I. Overview
Epilepsy is a paroxysmal discharge of neurons in the brain, causing various manifestations that can be detected clinically by both the patient and the observer, excluding spinal myoclonus due to spinal neuronal activity, tensor induced clonus or flexor spasm in paraplegia, migraine or epileptiform discharges due to inhibition of neuronal activity caused by cerebral hemorrhagic disease. When spontaneous seizures develop into chronic recurrent seizures, it can be called epilepsy.
Traumatic epilepsy refers to limited or generalized spasms secondary to craniocerebral injury, and can be divided into early epilepsy (within 1 week after injury) and late epilepsy (1 week to several years after injury); in early epilepsy, the seizures occurring within 24 hours after injury are called immediate seizures, and those occurring 2 to 7 days after injury are called recent seizures or delayed seizures. In terms of etiology, early epilepsy is mostly associated with cerebral contusions, depressed fractures, acute cerebral edema, subarachnoid hemorrhage and intracranial hematoma, which are mostly temporary seizures; late epilepsy is mostly caused by cerebral-membranous scar, old depressed fracture compression, cerebral abscess, intracranial foreign body, chronic subdural hematoma, etc., which are mostly persistent.
II. Epidemiology
1.Incidence
(1) It is generally accepted that the overall incidence of epilepsy observed clinically after craniocerebral injury is 5%-15%. Other statistics show that the incidence of epilepsy in the general population is 0.5%-2%, the incidence of post-traumatic epilepsy is 2%-2.5%, and the incidence in those with penetrating craniocerebral trauma is as high as 50%. The incidence after open and closed craniocerebral trauma is 20%~50% and 0.5%~5%, respectively, and the incidence of firearm and non-firearm open injuries is 42.1% and 16.4%, respectively.
(2) Early epilepsy accounts for 5%, 1/3 occurs within 1 hour after injury, 1/3 occurs 2~24 hours after injury, 1/3 occurs 2~7 days after injury, mainly related to intracranial hemorrhage, depressed fracture and foreign body irritation. Early epilepsy is more common in children, but the incidence of late epilepsy in children is significantly lower than that in adults.
(3) Late epilepsy accounts for about 84%, with more than half occurring within 1 year after injury, 70%-80% within the second year, and about 1/5 starting 4 years after injury and more persistent; mainly related to brain tissue scar formation, brain atrophy and intracranial infection, brain abscess formation, intracerebral cysts, brain penetrating malformations, foreign body retention and fracture fragments.
(4) Twenty-five percent of early epilepsy can be continued into late epilepsy, but the occurrence of late epilepsy is not related to the type and number of seizures in early epilepsy.
(5) The incidence of epilepsy gradually decreases with time, and the risk of seizures in the majority of patients 5 years after trauma is not different from that of the general population.
2. Risk factors
The incidence of traumatic epilepsy is 12 times higher than that of the general population. Factors associated with causing post-injury epilepsy include
(1) Site of injury The closer to the cortical motor area or the hippocampus and amygdala of the medial temporal lobe, the more likely epilepsy will occur.
(2) Type, nature and extent of injury The incidence of subdural hematoma and intracerebral hematoma in early epilepsy is 30% to 36%, the incidence of epidural hematoma, depressed fracture of the frontal or parietal bone is 9% to 13%, and the incidence of mild brain injury without neurological signs is only 1% to 2%.
(3) Age The incidence of early epilepsy after traumatic brain injury is high in children under 5 years old, and they are prone to persistent epilepsy; traumatic epilepsy is mainly concentrated in young people, and there are more males than females.
(4) Whether it is open brain injury The incidence of severe head trauma with neurological deficit and cortical injury is high, especially if the dura rupture is present.
(6) Penetrating brain injury is higher than non-penetrating injury (5 to 10 times). The incidence after open brain injury and closed craniocerebral trauma is 20%~50% and 0.5%~5%, respectively, and the incidence after firearm and non-firearm open injury is 42.1% and 16.4%, respectively.
(5) The incidence is high in those with respiratory distress and shock after injury, and is closely related to subarachnoid hemorrhage, acute cerebrovascular spasm, and intracerebral hematoma.
3.Predictors of the incidence of late epilepsy
(1) Early seizures after traumatic brain injury.
(2) Risk factors for late seizures Limited neurological deficits at the first check, projection-induced brain injury, frontal lobe injury, intracerebral hemorrhage, extensive cerebral contusion, prolonged post-injury amnesic symptoms, depressed fracture, and cortical-subcortical injury.
