The etiology of epilepsy is numerous and complex, with only about 1/3 of newly diagnosed cases having a clear etiology. In children, congenital neurological defects such as cerebral palsy may be the primary cause of epilepsy, while cerebrovascular disease is the most common cause in adults, accounting for approximately 12% of new cases. Different age groups, as well as different geographic and even ethnic groups, have different etiologies, but some patients have been unable to find a cause for their onset. Epilepsy with a definite cause is usually referred to as symptomatic or secondary epilepsy, and epilepsy in which no organic brain lesion or metabolic disease can be found is referred to as primary or cryptogenic epilepsy.
The epilepsy of primary origin, also known as idiopathic epilepsy, is a type of epilepsy that does not have any underlying cause other than genetic factors, and in which detailed history and physical examination and all available tests have failed to demonstrate the presence of organic lesions in the brain that cause seizures or signs of systemic metabolic disease, accounting for about 2/3 of epilepsy. It is characterized by age-dependent onset, generalized seizures, whole-brain EEG, bilateral symmetric synchronous spike and slow complex waves, and a significant family genetic predisposition. These patients have generalized tonic-clonic seizures, atonic seizures, or myoclonic seizures. Secondary epilepsy, also known as symptomatic epilepsy or acquired epilepsy, is only a symptom of brain disease or systemic disease and accounts for about 23% to 39% of all epilepsy patients. With the continuous progress of medical science and the introduction of advanced medical instruments, the detection rate of brain lesions has been greatly improved. A portion of the so-called primary epilepsy for which no cause could be found has found a cause. There are also some patients with the progress of the disease, the cause may gradually reveal, such as the early stage of some brain tumors, imaging also failed to suggest abnormalities, clinical performance is cool like primary epilepsy, and then the disease progresses, and then the review may find abnormalities, that is, the diagnosis rate of primary epilepsy will be relatively high, while the actual shrinking.
I. Genetic factors.
The chance of having epilepsy in the offspring caused by one father having epilepsy is about 6%, and 2 times higher in those whose mother has epilepsy. If both parents have primary epilepsy, the chance of having epilepsy in the offspring will rise to 9%-12%. The genetic factor has an important significance for primary epilepsy.
Prenatal and intrapartum injuries
Prenatal and intrapartum injuries and brain formation disorders are common causes of neonatal and infantile epilepsy. Early embryonic rubella, cytomegalovirus infection, uterine hemorrhage, radiation exposure, severe physical illness of the mother, certain drugs and chemical reagents can affect the development of the fetal brain, and the common ones are anencephaly, megalencephaly, microcephaly, cerebral microsomia, neuronal ectopia, cerebral penetration malformation, etc. The abnormal development of the midline brain structures include corpus callosum dysplasia, hyaline septal defect or cyst. Intrauterine asphyxia during the perinatal period, cranial hemorrhage, pelvic stenosis, high forceps, excessive speed of delivery, and oversized fetus can cause fetal brain injury, all of which may also be the pathological basis for seizures. In addition, the complex partial seizures that appear clinically after the age of 10 or even after the age of 20-30 have been surgically and pathologically confirmed to be due to the compression of the fetal head during delivery and the downward extrusion of the brain, resulting in vascular compression due to temporal lobe hook gyrus herniation, causing acute ischemia of the temporal lobe floor, and finally causing temporal lobe sclerosis and seizures.
Developmental defects
Developmental defects, which are associated with 5.5% of first-episode epilepsy cases and 18% of causal epilepsy cases, are the most important secondary factor in children. Three to six out of every 1000 surviving births have cerebral palsy and/or moderate to severe mental retardation, and 1/3 of these will develop epilepsy.
IV. Febrile convulsions
From 3 months to 6 years after birth, febrile convulsions can occur in about 3% to 4% of children, 90% of which occur before 3 years of age, with 15 months being the peak of the first febrile convulsions. Recurrent seizures account for 30% to 40% of cases, and three or more seizures account for 10% of cases. The possibility of secondary epilepsy after febrile convulsions is 2% to 3%. However, the following risk factors are present: 1. seizures lasting more than 15 minutes. 2. limited seizures. 3. presence of abnormal neurological status prior to onset. 4. recurrent seizures within 24 hours. 5. siblings or both parents with a history of epilepsy. The chance of developing epilepsy rises to 6%-15% if 2 or more of these 5 items are present. Another study has shown that each occurrence of febrile convulsions increases the risk of recurrence by a factor of 1, while age, sex, type of first attack, first temperature, and family history are not associated with recurrence rates.
V. Cerebrovascular disease
Cerebrovascular disease is a major cause of seizures in the elderly. The incidence of post-stroke epilepsy is 7.2 to 8.9%. Recent studies have shown that the incidence of epilepsy is 3% within 1 year after the acute phase and increases to 8.9% in 10 years; the incidence of epilepsy varies among different cerebrovascular diseases, including cerebral hemorrhage 4.5% to 17.6%, subarachnoid hemorrhage 6.2% to 19.2%, cerebral thrombosis 3.9% to 15.6%, cerebral embolism 9.3% to 18.2%, transient ischemic attack 4.5 The percentage of transient ischemic attacks is 4.5-5.5%. Seizures can still occur after the acute phase of cerebrovascular disease, whether hemorrhagic or ischemic, and about 33% of ischemic cerebrovascular disease occurs later in life. The occurrence of epilepsy is not necessarily parallel to the size of the lesion and the severity of the disease, but is closely related to cortical damage, with the highest incidence of frontal, temporal, and parietal lobe damage.
