and neurotransmitter function changes, SPECT can also measure brain Changes in blood flow, metabolism and neurotransmitter function, but no quantitative PET in terms of quantification, MRS can measure changes in certain chemicals such as acetyl aspartate, choline-containing substances, creatine and lactic acid in the epilepsy area.

6. Neurobiochemical examinations Ion-specific electrodes and microdialysis probes that have been applied can be placed in the epileptic area of the brain to measure certain biochemical changes between seizures, onset and after onset.

7. Neuropathological examination is a pathological examination of surgically resected epilepsy lesions. It can be determined that the cause of epilepsy is caused by brain tumors, scars, vascular malformations, sclerosis, inflammation, dysplasia or other abnormalities.

8. Neuropsychology This test can assess cognitive impairment and determine which side of the brain the epilepsy or region is on.

Diagnosis and identification of symptomatic epilepsy syndrome

Diagnostic criteria

The diagnosis of epilepsy is mainly based on the history of seizures. Witnesses provide a reliable and detailed description of the seizure process, supplemented by EEG epileptic discharge evidence to confirm the diagnosis. Symptomatic epilepsy can find clues in both the medical history and physical examination. Abnormal birth, head trauma, encephalitis, history of meningitis, etc., or other neurological symptoms such as severe headache, hemiplegia or sputum and mental retardation, etc., may also have systemic symptoms such as hypoglycemia episodes, metabolic or endocrine disorders , A-S syndrome, parasites such as schistosomiasis, paragonimiasis, swine mites, etc., for patients with age at onset of age, even if no abnormalities were found in physical examination and EEG, symptomatic epilepsy could not be completely ruled out. Review and do other auxiliary inspections if necessary.

For symptomatic epilepsy, the cause should be a diagnosis of a brain disease or a systemic disease.

The International Alliance Against Epilepsy (ILAE, 2001) recommends the idea of a diagnostic axis in the diagnosis of seizures and epilepsy syndrome, first describing the seizures, and then determining the type of seizure and epileptic syndrome, and then further investigation. The etiology and central nervous system damage are finally treated for the cause and injury.

Differential diagnosis

1. Seizure (seizure) needs to be differentiated from various seizure diseases

(1) snoring: snoring sometimes manifests as irregular contraction of the whole body muscle, and it occurs repeatedly, and it must be differentiated from the tonic-clonic seizure. The medical history can be found that the snoring episode occurs when someone is present and emotionally stimulated. Long, lasting for tens of minutes or hours, or even all day and night, often accompanied by crying and screaming, unconscious loss and incontinence, no bruises, if examined during the attack, muscle contraction can be seen Does not conform to the law of tonic-clonic, pupil, corneal reflex and tendon reflex do not change.

It is worth noting that some epileptic seizure patients, especially chronic patients, have different degrees of mental abnormalities, including emotional reactions, so the color of snoring can not rule out epilepsy, if prompted for psychomotor seizures According to the basis, further inspection is still required.

(2) syncope: syncope is also a short-term disturbance of consciousness, sometimes accompanied by a short-onset upper limb cramps, which needs to be differentiated from various seizures. Before vasopressive syncope, most have a history of emotional stimulation or pain stimulation; syncope due to reduced venous return More often standing, dehydration, bleeding or urination, coughing; erect hypotension stun occurs more when suddenly standing up; cardiogenic syncope occurs more often when running or running, most of the syncope before the onset of dizziness, Chest tightness, black eyes and other symptoms, not like the sudden onset of absence, the recovery of consciousness and physical strength is far slower.

(3) Hyperventilation syndrome: Anxiety and other neurosis patients may have numbness or paresthesia of the mouth and extremities due to active hyperventilation, which may be accompanied by dizziness and hand and foot convulsions. Excessive ventilation test to see if the same symptoms can be repeated.

(4) Migraine: Headache epilepsy must be differentiated from migraine. The headache of the former is sudden, the duration is not long, and it lasts for a few minutes. It is rarely accompanied by gastrointestinal symptoms such as nausea and vomiting. EEG can record Epileptic discharge, start and end have obvious boundaries, need continuous treatment of anti-epilepsy can be effective, and migraine attacks are gradual, often unilateral, mostly volatility headache, more long duration, usually several hours Or 1 to 2 days, often accompanied by nausea, vomiting and other gastrointestinal symptoms, EEG can not record epileptic discharge, mostly non-specific slow wave, migraine initially with tartaric acid tartaric caffeine can control seizures.

