What Is Post-Traumatic Epilepsy?

Symptomatic epilepsy is also called secondary epilepsy, which refers to seizures caused by abnormal brain structure or function and abnormal discharge of neural network due to some unexpected reason.

Basic Information

nickname
Secondary epilepsy
Visiting department
Neurology
Common locations
Brain neuron
Common causes
Perinatal ischemia and hypoxia, brain injury, intracranial infection, trauma, etc.
Common symptoms
Tonic clonics, myoclonus, hallucinations, hallucinations, dizziness, etc.

Causes of symptomatic epilepsy

1. Perinatal ischemic and hypoxic brain injury: mainly due to birth injury, asphyxia, intracranial hemorrhage, and hypoxic-ischemic encephalopathy. Among them, epilepsy caused by hypoxic-ischemic encephalopathy is the most common.
2. Congenital brain malformations: such as anencephaly, megacephaly, polycerebellar dysplasia, gray matter ectopic, perforation of the brain, congenital hydrocephalus, hypoplasia of the corpus callosum, arachnoid cyst, and megacephaly
3. Neurocutaneous Syndrome: The most common are nodular sclerosis and facial hemangioma.
4. Genetic metabolic diseases: such as phenylketonuria, hyperammonemia, cerebral lipidosis, vitamin B 6 dependence.
5. Intracranial infection: such as bacterial meningitis, viral encephalitis, brain abscess, fungal meningitis, cerebral parasitic disease, encephalitis after vaccination, etc.
6. Nutritional metabolism disorders and endocrine diseases: common hypoglycemia, hypocalcemia, hypomagnesemia, and hypothyroidism.
7. Cerebrovascular disease: such as cerebrovascular malformations and cerebrovascular inflammation.
7. Trauma: Intracranial hemorrhage caused by trauma, skull fracture, brain contusion, etc.
8. Brain tumors: such as gliomas, astrocytomas, tumors in the parietal, frontal, and temporal lobe regions often cause epilepsy.
9. Cerebral degeneration: macular degeneration, multiple sclerosis, subacute sclerosing panencephalitis.
10. Toxic encephalopathy: drug poisoning; food poisoning, carbon monoxide (CO) poisoning, organic phosphorus poisoning, heavy metal poisoning (mercury, lead, arsenic), etc.

Symptomatic epilepsy

1. Collection of clinical history
Medical history collection should include seizure history, birth history, growth and development history, febrile seizure history, and family history. The complete and detailed seizure history is most meaningful for the diagnosis of seizures and the determination of seizure types. In the collection of medical history, it is necessary to know in detail whether there are pre-seizure precursors, whether there are fixed first symptoms, whether there is automatism, and whether there are symptoms of localized seizures. These characteristics are of great value for the localization and positioning of seizures.
2. Imaging data
Computed tomography (CT) is a basic means of craniocerebral imaging, but because of its low resolution, it is difficult to identify small intracranial lesions. It is generally only used to determine whether intracranial lesions in patients with epilepsy have calcification, and epilepsy. Examination of early intracranial conditions.
Magnetic resonance scanning imaging (MRI, above 1.5T) has a high spatial resolution, can detect subtle intracranial lesions, and can detect most intracranial structural abnormalities through enhanced scanning. MR angiography can judge intracranial vascular abnormalities; hippocampal volume measurement and FLAIR scan are effective methods to judge hippocampal atrophy and sclerosis; magnetic resonance spectroscopy (MRS) can detect neurotransmitters and metabolites in the central nervous system, and can find Focal neuron damage and dysfunction are helpful in locating epileptic foci and are often used to judge hippocampal sclerosis and atrophy. The lesion area found by imaging examination is not equal to the epilepsy focus. Whether it is the responsible focus of epilepsy should be determined by combining clinical manifestations and electrophysiological examination.
3. EEG examination
EEG examination is the gold standard for localization of epilepsy. For preoperative assessment of epilepsy, long-range EEG monitoring with more than 32 leads has more diagnostic value. The preoperative location of epilepsy focus should pay great attention to the changes in the EEG during the seizure period. The starting area of abnormal discharge during the seizure period is an important basis for positioning the epilepsy focus. For patients evaluated before surgery, there should be 3-5 times of the EEG during the seizure period. Illustration. For the diagnosis of temporal lobe epilepsy, electroencephalogram recording should be combined with sphenoid electrode or oval hole electrode. If the patient has no seizures for more than three days during the EEG monitoring process or the patient has a lower frequency of seizures, the seizures can be gradually reduced under the guidance of a specialist.
