What Are Partial Seizures?

Partial seizures are the first clinical and electroencephalographic changes to indicate that the onset of neuronal group pathological activity is limited to a certain part of one hemisphere. The further classification of partial seizures is mainly based on the presence of a disturbance of consciousness and whether it is a secondary generalized seizure. Clinically it is divided into: simple partial seizures; only some partial seizures; partial seizures develop into comprehensive seizures. ^[1]

According to whether the seizure process is accompanied by a disturbance of consciousness, it is divided into simple partial seizures (unconscious disturbance during the seizure) and complex partial seizures (with different degrees of conscious disturbance).

If the discharge site is superficial (cortical), a more obvious partial discharge can be recorded, and the clinical manifestations are simple partial seizures, and the symptoms are related to the corresponding cortical function; as the discharge spreads, the corresponding site symptoms can evolve into complex partial seizures or The generalization is generalized tonic-clonic seizures, and conventional EEG can record the discharge process. If the discharge is deep in origin, or near the midline, such as the medial temporal lobe (hippocampus, amygdala) or medial frontal lobe, the discharge is likely to spread to the brainstem or contralateral side. Clinical consciousness disorders often occur, showing complex partial seizures; The generalization is generalized tonic-clonic seizures, but the scalp electrode EEG is not easy to record the discharge diffusion process.

1. Genetic factors Single or multiple genetic inheritance can cause seizures. It is known that more than 150 kinds of genetic defect syndromes show epileptic seizures or myoclonic seizures, of which 25 are autosomal dominant genetic diseases, such as knots. There are about 100 types of autosomal recessive diseases such as familial sclerosis and neurofibromatosis, such as familial black dementia, spheroid cell-type white matter dystrophy, and more than 20 types of sex chromosomal genetic defect syndromes.

2. Normal people can induce seizures due to electrical or chemical stimulation. The normal brain has an anatomical and physiological basis for seizures, and it is easy to be triggered by various stimuli. A certain frequency and intensity of current stimulation can cause a seizure discharge in the brain, which continues to discharge after the stimulation stops, leading to a generalized tonic seizure; only a short post discharge occurs after the stimulation is weakened, and if it is repeated regularly (even may Only once a day) stimulation, the post-discharge interval and diffusion range gradually increase until it causes a systemic attack, and even without any stimulation, kindling can occur spontaneously (kindling) leading to the attack. A characteristic change in epilepsy is that many neurons in a limited area of the brain are suddenly activated simultaneously for 50 to 100 ms, and then inhibited. EEG presents a high-amplitude negative-phase spike discharge followed by a slow wave. In the local area, the neurons can repeatedly discharge simultaneously for a few seconds to produce a simple partial seizure, and the discharge can spread to the brain for several seconds to several minutes to produce a complex partial or systemic seizure.

3. Electrophysiology and neurochemical abnormalities Excessive excitability of neurons can lead to abnormal discharges. Using intracellular electrodes to trace the overexcitation of the cerebral cortex in animal models of epilepsy found that neurons have continuous depolarization and hyperpolarization after the action potential burst, resulting in excitability. Post-synaptic potential (EPSP) and depolarized drift (DS) increase intracellular Ca2 and Na, increase extracellular K, decrease Ca2, and cause a large number of DS, and to the peripheral neurons several times faster than normal conduction diffusion. Biochemical studies have found that hippocampal and temporal lobe neurons can release a large amount of excitatory amino acids (EAA) and other neurotransmitters when depolarized. After activating NMDA receptors, a large amount of Ca2 flows in, resulting in further enhancement of excitatory synapses. Increasing extracellular K in epilepsy lesions can reduce the release of inhibitory amino acids (IAA), reduce the function of presynaptic inhibitory GABA receptors, and make excitatory discharges easily project to the surrounding and distant regions. When the epileptic foci migrated from isolated discharge to seizure, the suppression disappeared after DS was replaced by depolarization potential, neurons in adjacent areas and distant compartments with synaptic connections were activated, and the discharge was transmitted through local cortical circuits, long joint pathways (including Corpus callosum pathway) and subcortical pathways spread. Focal seizures can spread locally or whole brain, and some quickly turn into systemic seizures. The generation of idiopathic generalized epileptic seizures may be achieved through the thalamic cortex circuit of a wide reticular branch.

