What Are Complex Partial Seizures?

(I) Causes of Onset

Complex partial seizures of epilepsy

Complex partial seizures (CPS) of epilepsy are also called temporal lobe seizures, psychomotor seizures, showing partial seizures with varying degrees of disturbance of consciousness. Epileptic discharges originate in the temporal or medial frontal lobe. The origins, diffusion pathways, and speeds are different. The clinical manifestations can vary widely. Simple partial seizures can occur first (time can be long or short), and then disturbances of consciousness occur. Special sensations or pure autonomic symptoms are usually aura. Seizures originating from deep structures (medial temporal lobe, limbic system, etc.), such as psychotic episodes (aura), may be short, and disturbances of consciousness may soon appear; conscious disturbances may also begin, Even simply showing a disturbance of consciousness.

Affected area: whole body
Related diseases: Respiratory failure hemangioma hepatic encephalopathy cerebral hemorrhage fibromatosis nodular sclerosis uremia epilepsy glioblastoma dementia hyponatremia abnormal chromosome malnutrition
Related symptoms: Calcification hallucination eating-like autism venous thrombosis fear drooling increased intracranial pressure imitative autism cyst cyst cerebral perforation malformation hydrocephalus meningitis cerebral abscess cerebral ischemic gesture automatism fuzzy consciousness loss of consciousness sclerosis walker automatism

Affiliated Department: Department of Internal Medicine
Related inspections: Cerebrospinal fluid lactic acid

(I) Causes of Onset

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

1. Idiopathic epilepsy and epilepsy syndrome: suspicious genetic predisposition, no other obvious etiology, often onset at a specific age, characteristic clinical and electroencephalographic manifestations, diagnostic criteria are clearer. Either the clinically undetectable cause is idiopathic epilepsy.

2. Symptomatic epilepsy and epilepsy syndrome: it is a variety of clear or possible central nervous system lesions 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 technology, especially the development of functional neurosurgery for epilepsy, can detect the neurochemical changes in patients with symptomatic epilepsy and epilepsy syndrome.

(1) Local or diffuse brain disease: if the incidence of neonatal epilepsy caused by birth injury is about 1%, the combined birth injury during delivery is often accompanied by cerebral hemorrhage or cerebral hypoxia damage, and newborns with congenital brain malformations or birth defects Injuries and epilepsy are up to 25%.

(2) Systemic diseases: such as cardiac arrest, CO poisoning, suffocation, N2O anesthesia, accidental anesthesia, and respiratory failure can cause hypoxic encephalopathy, leading to myoclonic or systemic major attacks; metabolic encephalopathy such as Hypoglycemia most often causes epilepsy. Other metabolic and endocrine disorders such as hyperglycemia, hypocalcemia, hyponatremia, as well as uremia, dialysis encephalopathy, hepatic encephalopathy, and thyroid toxemia can cause epilepsy. attack.

3. Cryptogenic (cryptogenic) epilepsy: more common, clinical manifestations suggest symptomatic epilepsy, but no clear etiology has been found, it can start at a specific age, and there is no specific clinical and electroencephalographic manifestations.

4. State-related epilepsyattacks are related to special states, such as high fever, hypoxia, endocrine changes, electrolyte imbalance, drug overdose, long-term alcohol withdrawal, sleep deprivation, and excessive drinking, etc., which can also occur in normal people. Although the nature of the seizures is epileptic seizures, the epilepsy is not diagnosed because the relevant state is removed.

(Two) pathogenesis

1. Genetic factors: single gene or multiple gene inheritance can cause seizures. It is known that more than 150 kinds of gene defect syndromes show epilepsy or myoclonic seizures, of which 25 are autosomal dominant genetic diseases, such as Nodular sclerosis, neurofibromatosis, etc., there are about 100 autosomal recessive genetic diseases, such as familial melancholic dementia, globular 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 the anatomical and physiological basis for seizures, and is easily triggered by various stimuli. A certain frequency and intensity of current stimulation can cause the brain to produce a disease discharge (seizuredischarge), which continues to discharge after the stimulation is stopped, resulting in systemic tonic seizures; only a short post-discharge occurs after the stimulation is weakened, and if repeated regularly (even daily Only once) stimulation, the post-discharge interval and diffusion range gradually increase until systemic seizures are caused, and even without any stimulation, kindling can occur spontaneously (kindling) leading to seizures. 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 excitement of neurons can lead to abnormal discharges. Using intracellular electrodes to trace the overexcitation of the cerebral cortex of animal models of epilepsy, it was found that continuous depolarization and hyperpolarization occurred after the action potentials of the neurons erupted, generating excitement Sexual post-synaptic potential (EPSP) and depolarized drift (DS) increase intracellular Ca2 and Na, increase extracellular K, decrease Ca2, appear a large number of DS, and provide peripheral nerves at a rate several times faster than normal conduction Yuan spread. Biochemical studies have found that depolarization of hippocampal and temporal lobe neurons can release a large number of excitatory amino acids (EAA) and other neurotransmitters. After activating NMDA receptors, a large amount of Ca2 inflows, leading to 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 related to inhibitory neurotransmitters in the brain such as gamma; synaptic inhibition of aminobutyric acid (GABA) is weakened, and excitatory transmitters such as N-methyl-D-aspartate (NMDA) receptors are mediated Glutamate response is enhanced.