(3) Presence of pathologically abnormal EEG manifestations.
(4) Medical factors such as antiepileptic drugs can cause hypotension, which causes hemodynamic instability and further decrease of blood flow to the tissue in the brain injury area.
(5) Late epilepsy can occur in about 1/5 patients with epidural hematoma and about 1/2 patients with subdural and intracerebral hematoma; late epilepsy can occur in 1/3 of those with open cranial injury, especially firearm injury.
Third, pathology
Cortical contusion foci are the most important seizure factors. Microscopically, axonal fracture and stretching, secondary dense ball formation, gliosis; degeneration of damaged brain tissue, grayish color, hard texture, increased fibrous tissue content, yellowish tissue, striated tissue, fat-like tissue, granuloma tissue, formation of small sacs and cavities, accumulation of blood, fluid or pus in the cavity, multiple cerebral gyrus, cerebellar gyrus, etc.
4. Pathogenesis
It is now mostly believed that traumatic epilepsy is induced by traumatic brain injury on the basis of genetic factors. The ignition model does not explain the ability of 50% of patients to spontaneously remit. It is generally believed that factors that act as subthreshold stimuli or lead to lower cellular excitability thresholds during the formation of post-traumatic epilepsy include alterations in the biochemical environment inside and outside the cell after trauma, deposition of iron-containing heme in the neurofibrillary network, scarring left after traumatic brain injury, elevated levels of excitatory amino acids, and displacement of axonal endings. Specifically, the main hypotheses of traumatic epilepsy are.
(1) Mechanical effects of brain tissue injury Degenerative changes such as gliosis and scar formation and reduced or absent neuronal numbers after traumatic brain injury underlie the pathogenesis of traumatic epilepsy.
(2) Biochemical mechanisms of brain tissue injury Brain injury or cortical laceration causes extravasation and lysis of erythrocytes, deposition of hemoglobin on the neural network, and freeing of calcium ions from hemoglobin and transferrin, which are pathological histological features of post-traumatic epilepsy in humans. This iron salts and unsaturated fatty acids or subcellular organelle structures of ferrous heme can lead to free radical oxidant formation and non-enzymatic lipid peroxidation reactions, which can lead to impairment of cellular function.
(3) Cellular mechanisms of brain injury Caused by brain injury causes changes in the density and distribution of ion channels on neuronal cell membranes and alterations in plasma membrane ion permeability, resulting in increased extracellular potassium ions and decreased calcium ions, causing repeated episodes of cellular depolarization drift (PDS). Derangement of cellular hyperpolarization braking mechanisms can decrease and synchronize local neuronal activity from interictal to ictal firing.
(4) Pathophysiological mechanisms The main mechanisms are altered cerebral blood circulation, mechanical effects of meningeal scarring and gliosis, disruption of the blood-brain barrier and disruption of neuronal glial relationships, disruption of the axonal collateral inhibitory system, and instability of cellular metabolism and neurochemistry.
(5) Increased transcription of “immediate-early genes” (C-fos, C-jun, etc.) in neuronal cells after trauma leads to axonal outgrowth and synaptic reorganization, causing further increase in neuroexcitability and resulting in seizures.
V. Risk assessment
Specific risk factors for early onset seizures Penetrating traumatic brain injury, intracranial hematoma, hemorrhagic contusion, cortical laceration, linear or depressed skull fracture, coma >24 hours, focal neurological symptoms and children under 5 years of age.
Specific risk factors for late onset Penetrating traumatic brain injury, intracranial hematoma, hemorrhagic contusion, cortical laceration, depressed skull fracture, coma >24 hours, and early onset.
Patients with penetrating craniocerebral injury are at greatest risk for early and late seizures and seizure foci formation of the longest duration.
In the noncombatant population, the greatest risk factors for late seizures are subdural hematomas and cerebral contusions.
VI. Classification
Early epilepsy Within 3 to 4 days after injury, mostly seen under 5 years of age, especially under 2 years of age, mostly triggered by cerebral contusion, subarachnoid hemorrhage, intracranial hematoma or acute cerebral edema, and prone to persistent status epilepticus.
Delayed epilepsy Within a few days to 3 months after injury, mostly in children with penetrating injuries and depressed fractures.
