Generalized tonic-clonic seizures in epilepsy
Introduction
Introduction Systemic rigidity of epilepsy - clonic seizures (secondary generalization): simple partial seizures can develop into complex partial seizures, simple or complex partial seizures can be generalized into generalized tonic-clonic seizures, if the patient wakes up Remember that symptoms are a precursor to a focal episode. Sudden loss of consciousness without a clear description of aura symptoms, highly suggestive of seizures. Local sensory or motor symptoms, such as involuntary twitching of one limb, paresthesia of one side, and forced head turning, suggest a seizure of the contralateral frontal cortex. Fear, olfactory hallucinations or taste hallucinations, visceral sensations or familiarity often originate from temporal seizures.
Cause
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 (Situation related epileptic attack) is 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., 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.
Examine
an examination
Related inspection
EEG examination of cerebrospinal fluid lactic acid
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 meningeal or brain parenchymal inflammation, such as brain abscess, cerebral cysticercosis, meningitis or encephalitis secondary to epilepsy; increased CSF protein content suggests blood-cerebrospinal fluid barrier disruption, seen in intracranial tumors, cerebral cysticercosis and various inflammatory diseases leading to epilepsy .
1. 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.
2. 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.
3. 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.
Diagnosis
Differential diagnosis
1. Transient ischemic attack: There may be signs of focal symptoms of the paroxysmal nervous system, such as numbness and weakness of one limb, usually recovering within a few minutes, for the heart or aortic microemboli or a transient cerebral vasospasm To.
2. Migraine: It is a recurrent pulsatile headache caused by abnormal intracranial and extracranial arterial dysfunction. Typical migraine visual aura, ophthalmoplegia or hemiplegia type migraine need to be differentiated from partial seizures. Migraine prolonged aura for a long time, at least a few minutes, and then migraine, vomiting, etc., EEG in some migraine patients can see epileptic discharge, but there is still doubt about headache epilepsy.
3. Mental illness: Complex partial seizures sometimes need to be differentiated from mental illnesses. Epilepsy is episodes, sudden onset, and normal interictal spirit.
4. vestibular peripheral vertigo: manifested by paroxysmal visual rotation with vomiting, tinnitus, recurrent attacks, family genetic predisposition is mostly female, vestibular function test shows one or both sides of the function is reduced, EEG no abnormalities.
