Epileptic absence seizures

Introduction The absence of seizures is dominated by disturbances of consciousness, which is characterized by the absence of any aura and sudden onset of seizures. The patient's ongoing movement is suddenly interrupted, dazed, and can be accompanied by a double eye flip. If the patient is speaking, his speech will slow down or terminate; if he is walking, he may suddenly stand still and stay awake, or he may suddenly break free from the hand of the adult and walk a few steps forward, and suddenly he will cry back and find his parents. If the chopsticks with food are suddenly stopped in the middle of the mouth when eating, they can't answer the question. Some patients can stop the attack when they talk to them. This episode lasts from a few seconds to 30 seconds, and more than one minute is rare.

Cause

(1) Causes of the disease

The causes of epilepsy are extremely complex and can be divided into four main categories:

1. Idiopathic epilepsy and epilepsy syndrome: suspicious genetic predisposition, no other obvious cause, often in a certain age group, with characteristic clinical and EEG performance, the diagnostic criteria are clearer. It is not clinically undetectable that it is idiopathic epilepsy.

2. Symptomatic epilepsy and epilepsy syndrome: is a clear or possible central nervous system lesion affecting structure or function, such as chromosomal abnormalities, focal or diffuse brain diseases, and certain systemic Caused by disease. 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.

(1) localized or diffuse brain disease: the incidence of neonatal epilepsy is about 1%, such as birth injury, combined with birth injury and cerebral hemorrhage or cerebral hypoxia damage, neonatal cerebral congenital malformation or production Injury, the incidence of epilepsy is as high as 25%.

(2) systemic diseases: such as cardiac arrest, CO poisoning, asphyxia, N2O anesthesia, anesthesia accidents and respiratory failure can cause hypoxic encephalopathy, leading to myoclonic seizures or systemic episodes, 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 thyroid toxemia can cause epilepsy attack.

3. cryptogenic epilepsy: 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.

4. Situation related epileptic attack: seizures are associated with special conditions, such as high fever, hypoxia, endocrine changes, electrolyte imbalance, drug overdose, long-term drinking withdrawal, sleep deprivation and excessive drinking, etc. Can appear. Although the nature of the seizure is seizure, the removal of the relevant state does not occur, so the epilepsy is not diagnosed.

(two) pathogenesis

1. Genetic factors: single gene or polygene inheritance can cause epileptic seizures. More than 150 rare gene defect syndromes are known to present epileptic seizures or myoclonic seizures, of which 25 are autosomal dominant genetic diseases, such as Nodular sclerosis, neurofibromatosis, etc., about 100 autosomal recessive diseases, such as spheroid cell type white matter malnutrition, and more than 20 kinds of sex chromosome genetic defect syndrome.

2. Normal people can induce seizures due to electrical stimulation or chemical stimulation: normal brains have an anatomical and physiological basis for seizures and are susceptible to various stimuli. Current stimulation of a certain frequency and intensity can cause the brain to develop a seizure discharge, and the discharge continues after the stimulation stops, resulting in a systemic tonic attack; after the stimulation is weakened, only a short post-discharge occurs, if it is repeated regularly (or even possible Stimulation only once a day, the post-discharge interval and the spread range gradually increase until a systemic episode is caused, and even if no stimulation is given, spontaneous kinetic causes seizures. The characteristic change of epilepsy is that many neurons in the restricted area of the brain are synchronously activated for 50 to 100 ms, and then suppressed. EEG has a high amplitude negative phase spike discharge followed by a slow wave. Repeated synchronous discharge of neurons in the restricted area can occur in a partial partial seizure for a few seconds. The discharge can spread through the brain for several seconds to several minutes, and a complex partial or systemic episode can occur.