Late epilepsy More than 3 months after injury, mostly related to local meningeal-brain scar formation, ventricular penetration malformation, cerebral atrophy, hydrocephalus, intracranial local foreign body retention, late onset infection, etc. of cranial injury.
VII. Clinical manifestations
The clinical symptoms of epilepsy are characterized by diversity and complexity, and can manifest as different dysfunctions of sensation, behavior and autonomic nerves or both. Common types of generalized seizures include atonic seizures, myoclonic seizures, clonic seizures, tonic seizures, and tonic-clonic seizures. Focal (partial) seizures are seizure types in which seizure symptoms as well as the initial EEG of the seizure show that the EEG seizure is confined to a specific neurological region in one hemisphere, and can be divided into simple partial seizures without impaired consciousness and complex partial seizures with impaired consciousness, both of which can develop into full-blown seizures with tonic clonic convulsions.
Traumatic epilepsy is dominated by grand mal seizures and limited seizures. Children with prolonged and frequent uncontrolled seizures may have unresponsiveness, mental retardation and dullness.
The site of brain tissue injury usually corresponds to the site of post-traumatic epilepsy, and the clinical manifestations depend on the involved cortical and subcortical areas: prefrontal lesions are predominantly generalized seizures; injuries in and around the precentral and posterior gyrus of the cerebral cortex are predominantly limited motor seizures, Jackson seizures, and generalized spastic seizures, and partial seizure continuity is also seen; central and parietal lesions often cause contralateral limb The central and parietal lobe lesions often cause motor or sensory seizures in the contralateral limb; temporal lobe lesions often cause psychomotor seizures; and occipital lobe lesions often show visual seizures.
The incidence of early posttraumatic epilepsy is around 5%, with children under 5 years of age being particularly susceptible. Early post-traumatic epilepsy in children has two characteristics: seizures can be induced even with minor brain injury; even if the primary traumatic brain injury is not severe, persistent status epilepticus is likely to occur.
After the first seizure, there is often a certain interval, and then the frequency gradually increases. 25%-30% of these seizures stop within 2 years or a little longer by themselves, and half of them can improve or tend to stop in about 5 years, and most of those who still have seizures can be controlled by drugs, and the prognosis for a few intractable epilepsies that cannot be controlled is poor.
The majority of late seizures have at least one generalized seizure, but partial seizures are still the main type of late seizures and are more likely to recur and form long-term epilepsy, especially after the formation of epileptic foci.
About 1/3 of late traumatic seizures are temporal lobe epilepsy with psychomotor seizures, and about half of them are limited motor seizures or transform into generalized grand mal seizures.
Late epilepsy has a tendency to worsen and can evolve from partial seizures to generalized seizures, accompanied by memory loss, personality disorders and mental retardation in severe cases. The later the late seizures, the more likely the seizures will persist; 5 years after trauma, the risk of seizures falls to normal levels except for penetrating injuries.
VIII. Diagnosis and differential diagnosis
1.Diagnostic conditions
(1) A clear history of traumatic brain injury, especially open injury and firearm injury.
(2) No history of epilepsy before the trauma, no family history of epilepsy, or history of febrile convulsions.
(3) No other brain and systemic diseases that cause epilepsy, such as brain tumors and central nervous system infections.
(4) Have typical seizure manifestations.
(5) The seizure type is consistent with the site of traumatic brain injury and what is seen on the EEG.
(6) Skull X-ray plain film shows depressed fractures, fracture fragments, and metallic foreign bodies.
(7) CT and MRI show brain-dural adhesions, brain atrophy, brain softening foci, and brain penetration malformations.
(8) Electroencephalogram (EEG) shows typical spike waves, spike slow waves, paroxysmal slow waves, and more often spike waves and spike slow waves in children, but the positive rate is only 40%.
2.Caution
(1) Exclude other factors that may trigger epilepsy, such as hypoxia, metabolic abnormalities, intracranial occupancy, alcohol consumption, taking psychiatric drugs and tricyclic antidepressants, etc.
(2) Seizure manifestations (especially complex partial seizures) in those with impaired consciousness are easily overlooked, and nonepileptic seizures, myoclonus, and syncope are easily misdiagnosed as epilepsy and should be considered in conjunction with a history of trauma and ancillary findings.
(3) Todd syndrome is a focal neurological dysfunction after partial or generalized tonic-clonic seizures and is a temporary functional disorder 24 to 48 hours after seizure.