4. Seizures may be weakened by inhibitory neurotransmitters in the brain such as gamma aminobutyric acid (GABA), and excitatory transmitters such as N-methyl-D-aspartate (NMDA) receptors. Increased amino acid response.

Inhibitory transmitters include monoamines (dopamine, norepinephrine, serotonin) and amino acids (GABA, glycine). GABA exists only in the CNS, and is widely distributed in the brain, with the highest levels of substantia nigra and globus pallidum, which are important inhibitory transmitters of the CNS. Epilepsy-promoting transmitters include acetylcholine and amino acids (glutamic acid, aspartic acid, and taurine). CNS synaptic neurotransmitter receptors and ion channels play an important role in information transmission. For example, glutamate has three types of receptors: kainic acid (KA) receptor, gentisine receptor, and N-formyl -D-aspartate (NMDA) receptor. Glutamate accumulation during epileptic seizures, which acts on NMDA receptors and ion channels, makes synapses over-excited, and is one of the main causes of seizures. Outbreaks of endogenous neurons are usually voltage-dependent calcium current enhancement. Some focal epilepsy is mainly due to the loss of inhibitory intermediate neurons. Hippocampal sclerosis may cause epilepsy and loss of seizure due to abnormal return excitatory connections between surviving neurons. Possibly due to increased voltage-dependent calcium currents in thalamic neurons, diffuse cortical spine-slow wave activity occurs.

5. Pathological morphological abnormalities and epileptogenic foci. Cortical electrodes were used to explore the cortical epilepsy lesions that were discharged, and different degrees of glial hyperplasia, ectopic gray matter, microglioma, or capillary hemangioma were found. Electron microscopy showed that the electron density of synaptic clefts in epilepsy lesions increased, and vesicle emissions that marked synaptic transmission activity increased significantly. Immunohistochemistry confirmed that there were a large number of activated stellate cells around the epileptogenic focus, which changed the ion concentration around the neurons and made the excitement easily diffuse to the surroundings.

1. Principles of drug treatment Drug treatment of any disease should follow certain principles in order to improve the efficacy. It is particularly important in the treatment of epilepsy. Effective antiepileptics can control seizures in about 80% of patients with epilepsy. The following principles should be mastered in clinical application of antiepileptic drugs:

(1) medication according to the type of seizures: anti-epileptic drugs are best for a certain type of seizures, and have poor or ineffective effects on other types of seizures, and even have opposite effects. For example, ethosuximide has the best effect on the absence of seizures, but is not effective for other types of seizures. Phenytoin (sodium phenytoin) is effective for tonic-clonic seizures and has been reported to induce absence episodes. Antiepileptic drugs can be selected clinically according to the type of seizures.

(2) Choice of medication timing: It is clear that the diagnosis of epilepsy is a prerequisite for medication. If there are 2 or more seizures in a year, medication should be given. The recurrence rate after the first attack is 27% to 82%. The higher recurrence rate is seen in progressive or organic encephalopathy. The EEG has clear paroxysmal slow waves or frequent focal spines. Wave patients, also seen in partial seizures, neurological signs, mental retardation or mental disorders. If there is no such situation when the first attack occurs, the risk of recurrence is small, and the medication can be postponed for clinical observation. If there are clear triggering factors in patients, such as drugs, alcohol, fatigue, nervousness, light sensitivity, etc., these factors should be removed first, and then treated with medication according to the situation.

(3) Long-term medication: once a drug and a dose that can completely control the onset are found, it should be applied continuously. Generally, the drug should be discontinued if there are no adverse reactions after the seizure is completely controlled for 3 to 5 years. It should also be treated differently depending on the cause, type of attack, and frequency of attacks. If there is a history of encephalitis, birth trauma, symptomatic epilepsy should be taken for a long time, and discontinuation of medication for complex partial seizures should be cautious. Frequent attacks and abnormal EEG should also be taken for a long time. The dose should be gradually reduced when the drug is stopped, and it should be no less than six months from the beginning to the reduction.