3. Electrophysiological and neurobiochemical abnormalities: Excessive excitation of neurons can lead to abnormal discharge, and intracerebral cortex hyperexcitability is detected by intracellular electrodes in epileptic animal models. Continuous depolarization and hyperpolarization occur after neuronal action potential outbreaks, generating excitement. Post-synaptic potential (EPSP) and depolarization drift (DS) increase intracellular Ca2 and Na, increase extracellular K, decrease Ca2, produce large amounts of DS, and move to peripheral nerves several times faster than normal conduction. Yuan spread. Biochemical studies have revealed that a large number of excitatory amino acids (EAA) and other neurotransmitters are released during depolarization of hippocampus and temporal lobe neurons. After activation of NMDA receptors, a large amount of Ca2 influx leads to further enhancement of excitatory synapses. Increased extracellular K in epileptic lesions reduces the release of inhibitory amino acids (IAA), reduces presynaptic inhibitory GABA receptor function, and makes excitatory discharges easily projected to the surrounding and distant regions. When the epileptic foci migrated from the isolated discharge to the seizure, the post-DS inhibition disappeared by the depolarization potential, and the neurons in the adjacent region and the synaptic connection were activated. The discharge was through the cortical local loop and the long joint pathway (including The corpus callosum) and the subcortical pathway spread. Focal seizures 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.

4. Seizures may be associated with inhibitory neurotransmitters in the brain: such as gamma aminobutyric acid (GABA), synaptic inhibition is attenuated, and excitatory transmitters such as N-methyl-D-aspartate (NMDA) receptors are mediated. The glutamate response is enhanced.

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, and is an important inhibitory transmitter of the CNS. Epileptic triggering transmitters include acetylcholine and amino acids (glutamic acid, 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, gentrenine receptor and N-A. The base-D-aspartate type (NMDA) receptor. Glutamate accumulation during epileptic seizures, acting on NMDA receptors and ion channels, exacerbating synapses is one of the leading causes of seizures. 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 connections between surviving neurons. Cortically diffuse synchronous spine-slow wave activity may occur due to an increase in voltage-dependent calcium currents in the thalamic neurons.

5. Pathological morphological abnormalities and epileptogenic foci: Cortical epileptic lesions were detected by cortical electrodes, and different degrees of gliosis, gray matter ectopic, microglioma or capillary hemangioma were found. Electron microscopy showed an increase in the electron density of the synaptic cleft in the epileptic lesions, and markedly increased vesicle emissions marked by synaptic transmission. Immunohistochemistry confirmed that there were a large number of activated astrocytes around the epileptogenic foci, which changed the ion concentration around the neurons, making the excitability easy to spread to the surrounding.

an examination

Related inspection

Cerebrospinal fluid lactic acid electroencephalography

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

2. Cerebrospinal fluid examination: increased intracranial pressure suggests a space-occupying lesion or a CSF circulatory pathway disorder, such as a larger tumor or deep vein thrombosis. Increased number of cells suggest inflammation of the meninges or brain parenchyma, such as brain abscess, cerebral cysticercosis, meningitis or encephalitis secondary to epilepsy, increased CSF protein content suggests blood-cerebrospinal fluid barrier destruction, seen in intracranial tumors, cerebral cysticercosis and various inflammatory diseases leading to epilepsy .

3. Electrophysiological examination: Conventional EEG can only record 10% partial seizure waveform, 40% to 50% of focal discharge waveform. EEG monitoring technology, including portable cassette recording (AEEG), video EEG and multi-channel radio telemetry, can observe the awake and sleep EEG in natural state for a long time, and the detection rate is increased to 70%-80%. 40% of patients can record the onset waveform, which is helpful for the diagnosis, classification and location of epilepsy.