Intracranial electrode EEG is an invasive examination method, including epidural electrodes, subdural electrodes, deep electrode EEG, and stereotactic EEG. The monitoring time of intracranial electrode EEG is generally 7-10 days. In the absence of infection, the monitoring time can be extended to 3-4 weeks, and more than 3 records of usual episodes should be obtained. Intracranial electrode EEG can be free of interference from scalp and skull, and has higher sensitivity and accuracy.
Intraoperative EEG includes cortical EEG and deep EEG, which can further verify and clarify the location of epilepsy. However, during the intraoperative EEG recording, the EEG is recorded during the inter-seizure period. It is a complete epilepsy and requires careful comprehensive analysis and judgment.
4. Neuropsychological assessment
The contents of neuropsychological assessment include intelligence, memory, attention, feeling, language, executive function, etc. The intelligence test can use the Webster Intelligence Scale; the memory function can use the Webster Memory Scale; the language function test can use Boston diagnostic Aphasia test (BDAE) and Chinese test.
5. Single photon emission computed tomography (SPECT) and positron emission tomography (PET)
SPECT is a technique for injecting -ray tracer drugs into the body and detecting -ray emission in the body for imaging. It can reflect the status of cerebral perfusion and is an auxiliary method for preoperative epilepsy localization. The epilepsy foci showed low metabolism during the seizures and high metabolism during the seizures. The fusion of SPECT and MR images during seizures has high accuracy in the localization and positioning of epilepsy focus.
The attenuation of the radiopharmaceutical injected in the body during PET imaging produces an annihilation reaction between a positron and an electron in the tissue, generating two photons in opposite directions. PET can quantitatively analyze specific biochemical processes, reflecting the metabolism of glucose and the distribution of different neurotransmitter receptors. The epilepsy foci showed low metabolism during the seizures and high metabolism during the seizures.
SPECT and PET are important technologies for nuclear medicine imaging. Although they have high accuracy in detecting epilepsy focus, the spatial resolution of the image is low and there are some false negatives. They are often used in combination with EEG, magnetic resonance and other inspection methods. To improve positioning accuracy.
6. Functional magnetic resonance imaging (fMRI) and magnetoencephalography (MEG)
The fMRI technology based on blood oxygen level (BOLD) dependence is a relatively mature and perfect method for brain functional imaging research. It is currently mainly used for preoperative localization of brain functional areas (motor, language, sensory function).
Magnetoencephalography (MEG) is a non-invasive brain function detection method developed in recent years. It uses low-temperature superconductivity to detect biological magnetic signals in the brain. The time resolution reaches 1 millisecond, the spatial resolution is high, and the magnetoencephalography Epilepsy focus and functional area can be located, and epilepsy with a diameter less than 3mm can be detected. MEG mainly records inter-seizure magnetic signals. It has a high detection rate of epilepsy origins in the cerebral cortex and is not sensitive enough to locate epilepsy foci of deep origin.
7. Intracranial electrodes
It is the most advanced localized examination method for symptomatic epilepsy.

Symptomatic epilepsy treatment

1. General tonic-clonic seizures (mapileptic seizures)
Valproic acid is the first-line medication for newly diagnosed patients with generalized tonic-clonic seizures. If valproic acid is not applicable, use lamotrigine or levetiracetam. Lamotrigine may exacerbate myoclonic seizures if the patient also has myoclonic seizures or suspected adolescent myoclonic epilepsy. Carbamazepine and oxcarbazepine can be used in patients with only general tonic-clonic seizures. When first-line drug treatment is ineffective or intolerable, lamotrigine, clozam, levetiracetam, valproic acid, or topiramate can be used as add-on therapy.
Idiopathic generalized epilepsy: Propionate is the only drug of choice for systemic tonic, seizure and myoclonic seizures. After the failure of propionate treatment, lamotrigine, tolte, and levetiracetam are preferred for seizures of systemic tonic, and lamotrigine is preferred for absence episodes. Levetiracetam is used for myoclonus.