(4) Regular medication: Regular medication should be taken regularly and regularly, so that the steady-state effective blood concentration can be maintained to achieve the purpose of anti-epilepsy.

(5) Single drug treatment: Because the combined use of two or more antiepileptic drugs is likely to cause chronic poisoning, and the frequency of seizures is prone to increase, so it is advisable to use more than one drug. The second drug can only be added after confirming that the single drug treatment fails due to factors such as irregular medication. If the absence of seizures or myoclonic seizures cannot be controlled with a single drug, ethosuccinine and sodium valproate may be used in combination, or a combination of benzodiazepines may be effective. However, drugs with the same chemical structure, such as phenobarbital and primidone (eclofenone), clonazepam and diazepam, should not be used in combination. The use of two or more drugs is more contraindicated. The results of a multicenter study by Mattson (1990) showed that 40% of patients who responded to monotherapy were not effective with two drugs. Monotherapy should start from a small amount and gradually increase the dose until it reaches an effective dose for controlling seizures without adverse reactions, that is, reaching a steady-state effective blood concentration. Maintain this dose under blood concentration monitoring, and do not arbitrarily reduce or increase the dose. Due to drug-drug interactions, the combination of multiple drugs not only fails to improve the curative effect, but also reduces the toxic response. This has been confirmed by blood concentration studies. For mixed epilepsy, medications can be combined according to the type of seizure, but no more than 3 drugs are appropriate. If one drug is observed to be ineffective for 2 to 3 months or an adverse reaction occurs, you can gradually switch to another drug. Do not stop suddenly.

(6) Principles for adjusting the dosage of medicines: Generally, it is advisable to start with a small dose and then gradually increase it, and the minimum effective dose that can control the onset without generating a toxic reaction is appropriate. Due to individual differences, the principle of individualization is required for medication. Children need to calculate the amount of medicine according to their weight. Because infants and young children metabolize drugs quickly, the dosage is relatively larger than older children. The half-life of phenobarbital and phenytoin (sodium phenytoin) is longer, and the drug concentration can be changed to 1 time / d after the drug concentration is stable. Those with frequent seizures and difficult to control should not force the seizures completely and increase the dosage too much so as to cause adverse reactions. The quality of life of the patient should be considered. After treatment, the patient's seizures are significantly reduced and the degree is reduced, which is ideal for those who have no adverse effects on daily life and study or work.

(7) Drug replacement principle: The principle of adding new drugs and decreasing old drugs should be adopted for drug replacement. There is a transition period of at least 3 to 7 days. It is not advisable to discontinue the old medicines suddenly after adding new medicines, this will cause the seizures to worsen or induce the status of epilepsy.

(8) Drug reduction and withdrawal principles: Many advocate that after epilepsy is completely absent, then continue to take medicine for 3 to 5 years according to the type of seizures, the frequency of the seizures, and the size of the drug's toxic reaction, and then gradually stop the medicine. The principle of withdrawal of antiepileptic drugs is: The withdrawal process of GTCS is not less than 1 year, and the absence of seizures is not less than 6 months. For those who took a large amount of medication, the time required for withdrawal should also be longer; Do not stop abruptly, which can often lead to persistent epilepsy; Clear organic encephalopathy, positive signs of the nervous system, mental disorders, persistence Paroxysmal abnormalities, partial or mixed episodes of EEG all affect the withdrawal time; Some epilepsy patients with organic encephalopathy may need to take medication for life; Some people suggest that patients with onset of disease older than 30 years of age should be discontinued with caution, because The relapse rate after stopping the drug is more than 50%, which requires long-term or lifetime medication. According to statistics, about 70% of patients with epilepsy do not relapse after a certain period of remission. After stopping the drug, the recurrence rate of partial seizures was the highest, and the recurrence rates of GTCS and absence episodes were the lowest.

2. Selection of commonly used antiepileptic drugs For the effect of commonly used antiepileptic drugs, please refer to the treatment section of "Seizures and Epilepsy Syndrome".