4. Neuroimaging: The positive lateral radiograph of the skull can be found in abnormal intracranial calcification, sella and slope occupying lesions, sinusitis or space-occupying lesions. CT examination in children and adolescents with epilepsy common congenital cerebral perforation malformation, hydrocephalus, transparent septum cyst and perinatal craniocerebral injury and other old lesions, common cerebral ischemic lesions in adult patients, post-traumatic scars, intracranial space Lesions, cerebral cysticercosis or calcification, old patients often have old bleeding or infarction, chronic subdural hematoma, localized brain atrophy. Enhancement can show cerebral aneurysms, AVM, vascular-rich primary brain tumors or metastases. MRI examination showed that the detection rate of brain lesions in patients with epilepsy was over 80%, and the consistency with EEG recorded epileptic foci was 70%. MRI resolution above 1.0T can reach 3mm, and microscopic tumors that can not be recognized by CT, such as low-grade astrocytoma, ganglion glioma and hamartoma, can be found; the brain tissue volume changes, such as hippocampus and sputum Leaf and hemisphere atrophy, corpus callosum lack or thickening, gray matter ectopic and sputum sclerotherapy, etc., is the cause of some refractory epilepsy.

5. Single photon emission tomography: (SPECT) can detect the decrease of blood flow in the intermittent period of epileptogenic focus and increase the blood flow during the attack. Positron emission tomography (PET) can detect the reduction of glucose metabolism in intermittent episodes of complex partial seizures and increase the metabolism during episodes.

Differential diagnosis

Typical absence seizures can be divided into seven types:

1 loss of consciousness with consciousness disorder

It is manifested as only the disturbance of consciousness. The action that is going on at the time of the attack is abruptly terminated. It is mainly characterized by a sudden and sudden stop of daze and binocular condensation. It can also be stopped, lost, with no aura and no memories. Also, the patient can't understand the episode, but the action done before the attack can continue. If you don't pay attention, it is difficult to detect the episode.

2 Absence with the ingredients of mild clonic

The onset of the attack is completely the same as that of the only person with a disturbance of consciousness, but there are still trembling of eyelids, mouth horns or other muscle groups, from undetectable to systemic myoclonus. A clonic seizure of the eye can cause a rhythmic sleep. The clumps are often bilateral, but generally do not affect their posture, such as holding in the hands may fall.

3 absence with tension-free ingredients

It is characterized by the head or torso of the low tension caused by the loss of the front, accompanied by the falling of the head and upper limbs, the falling of the object in the hand, and occasionally the patient falling due to the loss of the whole body muscle tension, if the posture is maintained The muscle tension is asymmetrical, so the head can be turned to one side and the torso is tilted; if the patient is standing on both knees, it can be bent.

4 loss of consciousness with increased tension

In the absence of seizures, sudden increase in muscle tone can cause the patient's body to flex or stretch, which can be symmetrical or asymmetrical. The standing patient can be forced to retreat. If the tension is increased, the patient's head or torso can be pulled to one side. . Because the tension is often relatively light, it is not confused with a generalized tonic attack.

5 loss of heart with automatic disease

It can be accompanied by a seemingly targeted automatic disease, such as tongue, swallowing action, tongue extension, upper eyelid lifting, hand itching movement or purposeless walking. Sometimes the automatic disease is very short, such as Failure to observe carefully may not be discovered. The difference from the autonomic syndrome of complex partial seizures is:

a. Is there a warning?

b. Whether it stops suddenly.

c. Whether it is 3 times/second spine-slow wave on the EEG.

6 lost spirit with autonomic nervous phenomenon

It is manifested as a dilated pupil with a dilated pupil, pale or flushed skin, piloerection, salivation, tachycardia or urinary incontinence. The most common autonomic phenomena are pale perioral and enlarged pupil.

7 mixed absence seizures

A mixed episode of two or more of the above types.

(2) atypical absence of seizures

The occurrence and rest of the disturbance of consciousness is slower than the typical one, and the change of muscle tension is more obvious. At the end of the attack, there is often a behavior change, which lasts for 5-10 seconds. The EEG shows:

a. Low-amplitude high-frequency recruitment of epilepsy rhythm about 20 times per second.

b. Recruitative epileptic rhythm with high amplitude, slow frequency, and about 10 times per second.

c. Bilateral, substantially synchronous and symmetrical, somewhat rhythmic, low-frequency spine-slow waves of about 2 times per second, which are not easily induced by deep or rhythmic flash stimuli.

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