(4) Emerging motor, sensory, and speech deficits are alert for post-traumatic seizures.
(5) Those with symptoms disproportionate to mild post-traumatic head injury (e.g., epileptic seizures or blurred consciousness) should continue to be examined for the presence of other intracerebral lesions.
(6) Post-traumatic non-epileptic seizures (NES, pseudo seizures, cardiogenic seizures) often coexist with epileptic seizures and should be clarified by EEG (especially video EEG) and post-ictal lactate examination.
(7) Cranial trauma caused by seizures is not considered traumatic epilepsy.
3. Basic requirements
(1) First determine whether it is epilepsy, then determine the site of the epileptogenic focus, and the most accurate diagnostic method is EEG.
(2) Typical cases can generally be diagnosed based on the history of head trauma, clinical seizure characteristics and previous history of similar seizures; atypical cases or cases with first seizure for a long time after trauma require detailed medical history, combined with clinical manifestations, electrophysiological examination and imaging examination for comprehensive judgment.
(3) It should be noted that about 20%-30% of patients with non-epileptic seizures are misdiagnosed as epilepsy, especially syncope, psychogenic seizures, sleep disorders, deep sleep state and migraine should be identified; about 15% of patients misdiagnosed as epilepsy are treated with antiepileptic therapy; about 10% of patients with epilepsy are misdiagnosed as non-epileptic seizures.
4. Basic procedures
(1) The first stage is to rule out hysterical and psychogenic seizures, such as neurosis, syncope, nocturnal non-epileptic seizures with seizure characteristics (dream terrors, sleep apnea), extrapyramidal disorders and poisoning.
(2) In the second stage, whether the seizure is organic, episodic or initial, the diagnosis of electrolyte or metabolic disorders should be confirmed and corrected, head CT, cardiovascular system, blood and urine routine, electrolytes, blood glucose, blood osmolality, erythrocyte sedimentation rate and other examinations should be performed. The relationship between day and night, observation of reactivity, repetition ability, motor or sensory symptoms, aphasia, and performance after the seizure, etc.
5. Auxiliary examinations
(1) Structural imaging
Cranial X-rays are of little significance, and conventional cranial CT has been largely replaced by MRI.
(1) Cranial CT Intracranial hematoma and epidural hematoma with intracranial satellite foci shown by CT are significantly associated with post-traumatic epilepsy and are also helpful in the diagnosis of tuberous sclerosis.
② Cranial MRI is superior to CT in the diagnosis of diffuse axonal injury, medial temporal lobe and inferior frontal lobe contusions. Typical imaging findings include enlargement of the subarachnoid space and ventricular system, cortical atrophy, arachnoid cysts, and foci of anterior temporal gliosis. Magnified thin-layer scans perpendicular to the axial position of the temporal horn often clarify central temporal lobe sclerosis associated with recurrent partial seizures.
(2) Functional imaging
① Magnetic resonance functional imaging Localized hypovolemia or hypometabolism in the interictal period can be seen.
② PET 18F-fluorodeoxyglucose (FDG) or 15O positron emission tomography (PET) demonstrates reduced metabolism in the interictal epileptic focus to a greater extent than expected; PET is highly accurate in diagnosing temporal lobe epilepsy, but is less reliable for those epilepsies that are difficult to localize and have poor surgical outcomes.
(3) Single photon emission computed tomography (SPECT) Interictal scans are less accurate than seizure scans and often require medical staff to be ready to inject radionuclides into the patient 24 hours a day.
(3) Electroencephalography (EEG) is the primary tool for the diagnosis of epilepsy and provides information on the localization of the epileptogenic focus.
① Standard tests Single or multiple slow waves are common in all types of epilepsy, but a more meaningful differentiator between seizures is the form of epileptiform discharges, including spike, spike-slow complex, spike, and spike-slow complex waves; epilepsy originating from the cerebral cortex is often high amplitude spike, spike, spike-slow wave, or spike-slow wave complex; those with deep lesions are often spike or spike-slow complex waves with lower amplitude. The localization of epileptic foci is based on waveform, amplitude, and phase, but also on the synchronization of seizure waves (bilaterally synchronized paroxysmal slow waves are mostly central systemic seizures). The distribution of abnormal EEG discharges during the interictal period sometimes does not indicate the localization of epileptic foci; it may be difficult to localize epileptic foci because of multifocal epileptiform discharges, wide spread of abnormal discharges in one or both hemispheres, and drifting of abnormal discharges in one or both hemispheres (especially in pediatric patients).