Partial seizure prevention care

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

1. To prevent the occurrence of epilepsy, genetic factors make some children susceptible to convulsions, and seizures are caused by various environmental factors. In this regard, the importance of genetic counseling should be particularly emphasized, and family investigations should be conducted in detail to understand whether the patients' parents, siblings and close relatives have seizures and their seizure characteristics, and for some serious genetic diseases that can cause mental retardation and epilepsy, A prenatal diagnosis or neonatal screening should be performed to decide whether to terminate pregnancy or to treat early.

For secondary epilepsy, it is necessary to prevent its specific and specific cause, pay attention to maternal health before birth, reduce infection, nutritional deficiencies, and diseases of various systems, so that the fetus is less affected by adverse effects. To prevent childbirth accidents, neonatal birth injury is one of the important causes of epilepsy. Avoiding birth injury is of great significance in preventing epilepsy. If pregnant women can be checked regularly, new births will be implemented, and dystocia will be handled in a timely manner, you can avoid or reduce birth trauma. Attention should be paid to the febrile convulsions in infants and young children, and seizures should be avoided as much as possible, and medication should be used to control them immediately. Various diseases of the central nervous system in children should be actively prevented and treated in a timely manner to reduce sequelae.

2. Controlling seizures is mainly to avoid the predisposing factors of epilepsy and to carry out comprehensive treatment to control the seizures. Statistics show that patients have a relapse rate of 27% to 82% after the first seizure. It seems that most patients will relapse after a single seizure. Therefore, it is particularly important to prevent the recurrence of epilepsy symptoms.

Patients with epilepsy should be diagnosed in time and treated early. The earlier the treatment, the smaller the brain injury, the less the recurrence, and the better the prognosis. It is necessary to use medication properly and timely, adjust the dosage in a timely manner, pay attention to individual treatment, take a long course of treatment, and slow the withdrawal process, and adhere to regular medication. If necessary, evaluate the efficacy of the drugs used and monitor the blood concentration. Do not throw drugs randomly, not standard medication. Eliminating or reducing the primary causes of epilepsy, such as intracranial space-occupying diseases, metabolic abnormalities, and infections, are also of great significance for recurrent cases.

3. Reduction of the sequelae of epilepsy Epilepsy is a chronic disease that can last for years or even decades, and can cause serious adverse effects on patients' physical, mental, marital, and socioeconomic status. In particular, deep-rooted social prejudices and public discriminatory attitudes, the misfortunes and frustrations of patients in family relations, school education and employment, and restrictions on cultural and sports activities can not only cause patients to have stigma and pessimism, but also seriously affect patients' physical and mental health Developmental, and it bothers families, teachers, doctors and nurses, and even society itself. Therefore, many scholars particularly emphasize that the prevention of the social sequelae of epilepsy is as important as the prevention of the disease itself. The sequelae of epilepsy are both the patient's body and the whole society. This requires all sectors of the society to understand and support epilepsy patients. Minimize the social sequelae of epilepsy.

Diagnosis of partial seizures

1. Transient ischemic attack may show focal neurological symptoms and signs, such as numbness and weakness in one limb, usually complete recovery within minutes, caused by the shedding of microemboli in the heart or aorta or transient cerebral vasospasm .

2. Migraine is a recurrent pulsatile headache caused by abnormal contraction of the internal and external cranial arteries. Typical migraine visual aura, ophthalmoplegia or hemiplegia migraine need to be distinguished from partial attacks. Migraine has a long premonitory time, at least a few minutes, and then migraine, vomiting, etc., some patients with migraine EEG can see epileptic discharge, but still have doubts about headache epilepsy.

3. Complex and partial seizures of mental illness sometimes need to be distinguished from mental illness. Epilepsy is episodic, with sudden onset, and the spirit is normal between episodes.

4. Peripheral vestibular vertigo shows recurrent episodes of visual rotation with vomiting and tinnitus, which can be recurrent. Most of the patients with familial genetic predisposition are females. Vestibular function tests show that one or both sides have reduced function and EEG is normal.