Cerebral arteriovenous malformations often present with seizures in adulthood, with lesions near the central region and in the temporal lobe being the most common. According to statistics, the first symptom is epilepsy in half of the patients. They may present as partial seizures, disoriented seizures, and generalized tonic-clonic seizures. These patients may be accompanied by a history of migraine and/or subarachnoid hemorrhage. Intracranial venous or venous sinus thrombosis can also lead to epilepsy, with postpartum superior sagittal sinus thrombosis being the most common form of generalized tonic-clonic seizures, often accompanied by increased intracranial pressure and other limiting neurologic signs. The incidence of epilepsy in cerebrovascular disease is not very high, but the incidence of cerebrovascular disease itself is high, especially in the elderly population, so cerebrovascular disease is still one of the most common causes of epilepsy. Cerebral infarction or cerebral hemorrhage is more likely to cause seizures in children than in adults, 16% and 25%, respectively.
Craniocerebral trauma
Cranial trauma is also a common cause of seizures. It can be caused by gunshot, traffic accidents or even assault and accidents, and is related to the degree of trauma, trauma site and trauma time. Usually the more severe the cranial injury, the higher the incidence of epilepsy. There are generally 3 types of seizures according to the duration of onset: 1. Immediate seizures, which occur within a few hours after the injury, account for about 3%. It may be related to the stimulation of cranial hemorrhage, depression fracture, and brain cell damage, acetylcholine release, etc., and does not recur after one seizure. 2. Early seizure, within a few hours to 1 month after injury, accounting for 13%, may be related to trauma healing or secondary brain tissue reaction. 3. Late seizure, 1 month to several years after injury, accounting for 84%, mostly related to brain contusion, craniocerebral hematoma, cerebral scar. hematoma, meningeal brain scar, brain cyst, brain atrophy, etc.
VII. Intracranial infections
Intracranial infections, including bacterial, viral, fungal, parasitic and other infections, can lead to seizures.
Eight, brain tumor
Among symptomatic epilepsy, brain tumor is one of the common causes. About 1/3 of patients with intracranial tumors have seizures, while 50% of tumors in the cerebral hemispheres can have seizures. Slow-growing tumors such as meningiomas or low-grade gliomas are more likely to develop seizures than fast-growing tumors such as glioblastomas. Sometimes epilepsy is not only the first symptom, but even the only symptom of brain tumor, so it may be misdiagnosed as primary epilepsy.
IX. Metabolic disorders
Hypoglycemia, hyperglycemia, hypocalcemia, and uremia can all cause seizures. Most patients with blood glucose below 2.8 to 3.36 mmol/L (50-60 mg/dl) can have seizures. Common causes of hypoglycemia include islet cell tumors, insulin therapy, pituitary insufficiency, adrenocortical insufficiency, and hypothyroidism. Sudden rise in blood glucose and hyperosmolar state can trigger seizures.
X. Poisoning
Seizures can occur in 5% to 15% of alcoholics, and in both acute and chronic alcoholism, with 2/3 being associated with alcohol withdrawal. 20% or more of newly diagnosed adults with epilepsy have alcoholism as the most important risk factor. Seizures after alcohol cessation are usually chronic in alcoholics, but may also occur after only a few weeks of excessive drinking, and are more likely to occur with abrupt discontinuation or sudden reduction in high ethanol intake. The usual time between alcohol cessation and seizure is 18 to 24 hours, with 90% of seizures occurring 7 to 48 hours after alcohol cessation. Generally, there are often 2 to 4 seizures within 6 hours. 60% have multiple seizures, 3% have persistent status epilepticus, and 30% develop delirium tremens. In addition, ethanol may be a specific trigger in some epileptic patients, and the application of ethanol in epileptic patients may also be a trigger for seizures due to poor compliance, reduced absorption, and hepatic enzyme induction, which will lead to a decrease in the level of antiepileptic drugs. Seizures can occur with carbon monoxide poisoning, but are rare. Inhalation of high concentrations of oxygen or in hyperbaric chambers can have seizures.
XI. Other
The incidence of postoperative epilepsy after cranial surgery is related to the nature and location of the lesion, preoperative condition, and surgical access. The conditions with a high incidence of postoperative epilepsy include brain abscess, meningioma, glioma, and supratentorial aneurysm. Alzheimer’s disease 15% to 1/3 have seizures, and Pick’s disease can also have seizures but rarely. Neurocutaneous syndromes such as cerebral facet angiomatosis (Sturge-Weber syndrome), tuberous sclerosis, and neurofibromatosis can have seizures. About 5-10% of multiple sclerosis episodes have seizures. Systemic lupus erythematosus has seizures in 44% of patients with neurological comorbidities. Generalized tonic clonic seizures may appear early and are individually the first manifestation. Some drugs can induce seizures, such as penicillin (especially intravenous or intrathecal) and isoniazid, which consume a large amount of vitamin B6 in long-term application and can induce seizures if not supplemented; antidepressants such as promethazine and amitriptyline can cause seizures; drugs such as pentazocine, niclosamide, strychnine, camphor, indocin and other central stimulants such as overdose; other drugs such as insulin, prednisone, anticholinergics, aminophylline, chloroquine, chloroquine and other drugs can cause seizures. Other drugs such as insulin, prednisone, anticholinergics, aminophylline, chloroquine, baclofen, etc. can also induce seizures.