② Special electrodes Electrodes can be placed in inferior frontal, middle temporal, anterior temporal (for clear display of recurrent partial seizures), nasopharyngeal electrodes (for short-term recording only), subzygomatic electrodes (easy insertion, less artifacts and less pain after placement), and pterygoid electrodes (mainly for long-term EEG video monitoring). When recording temporal lobe complex partial seizures, the onset (and amplitude) of abnormal discharges during the seizure period appeared earliest (and largest) at the pterygoid electrode, and delayed (and decreased) in the order of subzygomatic, anterior temporal, and middle temporal.
③ Evoked Standard EEG is recorded during 30-60 minutes of wakefulness. Hyperventilation and flash stimulation may be used for epilepsy in which the patient’s status is inadequate; sleep EEG monitoring is feasible if awake EEG does not provide diagnostic evidence but epilepsy is still highly suspected.
④ Long-range (24-hour) EEG video monitoring For the most accurate method of identifying and selecting patients for epilepsy surgery. It can detect non-convulsive epilepsy (NCE) or non-convulsive continuous status epilepticus (NCSE) without obvious clinical manifestations after brain injury and high risk factors for seizures, and should be used as a routine examination for comatose patients with traumatic brain injury to help the diagnosis of the degree of coma and the estimation of traumatic brain injury, and also to observe critical conditions such as secondary brain hemorrhage and cerebral vasospasm after brain contusion in a timely manner. The use of anterior temporal electrodes is mostly recommended, and pterygoid electrodes are used only when seizure foci cannot be identified with the 10-20 system and anterior temporal electrodes.
⑤ Traumatic long-range cortical EEG video monitoring is mainly used in cases where the epileptic focus cannot be localized within the cerebral hemisphere (e.g., poor localization between two lobes, or if the epileptic focus is located in or close to a functional cortical area); commonly used electrodes are oval hole electrodes, subdural strip electrodes, deep electrodes, and subdural raster electrodes.
(6) Cortical EEG tracing method Mainly in craniotomy under awake or superficial anesthesia to determine the epileptic focus and the extent of surgical resection, and as a pre- and postoperative control.
(4) Intracarotid isopentobarbital test Primarily used preoperatively to determine the dominant language hemisphere and also to monitor memory integration function in the contralateral cerebral hemisphere (e.g., residual temporal lobe function after resection of epileptic foci).
(5) Prolactin measurement May be increased 20 to 40 minutes after generalized tonic-clonic and many complex partial seizures.
(6) Neuropsychological tests including personality tests (Minnesota Multiphasic Personality Test), memory tests, language function, and intelligence have been used in the early years to help localize epileptic foci, especially to determine the left and right hemispheres.
(7) Immediate early genetic testing Including c-fos, c-jun, Jun-B, and Jun-D. The expression of c-fos can be used as an objective and reliable method to localize the site of epilepsy and the transmission pathway.
IX. Treatment
1.Prevention priority and etiological treatment
Early post-traumatic epilepsy should be treated by first removing seizure-inducing factors, timely debridement, suture repair of dura, early use of dehydrating agents to reduce cerebral edema, application of antibiotics, prevention of infection, and reduction of scar formation.
Prophylactic treatment with drugs Early prophylactic application of antiepileptic drugs (such as phenobarbital, phenytoin sodium and carbamazepine) can reduce the risk of early seizures, with the best effect of prophylactic application within 1 week after the injury, but is not effective for late seizures.
2. Prerequisites for treatment
(1) A reliable diagnosis of seizures or epilepsy.
(2) Confirmation and exclusion of diseases requiring etiologic treatment Such as early seizures often require surgery for primary or secondary brain injury and complications, and late epilepsy with surgical removal of epileptic foci can improve the prognosis of patients with brain injury.
(3) Determine the indications for antiepileptic drug therapy.
(4) Selection of appropriate drug therapy.
(5) Treatment initiation, conduct, and conclusion.
3.Treatment principles
Traumatic epilepsy is generally treated by internal medicine, except for a few requiring surgery. Anti-epileptic drug therapy should be performed as early as possible in monotherapy, and intractable epilepsy should be diagnosed early and changed to other treatments or surgical treatment.
4. Emergency treatment of seizures
(1) Keep the airway open.
(2) Ensure that the patient is not injured by sharp or hot objects or open machines.