Focal attack
Carbamazepine, oxcarbazepine, or lamotrigine are used as first-line drugs in patients with newly diagnosed focal episodes. If carbamazepine, oxcarbazepine, or lamotrigine are inappropriate or intolerant, consider levothiracetam or valproic acid. If the first of the five antiepileptic drugs does not work, you can choose another one. If a second well-tolerated antiepileptic drug fails, consider combination therapy. When first-line treatment is ineffective or intolerable, carbamazepine, oxcarbazepine, lamotrigine, levetiracetam, valproic acid, topiramate, clobazan, gabapentin, zonisamide can be used as focal points Additional medication for sexual episodes. If the added treatment is ineffective or intolerable, other antiepileptic drugs to consider are phenobarbital and phenytoin sodium.
3. Surgically curable symptomatic epilepsy
(1) Epilepsy after trauma
Traumatic epilepsy refers to epileptic seizures secondary to craniocerebral injury. It can occur at any time after the injury. The earlier one appears immediately after the injury, and the late one can start a sudden attack many years after the head injury is healed. The incidence of epilepsy immediately after trauma is 1% to 4%, early epilepsy is 4% to 25%, and late epilepsy is 9% to 42%. Traumatic epilepsy is more common in young men, which may be related to more opportunities for head injuries. In addition, genetic factors are also related to traumatic epilepsy. In general, the more severe the brain injury, the greater the chance of epilepsy, and more open brain injury than closed.
Seizures after trauma. Frontal lobe epilepsy is usually a generalized seizure (major seizure); lesions in the central area often cause contralateral limb movement or sensory localized seizures; temporal lobe lesions cause psychomotor seizures, and occipital lobe lesions often have visual auras. The type of seizures is relatively fixed in most patients. MRI is the most effective method for detecting epilepsy after trauma, which can clarify the location and extent of trauma lesions.
EEG examinations often show slow wave discharge in focal epilepsy, and some cases can show diffuse discharge. Systemic anti-epileptic drugs should be given to recurrent early or middle-term epilepsy. Post-traumatic epilepsy is focal epilepsy, and first-line drugs such as carbamazepine, lamotrigine, and levetiracetam are generally used.
(2) Epilepsy caused by brain tumors or vascular malformations
The possibility of low-grade gliomas and angiopathy causing seizures ranges from 20% to 40%. This type of disease is an absolute indication for surgical treatment. Low-grade gliomas such as ganglion cell tumors are more common in the temporal lobe. DNET is more common in the frontotemporal lobe, and cavernous hemangioma can be found anywhere in the brain. Tumor and vascular malformations secondary to epilepsy should be completed under the guidance of neuroelectrophysiological monitoring. The tumor and the discharge area surrounding the tumor are removed, and antiepileptic drugs are routinely applied to prevent seizures.
(3) Focal cerebral cortical dysplasia
Focalortical dysplasia (FCD) is a disease caused by cerebral cortical neuron migration disorder or cell proliferation disorder, is a type of cortical developmental malformation, and is the most common cause of refractory epilepsy. In epilepsy surgery, FCD accounts for about 40% to 50% of children with epilepsy surgery and about 20% of adults with epilepsy surgery.
In 2011, the International Antiepileptic Coalition (ILAE) classified FCD as type III. FCDIa type refers to the presence of mature neurons in the cortex, but there is a radial laminar structure defect; FCDIb type refers to the presence of a large number of immature small neurons and hypertrophy. Conical neurons; FCDIc type refers to the presence of both Ia and Ib abnormalities. FCDIIa type refers to the presence of heteromorphic neurons; FCDIIb type refers to the presence of balloon-like cells and heteromorphic neurons. FCDIIIa refers to the presence of lamellar structural defects of the temporal lobe, accompanied by hippocampal sclerosis; FCDIIIb refers to tumors in the cortical lamellar structure that are close to the ganglia or glial; FCDIIIc refers to the deformities in the cortical lamellar structure immediately adjacent to vascular malformations; FCDIIId Type refers to the abnormality of the lamellar structure of the cortex accompanied by any acquired damage in the early postnatal period, including inflammatory response, ischemic damage, trauma, etc.
