Seizures

Introduction The simple partial seizure of epilepsy has a short duration, usually no more than 1 min, and the start and end are abrupt, and the consciousness remains, unless the secondary part of the seizure or the tonic-clonic seizure (secondary generalization) ).

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 seizures.

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

Attacks are associated with special conditions, such as high fever, hypoxia, endocrine changes, electrolyte imbalance, overdose, long-term drinking withdrawal, sleep deprivation and excessive drinking, etc., normal people can also 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 general trait examination brain ultrasound examination

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 cell number suggests inflammation of the meninges or brain parenchyma, such as brain abscess, cerebral cysticercosis, meningitis or encephalitis secondary to epilepsy. Increased CSF protein content suggests a disruption of the blood-cerebrospinal fluid barrier, which is 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 cannot be recognized by CT, such as low-grade astrocytoma, ganglion glioma and hamartoma, can be found. The changes in brain tissue volume, such as hippocampus, temporal lobe and hemisphere atrophy, corpus callosum lack or thickening, gray matter ectopic and sacral sclerotherapy, are the causes 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

1. Partial exercise seizures:

1 focal seizures: starting with local twitching, involving a side of the face such as the mouth or the distal part of the limb such as the thumb or toe, etc., the lesion is mostly in front of the central ditch, such as temporary local limb weakness or hemiparesis after the attack ( O.5~36h elimination), called Todd.

2 Jackson Attack: Focal motor seizures gradually expand along the cerebral cortex motor area, and clinical manifestations (most common) twitching extend from the contralateral thumb along the wrist, elbow, and shoulder.

3 Rotational episode: The head eye is tilted to one side and the torso is connected. Even the whole body can be rotated. The lesion is in the frontal lobe, occasionally in the occipital lobe, and a few are in the ipsilateral cortex.

4 Postural seizures: abnormal postures, such as abduction of one side of the upper limb, half flexion of the elbow, eyes of the side of the hand, the lesions are mostly in the additional sports area.

5 linguistic seizures: vocalization of the throat, involuntary repetition of monosyllabic or words, language interruption, etc.

2, part of the feeling (soul or special feeling) sexual seizures:

1 Somatosensory seizures: manifestations of numbness and acupuncture of the limbs, mostly in the mouth, tongue, fingers or toes. The lesions are located in the central posterior sensation zone, and can even slowly spread into sensory Jackson epilepsy.

2 special sensory episodes:

A. Visual seizures: mostly flashes, simple visual hallucinations, visible structural illusions such as characters, scenery, etc., lesions in the occipital lobe.

B. Auditory seizures: Auditory hallucinations are as simple as noise, complex as music, and lesions on the lateral side of the temporal lobe or on the island.

C. Olfactory seizures: mostly stench or other unpleasant odors, lesions in the temporal lobe, hook back, amygdala or island back.

D. Taste episodes: may be sweet, sour, bitter, salty or metallic, with lesions in the amygdala and islands.

E. Dizziness episode: showing a sense of rotation, floating or sinking, the lesion is in the island or the parietal lobe.

3, autonomic seizures: facial and body pale, flushing, sweating, standing hair, dilated pupils, vomiting, belly sounds, polydipsia and urination, etc., rarely appear alone, attention and non-epileptic autonomic symptoms Identification. Most of the lesions are located in the amygdala, islands, or cingulate gyrus, which are prone to spread and cause disturbance of consciousness, which becomes part of a complex partial seizure.

(4) Mental seizures: appear alone, often a complex partial seizure aura, and can be followed by a comprehensive tonic-clonic seizure.

1 language disorder episode: incomplete aphasia or repeated language, the lesion is on the lateral side of the temporal lobe.

2 memory disorder episodes: memory distortion or dream-like state, seemingly familiar or familiar with strange things, familiar or unfamiliar with strange things, occasionally quick memories of past events, forced thinking, lesions in the hippocampus.

3 cognitive disorders: environmental distortion, disengagement, personality disintegration, dream state and time disorders, etc., the lesions are mostly in the hippocampus.

4 Emotional episodes: such as unnamed fear, unreasonable anger, depression, and euphoria, the lesion is brought back in the buckle.

5 illusion episode: the visual object becomes larger and smaller, becomes farther and closer, the sound becomes stronger and weaker, and the personality disintegrates, as if he is not on himself, feels his body weight, size change, etc., the lesion is in the hippocampus or the occipital lobe .

6 Structural hallucinations: Hallucinations include body sense, sight, hearing, smell and taste. They can be simple illusions such as flashes, noises, or complex forms such as characters, scenery, speech, and music. The lesions are in the hippocampus or the occipital lobe.

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