(3) A dental pad can be inserted between the patient’s upper and lower teeth before a tonic seizure. Tracheal intubation with inotropes is feasible in very complicated grand mal seizures (especially those with blood oxygen <85% or gcs score <7). < span="">
(4) Get a history of trauma, monitor drug concentrations, brain CT, MRI, and EEG.
(5) Management of persistent status epilepticus (tonic-clonic grand mal seizures).
① Intubate the trachea, administer oxygen, prepare the ventilator, remove secretions, monitor vital signs, blood glucose and blood gas, and maintain a reasonable body and head position.
② Establish two intravenous accesses, infuse antiepileptic drugs and routine fluids respectively, and strictly record the in and out volume.
③ Firstly, push 50％ GS 40ml intravenously, then drip saline and vitamin C 500mg.
④ Slowly infuse Valium 10mg intravenously, then pump with Valium 20mg/NS 200ml at a rate <2ml/h; after the seizure stops, change to Depakene input with the first dose of 800mg, followed by 400mg/5% GS 500ml at 1~2ml (kg?h) infusion to maintain the concentration to 300~600mmol/L; lorazepam is preferred for pediatric patients. The dose is 0.5mg/kg.
⑤ Maintain partial pressure of oxygen >12kPa and partial pressure of carbon dioxide 4.0~5.7kPa, and provide physical cooling for hyperthermia.
⑥ If the concentration of Depakene reaches the treatment standard but not completely controlled, 2.5% thiopental sodium (0.5g/NS 20ml) can be slowly injected intravenously until the epilepsy is completely stopped, and care should be taken to avoid respiratory depression.
(7) Pay attention to complete control of seizures under the condition of monitoring blood concentration for at least 24~48 hours to avoid recurrent seizures.
5. Drug treatment
(1) Efficiency
About 2/3 of patients can be controlled satisfactorily under the condition of maintaining appropriate antiepileptic drug concentration, but the medication principle of using the smallest drug dose to control seizures without significant toxic side effects must be followed.
(2) Indications for drug therapy
The main indications are chronic, recurrent autonomous seizures and prophylactic medication for some patients, while the patient’s health status and social status need to be evaluated; long-term treatment usually starts after the second grand mal seizure, and medication is recommended for those with more than 2 grand mal seizures per year.
(3) Indications for prophylactic drug therapy
① Severe closed craniosynostosis
② Open cranial penetrating injury in the temporoparietal region
③Secondary mesencephalic syndrome
④ Early onset of seizure within 1 week after injury
⑤ Cerebral contusion combined with EEG lesions and confusion for more than 3 hours
(6) Combined family history of epilepsy
(7) Central temporoparietal penetrating brain injury
⑧ Traumatic intracerebral hematoma or cortical hemorrhage.
(4) Principles of drug therapy
① Start with a single drug, and strive for a drug that can control seizures with minimal toxic side effects and long-term maintenance at low doses.
② If a combination of drugs is required to control seizures, a second drug should be taken.
③ Consider the saturation time to reach steady state and avoid unnecessary adjunctive dosing.
④ Use one-time dose administration as little as possible to reduce toxic side effects.
⑤ The dose should be as small as possible and increased only when necessary.
(5) General approach to drug therapy
① Children at high risk for seizures can be treated prophylactically with antiepileptic drugs, preferably about 1 week after trauma.
② Early-onset epilepsy is mostly temporary and should be treated with antiepileptic drugs for 3-6 months, supplemented with dehydration; late-onset epilepsy should be treated with drugs for at least 2 years, with complete control for 1~2 years before gradual dose reduction.
(3) Generally, medication should be administered according to the type of seizure, so as to completely control the seizure with minimum dose and avoid obvious side effects of medication, emphasizing the medication principles of systematic and regular, sufficient amount and full course, no combination of medication if single medication is effective, regular review, observation of toxicity and slow discontinuation of medication.
④ In persistent epilepsy, Valium and phenytoin sodium are usually administered intravenously, supplemented with dehydrating drugs and hormone therapy, and attention is paid to keeping the airway open.
⑤ Calcium antagonists such as nimodipine and ciprofloxacin are effective in the treatment of intractable epilepsy.
(6) Duration of drug therapy
(6) The general recommended duration is 3 to 5 years, with at least 1 to 3 years of dose reduction.