FCD generally develops earlier in children, and the age of onset of FCDII is earlier than FCDI. FCD can occur in any part of the brain. The most common are the frontal and temporal lobes. About 30% of FCDs affect more than two brain lobes. The FCDI type is common in the temporal lobe, and the FCDII type often occurs in the cerebral lobes other than the temporal lobe, and is more common in the frontal lobe. FCD mainly affects the cortex and subcortex, but some FCD extensively involve white matter, and some from the cortex to the lateral ventricle. FCD is more frequent than epilepsy induced by tumor and hippocampal sclerosis.
There is no specific difference between the performance of FCD on EEG and refractory epilepsy. It usually presents as a limited rhythmic discharge, and the scalp EEG before and during the onset of surgery can only locate 50% to 70% of FCD patients.
Surgery is an effective method to treat refractory epilepsy caused by FCD. The prognosis of surgery is related to the location of the brain lobe and whether the epileptogenic focus is completely removed. With the advancement of surgical methods, the postoperative epilepsy remission rate reaches 80%.
(4) tuberous sclerosis
Nodular sclerosis (TSC) is an autosomal dominant inherited neurodermal syndrome, which is mostly caused by abnormal organ development in the ectodermal tissue, and may involve multiple organs such as the brain, skin, peripheral nerves, and kidneys. Clinical features It is facial sebaceous adenoma, seizures, and decreased intelligence. The incidence rate is about 1/6000 live babies, and the male to female ratio is 2: 1. More than childhood onset, more men than women.
Head CT and MRI can identify intracranial epilepsy lesions. Intracranial lesions are mostly high-signal nodules of several to dozens of FLAIR sequences. They are located in the cortex and the ventricle, and the intraventricular nodules are distributed symmetrically. There is calcification.
The EEG interval and seizure period can be manifested as focal or diffuse spike slow wave discharge.
Childhood can be treated with rapamycin, and some patients can control nodular growth to a certain extent. Early anti-epileptic drugs to control seizures can help prevent secondary epilepsy encephalopathy and cognitive behavioral damage. For drug-refractory epilepsy, responsible nodules (nodules that cause epilepsy) can be surgically removed, and most patients can achieve satisfactory results.
(5) hypothalamic hamartoma
It is a rare, congenital brain dysplasia that occurs frequently around the lower hindbrain. The disease is common in infants and preschool children, and clinical symptoms are related to the location and size of the "tumor" and the composition of the "tumor". The first symptoms of most patients are seizures and precocious puberty; some cases can be manifested as mental, behavioral and intellectual disorders; a few cases are combined with other organs' abnormal development, such as multi-finger, facial deformity, heart defects, etc .; very few cases Without any symptoms.
According to the relationship between the growth site of the hamartoma and the third ventricle, Arita et al. Divided it into a parathalamic type and an intrahypothalamic type. The former mainly involves the papillary body and / or pituitary stalk. The upper edge of the tumor does not affect the floor of the third ventricle; the latter grows up and down from the pituitary stalk and extends to the bottom of the third ventricle or the tumor extends into the footwell.
The clinical symptoms of hypothalamic hamartoma are related to the physiological functions of the hypothalamus and its surrounding structures. In addition to the typical onset of giggles, other forms of seizures appear with age. Other accompanying symptoms include central precocious puberty, behavioral disorders, and progressive cognitive decline.
The magnetic resonance imaging can clearly show the locality of hamartoma and the relationship between hamartoma and surrounding tissues, which is of great significance for determining the surgical approach and guiding the operation during surgery. Therefore, high-resolution magnetic resonance can replace other methods in diagnosis. Cortical and deep gray matter signals of hamartomas in most patients are compared. T2 weighted images are high signals, and T1 weighted images are low signals compared to normal gray matter.
The treatment of hypothalamic hamartoma is mainly surgical treatment: surgical methods include thermal coagulation damage treatment, surgical resection, and thermal coagulation damage treatment is recommended.
(6) Facial Hemangioma
Cerebral facial hemangioma syndrome is often called Sturge-Weber syndrome, which is a congenital neurocutaneous syndrome. It is mainly manifested as the trigeminal nerve distribution area on one side, and the purple-red hemangiomas that are more commonly distributed on the branch of the eye nerve can be severely spread on one side of the face. On the ipsilateral intracranial side of the cerebral hemi-brain, there are different extents of pial meningeal vascular hyperplasia, and the patient mainly presents with seizures. Children often have delayed development and mental retardation. If the choroid has lesions, it can cause glaucoma, optic nerve atrophy, and blindness.