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 epilepsy foci with cortical electrodes were explored, and different degrees of glial hyperplasia, ectopic gray matter, microgliomas, or capillary hemangiomas 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. Routine examination of blood, urine, stool and determination of blood glucose, electrolytes (calcium, phosphorus).

2. Cerebrospinal fluid examination: An increase in intracranial pressure indicates a mass lesion or a disorder of the CSF circulation pathway, such as a larger tumor or deep vein thrombosis. An increase in the number of cells indicates inflammation of the meninges or parenchyma, such as secondary epilepsy of brain abscesses, cerebral cysts, meningitis, or encephalitis; an increase in the CSF protein level indicates a breakdown of the blood-cerebrospinal fluid barrier, which is found in intracranial tumors, cerebral cysts, and various inflammatory diseases that cause epilepsy .

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: X-ray plain radiographs of the head and side can find abnormal intracranial calcification, saddle and slope occupying lesions, sinus inflammatory or occupying lesions, etc. 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 with a resolution of more than 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; 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 the decrease of blood flow during the epilepsy period and the increase of blood flow during the seizure period. 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.

The following types are common:

(1) Performance consciousness disorder: common consciousness ambiguity, rare loss of consciousness, psychiatric or psychosensory symptoms during seizures, consciousness disorder can be covered up, manifestation of false absence, children should pay attention to distinguish from the absence of seizures; mostly originate from the temporal lobe.

(2) Performance disorder and autism: aura may appear before the loss of consciousness in a seizure, and the patient may retain some memory. The classic complex partial seizures begin with auras, common upper abdominal paresthesias, and emotional (fear), cognition (seemingly acquaintance), and sensory (olfactory hallucinations) symptoms, followed by loss of consciousness, stunnedness, and cessation of movement. The seizures usually last 1 to 3 minutes . Complex partial motor seizures are more coordinated and adaptive with unconscious activity and amnesia, which is called automatism. About 75% of patients have cheek-tongue movements, and about 50% of facial or neck movements can be generalized. Automatic behavior is not unique to complex partial seizures, other (such as absence) or post-seizure disturbances of consciousness, even non-epileptic seizures can occur. Complicated partial seizures cause disturbance of consciousness to release advanced control functions and release the original automatic behavior.

According to the clinical manifestations, the symptoms are divided into:

Food-like automatism: showing eating or tasting movements, such as licking lips, tongue extension, pouting, and throat clearing, often accompanied by salivation, chewing, swallowing or nasal spray, etc., to a certain degree of stereotypes.

Imitative automatism: Emotional expressions and physical movements such as horror, happiness, anger and thought can be seen.

Gesture autism: simple gestures such as wiping face, pouting mouth, tongue, twisting hands, grasping objects and playing with genitals, making confusion or comprehension, etc .; complex gestures such as buttoning or undressing, turning pockets, dusting, finishing Clothes, moving furniture, overturning a bed, or performing some professional activities.

Verbal autism: mumbling, recitation, accompanying sounds or laughter, common repeated phrases or sentences, which need to be distinguished from phonic episodes.

Ambulatory automatism: walking towards a target, avoiding obstacles, and sometimes even riding a bicycle or driving through downtown, the attack lasts for several seconds to several minutes, and the continuous attack can last for several hours to several days.

Pseudo-autonomous motor autism: It is also called semi-automatic autism. It is seen during frontal lobe epilepsy. It often has violent swing, rolling, and running-like movements. It has a certain rhythm. It needs to be distinguished from rickets clinically.

Spontaneous automatism: sexual excitement and movement, common in male frontal lobe epilepsy.

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

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. 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. Control of seizures: mainly to avoid the predisposing factors of epilepsy and 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. Reduce 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.

What Are Complex Partial Seizures?

Complex partial seizures of epilepsy

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