(7) Phenytoin sodium has a more definite effect in patients with prophylactic indications, but it needs to maintain the blood drug concentration at therapeutic levels for at least 3~6 months before the dose can be gradually reduced.
(8) Generally, drug taper is required once every 2-3 months. Whether to discontinue the drug after several years of drug control is based on EEG monitoring and combined with seizure type and psychosocial factors.
(7) Selection of antiepileptic drugs
Partial seizures or partial secondary grand mal seizures are mostly treated with carbamazepine (carbamazepine); recurrent partial seizures are better with valproate (sodium valproate); generalized seizures without significant focal electrical activity are preferred to valproate; a new antiepileptic drug can be added if the preferred drug is not sufficiently effective.
(8) Contraindications to antiepileptic drugs
① Sodium valproate (family history of liver disease, pancreatic disease and hemorrhagic constitution).
② Benzodiazepine?BZ, DPH (myasthenia gravis, acute glaucoma, drug dependence)
③ Phenobarbital Pb, paroxetone Pr, DPH, carbamazepine, sodium valproate (hepatic porphyria)
④ Carbamazepine, extragastric DPH (atrioventricular block)
⑤ DPH (progressive myoclonic epilepsy, moderate to severe ketoacidosis, tendency to osmolar hypertension)
⑥ Ethosuximide, gamma-vinyl-gamma-aminobutyric acid (history or propensity for psychosis)
(7) DPH, carbamazepine Primary generalized spontaneous akathisia epilepticus.
(9) Monitoring of drug therapy
① Monitoring time It usually takes 5 half-lives for drug administration and excretion to reach equilibrium. 14 days of monitoring is required during treatment, and 1 month for longer half-lives (e.g., DPH or phenobarbital), and every 6 months thereafter.
② Monitoring content Frequency of seizures, history information, seizure form, physical and mental status, EEG and laboratory biochemical values (liver function, blood glucose, antiepileptic drug concentration); blood coagulation status, amoniak and amylase are required for those treated with sodium valproate.
③ Indications Suspected antiepileptic drug toxicity; uncontrollable seizures; pregnancy; concomitant other diseases (liver disease, renal disease, hypoproteinemia, absorption disorder syndrome); adjustment of individual medication; combination of medications; epilepsy in the elderly.
6. Behavioral therapy
The aim is to increase the seizure threshold by stimulating mental performance, and to reduce sensitivity in reflex epilepsy; biofeedback training is also available.
7. Surgical treatment
Surgical treatment is the removal of epileptic lesions localized by EEG, CT, MRI, SPECT or PET, with depressed fractures should be reset, intracranial foreign bodies should be removed, and hematomas or abscesses should be actively removed; antiepileptic drugs need to be continued for a period of time after surgery.
(1) Etiological treatment
The aim of treatment for traumatic epilepsy is to eliminate the cause as much as possible and improve the patient’s prognosis.
② In patients with cranial firearm injuries and open brain injuries, early treatment of the traumatic tract or wound is important.
③ Those who develop early epilepsy should search for the cause, promptly rectify depressed fracture fragments, remove intracranial hematoma and contused brain tissue, and actively control cerebral edema and intracranial infection.
(2) Treatment of epileptic foci
① Single or combined drug therapy can effectively treat 80%-85% of epilepsy, and about 15% require surgical treatment.
② Indications for surgery Post-traumatic epilepsy cannot be controlled by regular medication for 2~3 years, and the seizure frequency is severe (i.e., seizures cannot be controlled by regular antiepileptic medication for 2~3 years, and there is still more than one seizure or significant aggravation within one week) before surgery is considered, or surgery is required for drug-resistant epilepsy or refractory epilepsy; clinical, electroencephalographic and radiological examinations confirm (e.g., hippocampus or amygdala (2) Surgery should only be considered for drug-resistant epilepsy or refractory epilepsy; clinical, electroencephalographic and radiological examinations confirm that there is a clear local epileptogenic focus (e.g. hippocampus or amygdala atrophy, sclerosis); or persistent limited epilepsy with frequent seizures does not cause or aggravate the original neurological dysfunction after resection.
(3) Relative contraindications to surgery Neurotic patients with low IQ, strong emotional instability and poor tolerance, and lack of family support to adapt to society should not be operated on. Caution should be exercised in intractable epilepsy because post-traumatic epilepsy has a tendency to heal spontaneously (about 50% remit within 5-10 years, and 2/3 can be satisfactorily controlled with antiepileptic drug therapy) and is often polygenic, and control is still unsatisfactory after removal of the major lesion.