Facial hemangioma can be treated with cosmetic surgery or laser treatment, and patients with severe seizures can be treated with lobes or hemispheres with good surgical results.
(7) Rasmussen encephalitis (syndrome)
Rasmussen encephalitis (Rasmussenencephalitis, RE) is a sporadic disease of unknown etiology that originates in childhood. It is mostly manifested as partial epilepsy or persistent epilepsy in the early stage, and its imaging manifestations are progressive hemisphere atrophy and T2 And / or FLAIR exception signal. Drug treatment has no obvious effect, and the development of the disease to the advanced stage will lead to hemiplegia and mental retardation in children. Antiepileptic drugs have poor efficacy, and some patients with hormonal shock therapy or immunoglobulin therapy can provide short-term relief. The constant seizures and hemiplegia seriously affect children's normal development, education and adult work. Removal of the affected hemisphere is the only effective method to control epilepsy.
RE therapy has two goals: to stop seizures and to impair neurological function. Focal resections in patients with RE generally do not control seizures, and hemisphere excision and hemisphere dissection are the only effective methods to achieve complete control of epilepsy. It is advocated that once the diagnosis of RE is confirmed, surgical treatment should be carried out as soon as possible. RE disease itself determines its drug refractory and patients' inevitable cognitive decline and motor nerve function damage. Early surgical treatment can effectively control seizures and protect them. Healthy lateral brain development to compensate for the function of the diseased lateral brain. Hemisphere disconnection is recommended for RE encephalitis.
In RE patients, the complete remission rate of epilepsy ranges from 62.5% to 85%. In the recently reported cases of RE surgery, functional hemisphere resection and cerebral hemisphere dissection are mostly used. Professor Luan Guoming concluded that the complete remission rate of surgical epilepsy in 20 patients with RE was 80%. The hemispheric disconnection technique has lower complications than the anatomic hemisphere. One disadvantage compared with anatomic surgery is the incomplete residual seizures. In experienced centers, this technique does not affect surgical outcomes. After hemisphere surgery, patients' cognitive function has improved to a certain extent compared with before surgery. After regular limb and language rehabilitation exercises, the patient's proximal muscle strength can reach level IV or higher. They can walk without relying on external force, but the distal end The fine movement function of the limb, especially the hand, is lost, and the patient can communicate more skillfully after the operation.
(8) Temporal lobe epilepsy
Medial temporal lobe epilepsy can be directly related to complex febrile seizures. Seizures in children are a common cause of epilepsy in the medial temporal lobe. About 2% to 4% of children with febrile seizures may develop epilepsy, with a higher incidence in those with a family history of epilepsy. Medial temporal lobe sclerosis is an important cause of medial temporal lobe epilepsy, and perinatal injuries and febrile seizures are one of the causes of medial temporal lobe sclerosis. The temporal lobe damage caused by febrile convulsions and birth trauma in children is mostly bilateral, with a wide range. Adult temporal lobe lesions are mostly unilateral, and the range is limited. In addition, medial temporal lobe tumors, vascular diseases such as cavernous vascular malformations, craniocerebral trauma, intracranial infections, hypoxia, degenerative diseases, and abnormal cortical development are also common causes of temporal lobe epilepsy.
Indications: unilateral medial temporal lobe epilepsy with hippocampal sclerosis; medial temporal lobe epilepsy with structural lesions, such as medial temporal lobe tumors, vascular malformations, cortical dysplasia, trauma and ischemic damage, etc. ; Cryptogenic temporal lobe epilepsy, who is confirmed by comprehensive preoperative assessment to be located on one side of the temporal lobe.
Contraindications: Patients with severe medical conditions who cannot tolerate surgery; Patients with independent origins of epilepsy on both temporal lobe, contraindicated bilateral temporal lobe resection.
Surgery: Resection of anterior temporal lobe and medial structure, one side of temporal lobe epilepsy, but it cannot be clearly distinguished that epilepsy originated from the medial temporal lobe structure or temporal cortex. Selective resection of the medial temporal lobe, and intracranial electrodes confirm that epilepsy originated from the lateral temporal lobe structure. This surgical method is feasible.