Partial seizure test

Laboratory inspection:

1. Routine examination of blood, urine, stool and determination of blood glucose, electrolytes (calcium, phosphorus).

2. Increased intracranial pressure on cerebrospinal fluid examination indicates space occupying lesions or impaired CSF circulation pathways, such as larger tumors or deep vein thrombosis. An increase in the number of cells indicates inflammation of the meninges or parenchyma, such as secondary epilepsy of brain abscess, cerebral cysticercosis, meningitis, or encephalitis; an increase in the CSF protein level indicates the destruction of the blood-cerebrospinal fluid barrier, which is found in intracranial tumors, cerebral cysts, and various inflammatory diseases that cause epilepsy .

Other auxiliary checks:

1. Electrophysiological examination Conventional EEG can only record 10% of partial seizure waveforms and 40% to 50% of focal discharge waveforms. Using EEG monitoring technology, including portable cassette recording (AEEG), video EEG, and multi-channel radio telemetry, etc., can dynamically observe the awake and sleeping EEG under natural conditions for a long time, and the detection rate is increased to 70% to 80%. The seizure waveform can be recorded in 40% of patients, which is helpful for epilepsy diagnosis, typing and localization of lesions.

2. Neuroimaging examination of the skull X-ray plain radiographs can find abnormal intracranial calcification, saddle and slope occupying lesions, sinus inflammatory or occupying lesions. CT examinations are common in children and adolescents with epilepsy, such as congenital cerebral perforation malformations, hydrocephalus, hyaline septal cysts, and perinatal craniocerebral injury. They are common in adult patients with ischemic lesions, scars after trauma, and intracranial occupying. Lesions, cysticercosis or calcification, old patients with old bleeding or infarction, chronic subdural hematoma, localized brain atrophy and so on. Enhancement can show cerebral aneurysms, AVM, vascular-rich primary brain tumors or metastases. The detection rate of brain lesions in patients with epilepsy by MRI was more than 80%, and the consistency with epilepsy foci recorded by EEG was 70%. MRI resolution above 1.0T can reach 3mm, and microtumors that can not be recognized by CT can be found, such as low-grade malignant astrocytoma, ganglioglioma, and hamartoma, etc .; it shows changes in brain tissue volume, such as hippocampus, temporal Leaf and hemisphere atrophy, lack or thickening of the corpus callosum, ectopic gray matter, and sclerosis of the middle temporal gyrus are some of the causes of intractable epilepsy.

3. Single-photon emission tomography (SPECT) can detect decreased blood flow during epilepsy and intermittent blood flow during seizures. Positron emission tomography (PET) showed that glucose metabolism was reduced during the intermittent phase of seizures caused by complex partial seizures and increased during the seizure period.

Partial seizures

Epileptic disease (epileptic disease) is a definite pathological state caused by a specific cause, not just the type of attack. Epileptic encephalopathy is an epilepsy-like discharge itself that causes progressive brain dysfunction. Therefore, the brain dysfunction caused by different etiology and after the attack is different, and the clinical complications are also different. But their common point is that they may cause accidents such as trauma or suffocation due to the attack.

Partial seizure prognosis

The prognosis of epilepsy is related to many factors, such as etiology, age of onset, type of seizures, frequency of seizures, EEG manifestations, treatment time, and response to antiepileptic drug treatment. In 1985, an epidemiological survey of rural epilepsy in 22 provinces and cities in China found that 40.4% of those who had seizures with natural remission for more than 2 years accounted for 27.1%. After reasonable and regular drug treatment for epilepsy patients, the complete control rate of seizures is 50% to 85%. The prognosis is affected by many factors, including improper treatment.

Reasons for treatment failure: incorrect determination of the type of seizures and improper medication; incorrect estimation of the frequency of seizures and insufficient medication doses; irregular medications that cannot maintain steady-state effective blood concentrations; epilepsy itself is refractory epilepsy. There is no uniform diagnostic standard for refractory epilepsy. It is generally believed that the use of first-line antiepileptic drugs has reached the steady-state effective concentration or reached the maximum tolerated amount, and the seizures cannot be controlled. The seizures occur more than once a month and are observed for 6 months ~ 3 years before being identified as refractory epilepsy.