④ Surgical indications for reference: refractory epilepsy, where first-line antiepileptic drugs have been ineffective for more than 2 years of systematic and regular treatment; the origin of the seizure, i.e., the epileptogenic focus, has been clearly identified; consideration of the postoperative period does not cause important functional deficits; and the patient and family have a good understanding of the treatment and a strong desire for surgery.
(3) Preoperative diagnosis
① Diagnostic steps The first step is the localization of the epileptogenic focus, and the second step is to clarify whether the epileptogenic focus is located in an important functional area (language area, central zone, and brain areas that bear memory functions, etc.).
② Caution Even if a morphological lesion is found, the site of localized epileptic activity must be further determined, and the site of abnormal EEG during seizures is usually the site of the epileptogenic focus.
(4) Purpose of surgery Removal of the epileptogenic focus or blocking the spread of local epileptiform activity to improve or eliminate symptoms.
(1) Epileptogenic foci resection includes cortical resection, lobectomy (temporal lobectomy, lobectomy, hemisphere resection), and selective amygdala-hippocampal resection.
When the epileptogenic foci are located in important functional areas such as motor, sensory or speech, only part of the epileptogenic foci can be removed, but not all of the scar can be removed, and every effort should be made to preserve the soft meninges and nearby blood vessels.
③ Functional surgery includes corpus callosotomy, multiple submural transverse fiberotomy (MST), electroencephalography, brain stereotactic surgical radiation (gamma-knife, X-knife), and brain stereotactic disruption.
④ Anterior temporal lobectomy has become the main treatment for temporal lobe epilepsy. When performing left temporal lobectomy, care should be taken to avoid causing aphasia. Generally, the left temporal lobe can be resected 125px from the temporal apex backward, and the right temporal lobe can be resected 150px, preferably not exceeding the Labbe vein.
At present, full joint dissection (the whole corpus callosum, hippocampal joint and anterior joint) is rarely used, and anterior 2/3 dissection of the corpus callosum (5-150px in length, 2mm in width, 0.9-25px in depth) is mostly used; care should be taken not to cut through the ventricular canal, and bilateral cingulate cortex dissection (37.5px×50px) can be performed at the same time for those with psychosis and mania and enhanced excitability. 50px).
(6) Multiple subchondral transverse fibrous resection is indicated for those with epileptic foci located in important functional areas, and the epileptogenic foci cannot be completely resected.
(7) Hemispherectomy includes anatomical hemispherectomy, modified anatomical hemispherectomy, functional hemispherectomy, hemispherectomy with preservation of white matter, and hemispheric dissection. The aim is to preserve the basal ganglia and thalamus, and to remove one hemisphere in its entirety; care should be taken to gradually block the cortical arterial flow, and the basilar arterial ring and the arteries distributed in the basal ganglia of the thalamus should be preserved.
(8) Stereotactic brain dissection includes amygdala dissection, Forel H dissection, internal capsule dissection, posterior internal hypothalamus dissection, pallidum or combined pallidum dissection, fornix dissection, etc.
⑨ Electroencephalographic stimulation is the use of deep brain electrodes to place and stimulate certain nuclei in the brain to produce inhibitory neurotransmitters in the brain tissue and reduce the excitability of the cerebral cortex for the purpose of treating epilepsy, mainly cerebellar hemisphere stimulation, thalamic base nucleus stimulation and vagus nerve stimulation, etc.
X. Prognosis
1. Stage I The first seizure after trauma is treated by removing the cause.
After several years, most of them have a few recurrences in a relatively short period of time, and then enter into lasting remission; 70% of them are maintained without seizures after stopping medication, and 30% continue without remission, forming a potentially chronic intractable epilepsy.
3, Stage 3 Lifetime remission (cure) or becoming chronic intractable epilepsy.
4. In patients with persistent seizures, drug treatment can lead to final remission in 20% of patients, and the rest need to be combined with surgery or other methods of comprehensive treatment; generally, temporal lobectomy has the best effect, and patients with temporal lobe structural lesions and unilateral temporal lobe epilepsy have the best effect, those with bilateral temporal lobe lesions with one dominant lesion have a slightly worse effect, and those with extratemporal lobe lesions have a poorer effect; postoperative drug antiepileptic treatment needs to be maintained for at least two years .