(9) Frontal lobe epilepsy
Various intracranial abnormalities involving the frontal lobe can cause frontal lobe epilepsy. For example: tumors, vascular malformations, cortical dysplasia, trauma, etc. There are many patients with no obvious abnormal changes in imaging examination, which is called cryptogenic epilepsy. Frontal lobe seizures are complex and changeable, but they have some common features. In general, frontal lobe seizures have the following characteristics: the onset and end of the attack are short, and the duration is short, which can be as short as a few seconds to tens of seconds, usually not more than 1 minute; the seizures are frequent, often clustered, up to several times a day or even Hundreds of seizures; There is no or only a short hazy state after seizures, and consciousness usually recovers quickly; Frequent seizures during sleep; Outstanding symptoms of tonicity or exercise posture; Common complex gestural automatics when onset Various forms of seizures can be quickly followed by generalized seizures or seizures.
Indications: The MRI shows clear lesion boundaries; EEG localization and MRI localization of lesions coincide between seizures and periods; The symptomatic manifestations of epileptic seizures coincide with the origin of the frontal lobe, electrophysiological location, and imaging location; The epilepsy foci are reachable during surgery and do not involve the cortex of important functional areas; There are no other potential epileptic abnormalities.
Contraindications: Primary generalized seizures; Cases with diffuse brain damage or multiple epileptogenic lesions; Patients with severe medical conditions who cannot tolerate surgery.
Surgical methods: selective epilepsy resection; the predominant hemisphere of total frontal lobe resection in the central region should retain 2.5 cm of brain tissue in the posterior frontal gyrus (Broca's region).
Frontal lobe epilepsy surgery is not as effective as temporal lobe epilepsy, mainly because preoperative epilepsy focus assessment is difficult, sometimes important functional areas cannot be completely removed, and intracranial buried electrodes and cortical electrical stimulation are used to locate the epilepsy focus before surgery. And determining the relationship between epileptogenic focus and brain functional area can improve the efficacy of surgery and the quality of life of patients after surgery.
(10) Island Leaf Epilepsy
In limbic epilepsy without structural lesions, the island leaf is part of the epilepsy network. In island leaf epilepsy with structural lesions, island leaf brain tumors are mainly gliomas, which are more common in low-grade gliomas, such as low-grade astrocytomas, oligodendrocyte gliomas, and ganglion cell tumors. Others, such as cortical dysplasia, etc., or vascular lesions such as vascular malformations, bleeding, infarction, etc., or various encephalitis such as herpes encephalitis. Most of these lesions are first symptoms of epilepsy.
Due to the complex anatomical structure of the island leaf, it is difficult to diagnose and operate the island leaf epilepsy. Epilepsy electrode placement is the gold standard for diagnosis of island leaf epilepsy. The operation of island leaf epilepsy is generally treated by island leaf resection or island leaf burns. With the advancement of diagnosis and treatment technology, the total postoperative seizure-free rate of island leaf epilepsy has reached about 70%.
(11) Central area epilepsy
Common causes of epilepsy in the central area are mass lesions. 63% of seizures from the central area are associated with tumors. The most common are astrocytomas, followed by meningiomas, oligodendroglioma, hemangiomas, and metastases. tumor.
The surgery for epilepsy in the central area uses microsurgical techniques to accurately and selectively remove epilepsy foci; small areas of epilepsy in the functional area must be carefully weighed against the advantages and disadvantages of epilepsy relief and loss of function. Cortical electrical stimulation technology in the awake state is the gold standard for brain function positioning. Performing functional area surgery on patients who can cooperate with awake electrical stimulation during surgery will greatly improve the protection of nerve function during surgery. Low-power electrocautery is a safe and effective method for treating epilepsy in the central area.
The main complications after surgery in the central area are motor and / or sensory function impairment. Generally, sensory function impairment does not seriously affect patients' daily work and life. Central facial paralysis, contralateral limb muscle decline, and fine movements occur early after surgery. Functional decline, generally relieved and recovered gradually after symptomatic treatment and functional exercise.
(12) Parietal and Occipital Lobe Epilepsy
There are many similarities with the etiology and mechanism of frontal and temporal lobe epilepsy and surgical treatment, which will not be described in detail.