(5) Transient ischemic attack (TIA): TIA refers to a transient blood supply to the carotid or vertebral-basal artery system, resulting in focal neurological dysfunction in the blood supply area, corresponding symptoms and signs, general symptoms Within 5 minutes, the peak is reached. One episode usually lasts for 5-20 minutes, and the longest is no more than 24 hours, but it can be repeated. This disease should be differentiated from localized seizures. TIA is more common in the elderly, often with arteriosclerosis, hypertension. Risk factors such as coronary heart disease and diabetes mellitus, the duration of symptoms varies from a few minutes to several hours. Symptoms are limited to one limb, face, etc., and can be recurrent. Physical examination shows signs of cerebral arteriosclerosis, EEG examination is normal, cranial Brain CT scan is normal, a few can have lacunar infarction, and epilepsy can be seen in various ages. Except for epilepsy secondary to cerebrovascular disease in the elderly, the aforementioned risk factors are not prominent in patients with epilepsy, and seizures persist. The time is usually a few minutes, rarely more than half an hour. The symptoms of localized epilepsy begin to extend to the whole body after an upper limb. There is no abnormality in the physical examination after the attack. EEG can find limitations. Or epileptiform EEG waves, CT can be found in brain lesions.

(6) narcolepsy: narcolepsy is a type of sleep disorder, an unexplained sleep disorder, manifested as paroxysmal irresistible sleep, may be accompanied by cataplexy, sleep paralysis and sleep illusion, etc. , manifested as quarantine sleeping quadruple syndrome, only 10% of patients have all the symptoms of the above four signs, the disease mostly in childhood and adolescent onset, the most from 10 to 20 years old, each episode lasts for several minutes Up to 10 hours, usually 10 to 20 minutes, automatically awake and immediately resume work, several times a day, more normal neurological examination, a small number of patients with obesity and hypotension, sleep monitoring can find specific abnormalities, daytime seizures fall asleep Rapid eye movement sleep (REM); nighttime sleep is different from healthy people, the sleep cycle starts from REM, while healthy people start with non-rapid eye movement sleep (NREM). This disease should be differentiated from absence seizures, loss of dementia. The age of onset of epilepsy is earlier than that of narcolepsy. Children are more common. Absence epilepsy is a sudden loss of consciousness rather than sleep. Some episodes of absence epilepsy are accompanied by loss of tension, but the duration is short, usually only a few seconds. EEG See 3 / s of spike - slow wave synthesis, absence epilepsy is a characteristic change, there are important differential value.

In addition, epilepsy should be differentiated from paroxysmal psychosis and paroxysmal other visceral symptoms.

2. Symptomatic (epilomatic) epilepsy and the etiology of epilepsy syndrome

(1) Systemic diseases that cause epilepsy:

1 low glycemic: after the onset of fasting or strenuous exercise, usually first heart palpitations, dizziness, sweating, nausea, irritability and other symptoms, and even behavioral disorders, those with a history of these should do fasting blood glucose measurement for further diagnosis.

2 hypocalcemia: for patients with hand and foot convulsions, long-term diarrhea, steatorrhea or thyroid surgery, or patients with rickets deformed in the physical examination, blood calcium and phosphorus should be measured.

3 Amino aciduria: For children with mental dysplasia, pale skin color, increased muscle tone, or accompanied by tremors and hand and foot movements, suspected phenylketonuria, urine test, other rare There are many types of urine with different colors, odors, and when necessary, do the corresponding biochemical tests.

4 acute intermittent blood porphyria: abdominal pain, vomiting, diarrhea and peripheral neuropathy associated with epilepsy, should be done urine or blood tests.

(2) Brain diseases that cause epilepsy: medical history (history of birth injury, history of febrile seizures, history of encephalitis meningitis, history of traumatic brain injury, history of stroke, etc.) and age of onset can provide some evidence, such as intracranial tumors found in physical examination Localization signs and optic disc edema, head murmurs of cerebral arteriovenous malformations, subcutaneous nodules of cysticercosis (cysticercosis), etc., can provide clues to the cause, the cause is unknown, except for those with obvious diffuse encephalopathy In addition, it is often necessary to do further examinations, such as cerebral angiography, nuclear scanning, CT, MRI and so on.

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