complex partial seizures
Introduction
Introduction Complicated partial seizure (CPS) of epilepsy, also known as temporal lobe episodes, psychomotor seizures, with partial seizures with varying degrees of disturbance of consciousness. Epileptic discharge originates from the temporal or frontal lobe. The origin, diffusion pathway and velocity are different. The clinical manifestations may vary greatly. A partial partial seizure may occur first (the time may be long or short), and then the disturbance of consciousness may occur. Special sensations or simple autonomic symptoms are often aura, and the onset of deep structures (medial temporal margin, limbic system, etc.) such as psychotic seizures (aura) may be short, and soon consciousness disturbances may occur, or conscious disturbances may begin. Even simply manifesting a disturbance of consciousness.
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 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. The amino acid response is related.
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
Cerebrospinal fluid cytology neurological 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 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 .
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.
Diagnosis
Differential diagnosis
The following types are common:
(1) manifestation of consciousness disorder: common confusion, loss of consciousness is rare, seizures often have mental or psychosensory symptoms, consciousness disorders can be concealed, performance false sense of absence, children should pay attention to the identification of absence seizure; more originated from temporal lobe.
(2) manifestation of consciousness disorder and automatic disease: aura can occur before the loss of seizure consciousness, the patient can retain some memory. Classical complex partial seizures begin with aura, common upper abdominal paresthesia, and emotional (fear), cognitive (like-acquaintance), and sensory (olfactory hallucinations) symptoms, followed by loss of consciousness, dullness, and stop of action, usually lasting 1 to 3 minutes. . Complex partial seizures show more adaptive adaptive unconscious activities with forgetting, called automatism. About 75% of patients have buccal tongue movements, and about 50% have facial or neck movements, which can be secondary to generalization. Automated behavior is not unique to complex partial seizures, and other (such as absence of seizures) or post-onset disturbances of consciousness, even non-seizures can occur. Conscious disturbances occur in complex partial seizures, the advanced control functions are removed, and the original automatic behavior is released.
According to clinical manifestations, the automatic syndrome is divided into:
1 eating automatic disease: performance eating or tasting action, such as lip, tongue, mouth and throat, often accompanied by salivation, chewing, swallowing or nasal spray, etc., have a certain degree of stereotype.
2 imitative autonomic syndrome: visible emotional state expressions and physical movements such as horror, happiness, anger and thinking.
3 Gesture Automated Disorder: Simple gestures such as wiping face, pouting, licking tongue, twisting hands, grasping objects and playing with the genitals, making confusion or comprehension. Complex gestures such as buttoning or undressing, flipping pockets, whisking, organizing clothes, moving furniture, smashing beds or performing some professional activities.
4 lexical autonomic disorder: muttering, reciting, accompanied by vocal or laughter, common repetitive phrases or sentences, need to be identified with the pronunciation of seizures.
5 ambulatory automatic disease: walking to a target, encounter obstacles can be avoided, sometimes even riding a bicycle or driving through the downtown, the attack lasts for a few seconds to a few minutes, continuous episodes can last from several hours to several days.
6 pseudo-automatic motility automatic syndrome: also known as semi-target autonomic syndrome, seen in the frontal lobe seizure period, common severe swing, rolling, running-like movements, a certain rhythm, clinical need to identify with snoring.
7 Sexual autosis: sexual excitability and movement, common in male frontal lobe epilepsy.