(13) Hemi-brain pathological epilepsy
Hemisphere megacephaly; Sturge-Weber syndrome; Rasmussen encephalitis; epilepsy caused by diffuse lesions on one side of the hemisphere caused by trauma, bleeding, meningoencephalitis, etc. are indications for hemisphere resection / dissection. In 1929, WalterDandy first applied anatomical cerebral hemisphere resection to treat patients with diffusely growing gliomas on one side of the hemisphere. There have been several improvements so far. At present, hepatectomy is most commonly used for surgery. The dissection technique minimizes the removal of the brain tissue and maximizes the dissection of the brain tissue. The purpose is to reduce the perioperative period and long-term complications, while maintaining the effect of surgical control of seizures consistent with anatomical hemisphere resection.
Cerebral hemisphereectomy is used to treat intractable epilepsy, and the complete remission rate of seizures is between 80% -90%. Patients can walk independently after surgery, and their cognitive function is significantly improved compared with before surgery.
4. New ideas for surgical treatment
Epilepsy surgery is an emerging discipline, with new ideas and new technologies emerging. The treatment concept of epilepsy surgery represents the current direction of the latest knowledge of epilepsy surgery. It is a direction guide to the advancement of surgical treatment and a fundamental guarantee for the correct view of epilepsy surgeons. .
(1) Secondary epilepsy should be treated as soon as possible
The traditional view is that "the combination of two drugs still cannot effectively control seizures for two years, and more than 4 seizures per month are called drug-refractory epilepsy, which can be used as an indication for surgery." With clinical research According to observations, this view is currently considered to be wrong. The views of many well-known epilepsy centers at home and abroad believe that all non-benign secondary epilepsy should be comprehensively evaluated. If the onset of epilepsy can be identified, surgery should be performed as soon as possible. Treatment, he believes that seizures will damage the development of the nervous system, causing patients, especially children, to decline or fall back in intelligence, and that the frequency of seizures will gradually increase with the progress of time, and epilepsy drugs will also increase damage to nerve function and the whole body.
(2) Children's brain function has good plasticity
For many years, epilepsy experts have been arguing about early diagnosis of epilepsy, early surgery, or surgical intervention when the drug can not be controlled, especially for one side of the brain that is more serious and requires multiple lobe resections, even the brain. Patients with hemisphere resection. At present, most surgical experts have formed a unified view. Frequent discharge of epileptic focus and frequent seizures will lead to developmental disorders of brain function. Children's brain function has good plasticity. Even if there is a certain degree of brain damage after early surgical treatment, It can also have a strong compensatory ability because the child's brain is still developing, and will not cause more serious neurological damage.
(3) Highly selective resection of precise positioning of epilepsy foci is the mainstream direction of the development of epilepsy surgery
There are functions in any part of the brain. For example, the "dumb areas" of brain functions such as the frontal pole and temporal pole are relative to the primitive cortical functional areas such as language, motor, and vision. Based on this concept, we believe that the surgical treatment of epilepsy should not use large-area brain tissue resection, but should be developed in the direction of precise positioning of highly selective resection of epilepsy focus. Highly selective resection of epilepsy foci under the guidance of intracranial electrodes is the removal of epilepsy foci with the greatest possible preservation of brain tissue, and it is the mainstream development direction of epilepsy surgery.
(4) Neuromodulation is a new bright spot in epilepsy surgery
More than 50% of patients with intractable epilepsy are not suitable for resection surgery due to various reasons, such as scattered or inaccurate positioning of epileptogenic focus, or inability to be removed because of epileptic focus in the functional area. Unable to effectively control seizures, and have large systemic side effects. For such patients, neuromodulation techniques are an effective treatment option. Neuromodulation is defined as a treatment model that uses the electrical or chemical means to obtain a therapeutic effect by changing the function or state of the nervous system at the level of neuroscience. This technology involves multiple disciplines and multiple diseases. In terms of epilepsy treatment, it is a brand-new field that has gradually been recognized and developed rapidly after pain and sports diseases, such as vagus nerve stimulation, bilateral hippocampal electrical stimulation, and cortical electrical stimulation. Neuromodulation technology has the advantages of minimally invasive, reversible treatment and small side effects in the treatment of epilepsy. It is a new direction and new hot spot in the treatment of epilepsy.

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