1.What is hippocampal structure? The human brain is divided into two hemispheres, and each hemisphere is divided into frontal lobe, parietal lobe, occipital lobe and temporal lobe by some sulci and fissures, and each lobe is divided into several brain gyri, and the hippocampus is part of the temporal lobe, which is called hippocampus because its shape is similar to that of a seahorse, and is an important part of the medial structure of the temporal lobe. 2.What is hippocampal sclerosis? The basic pathological changes of hippocampal sclerosis are selective neural loss and glial cell proliferation in the hippocampus, and in the general structure, the hippocampus becomes smaller and harder. 3.The cause of hippocampal sclerosis? The causes of hippocampal sclerosis are still unclear. Based on the medical history of many patients, it is believed that the occurrence of hippocampal sclerosis is related to some adverse brain events such as heat cramps and head trauma during infancy and childhood. Nearly 1/3 of patients with temporal lobe epilepsy associated with hippocampal sclerosis had a history of heat cramps during infancy and childhood. However, recent data suggest that the above-mentioned causes may only be contributing factors, while the most fundamental cause may be minor abnormalities in the hippocampus development. 4. What is the relationship between hippocampal sclerosis and temporal lobe epilepsy? Before the 1950s, it was widely believed that hippocampal sclerosis might be the result of long-term seizures, but later a large amount of clinical data and basic research results showed that hippocampal sclerosis was before and temporal lobe epilepsy was after, and hippocampal sclerosis was an important cause of epilepsy, and long-term seizures could lead to hippocampal neuron loss, but not hippocampal sclerosis. 5. What are the clinical characteristics of hippocampal sclerosis temporal lobe epilepsy? Temporal lobe epilepsy with hippocampal sclerosis is a medial temporal lobe epilepsy syndrome with typical seizure syndromes, mainly complex partial seizures and secondary generalized seizures. Complex partial seizures are manifested as psychomotor seizures, with aura of epigastric discomfort, rising sensation and fear, etc. The aura may appear in isolation and continue to progress with blurred consciousness, mouth and hand automaticity, etc. There is usually a long period of blurred consciousness after the seizure. Temporal lobe epilepsy with hippocampal sclerosis is the most common type of epilepsy in adults. In addition to the seizure syndromes characteristic of medial temporal lobe epilepsy described above, there is also a history of febrile convulsions during infancy in 1/3 of cases, and 2/3 of cases will be insensitive to drug therapy and become intractable. As the disease progresses, there is mostly progressive memory loss manifested. 6. What is the diagnosis of hippocampal sclerotic temporal lobe epilepsy? First of all, medical history, clinical seizure characteristics and EEG characteristics are emphasized. In addition, most importantly, hippocampal sclerosis can be diagnosed by high-resolution magnetic resonance at present. 7.Treatment of hippocampal sclerosis temporal lobe epilepsy? Treatment of temporal lobe epilepsy with hippocampal sclerosis is similar to the treatment of other types of epilepsy, starting with medication, generally carbamazepine is preferred. However, most of them become resistant to medication as the course of treatment is prolonged and become intractable, requiring surgical treatment. It is worth noting that the surgical treatment should not be too conservative. In general, surgery can be performed when some conventional antiepileptic drugs such as carbamazepine, sodium valproate and phenytoin sodium do not work well, and long-term repeated trials of drug therapy are not advisable, because even if the seizures are controlled when the patient’s memory is severely impaired, the quality of life cannot be significantly improved. Currently, the main surgical approaches are anterior temporal lobectomy, transcortical ventriculo-selective hippocampal amygdala resection, trans-lateral fissure-selective hippocampal amygdala resection, and trans-inferior temporal selective hippocampal amygdala resection. All four surgical approaches emphasize the resection of medial temporal lobe structures. We appreciate that the four surgical approaches are basically similar in terms of resection of structures in the medial temporal lobe. When resecting the medial temporal lobe structures, regardless of the approach chosen, it is necessary to go through the inferior horn of the lateral ventricle. It is critical to be familiar with the anatomic landmarks associated with the inferior horn of the lateral ventricle. These landmarks include the lateral ventricular sulcus, lateral bulge, hippocampal fissure, choroidal fissure, internal olfactory sulcus, and terminal stripe. The same is true for the resection of medial temporal lobe structures, including the hippocampus, hook gyrus, amygdala, and parahippocampal gyrus. Of course, each surgical approach has its own characteristics. We now prefer transcortical ventricular selective hippocampal amygdala resection and transtemporal selective hippocampal amygdala resection. Because in these two surgeries, only a small incision is needed in the temporal region and a small bone window is made in the temporal region, the surgery is less invasive and is a minimally invasive lock-hole surgery. 8. What are the results of surgical treatment for temporal lobe epilepsy with hippocampal sclerosis? The rate of complete control of epilepsy after surgery is over 80%. Other postoperative conditions: Early-onset postoperative epilepsy: Early-onset postoperative epilepsy refers to seizures that appear within 1 week after surgery, mostly tonic clonic seizures. Early-onset postoperative tonic-clonic seizures may be related to postoperative acute cortical damage stimulation, and we appreciate that they are more likely to be related to the temporary discontinuation of conventional antiepileptic drugs in the postoperative period. Therefore, if there is no obvious vomiting after postoperative anesthesia awakening, the preoperative medication is promptly resumed. In the transitional phase, intramuscular, subcutaneous and intravenous preparations can be applied instead. Early-onset postoperative seizures that are inconsistent with the habitual seizure form, especially when tonic-clonic seizures are present, do not predict a poor long-term outcome of surgery. The running down phenomenon was introduced by Rasmussen in 1962, when it was found that some patients had seizures for the first few years after temporal lobectomy, but the seizures gradually decreased to a cessation. In general, this phenomenon occurs in patients who have improved the frequency and extent of epileptic seizures after surgery, and rarely in patients with poor control. Late recurrence refers to the absence of seizures after surgery, followed by seizures one or more years later. The mechanism of late recurrence is unclear and may be related to the maturation and expansion of the secondary local epileptogenic focus. Complications: In a strict sense, new postoperative complications related to surgical operation include two cases: one is functional impairment caused by injury to non-resected target neurovascular tissue, etc., which can be called complications, and the other is functional deficit caused by removal of target brain tissue, which should not be called complications. Under the current microscopic technology conditions, the main complications include: (1) vasospasm: In trans-lateral fissure surgery, it is necessary to separate the lateral fissure, so it is easy to cause spasm of the internal carotid artery and middle cerebral artery, resulting in postoperative hemiplegia, aphasia and other complications. The operation must be lightly rubbed, avoid electrocautery when operating in the lateral fissure area, keep it moist, and promptly apply cherry soda cotton or gelatin sponge. Postoperatively, hemostatic drugs are generally not used. (2) Diplopia: When removing the medial temporal lobe structure, especially the hook gyrus, to the medial aspect of the cerebellar curtain cut, it is easy to cause damage to the motoneurotic nerve and the talocrural nerve, causing diplopia. The cause of diplopia is due to intraoperative damage to the talocrural nerve, which usually recovers within 1 month.