Developmental and epileptic encephalopathy (DEE) is a group of diseases that severely affects the neurological development of children, characterized by frequent seizures and significant neurodevelopmental impairments. These diseases not only impact the quality of life of affected children but also impose a heavy burden on families and society. In recent years, the development of brain network theory has provided a new perspective on understanding the pathological mechanisms of DEE, especially the role of structural and functional brain networks in the process of epilepsy. This review systematically summarized the research progress of structural and functional brain networks in DEE, highlighted their importance in seizure activity, disease progression, and prognosis evaluation.
目的 探讨胰性脑病的可能的发病机制、发病情况及防治措施.方法 计算机检索中文科技期刊全文数据库(1989～2004),收集有关胰性脑病的临床研究,并进行统计分析.结果 共纳入43篇文献,435例患者.胰性脑病在重症急性胰腺炎中的发病率远高于轻症急性胰腺炎;发病年龄趋向中、老年;病死率为43.67%;病因仍以胆系疾病为主;伴发低氧的几率不高于未并发胰性脑病患者.结论 胰性脑病的发生可能是多因素共同作用的结果,仍需进一步探讨其发病机制.血清髓鞘碱性蛋白有望成为有价值的诊断指标.防治以治疗原发病急性胰腺炎为主,重在预防.胰酶抑制剂和早期营养支持有一定预防作用.
Objective To study the effects of malondialdehyde (MDA), superoxide dismutase (SOD) and tumor necrosis factor-α (TNF-α) on brain tissue in rats with pancreatic encephalopathy (PE). Methods Thirty-six Wistar rats were randomly divided into control group (n=6) and PE model group (n=30). In control group, rats were injected with normal saline by internal carotid artery (0.1 ml/100 g) and were killed on the first day after the injection. In PE model group, rats were injected with phospholipases A2 (0.1 ml/100 g, 1 000 U/0.1 ml) by internal carotid artery, to establish animal model of PE in rat and 10 rats were killed on day 1, 3, 7 respectively after the injection. The changes of water content in the brain were measured. Leucocytes aggregation and margination in the microvessels, and the changes of cerebral cells and nerve fibers were observed. The levels of MDA, TNF-α and the activity of SOD were tested in the brain homogenate in rats. Results In PE model group, water contents of brain increased; The phenomena of leucocytes accumulation and margination, cellular edema of neurons and demyelination of nerve fibers became more obvious; The levels of MDA and TNF-α increased significantly than those in the control group, while the activity of SOD reduced (P＜0．05， P＜0.01)． Conclusion Inthe rat model of PE, MDA, SOD, and TNF-α play important roles on the occurrence and development of brain injury.
ObjectiveTo investigate the effect of dexamethasone on mammalian target of rapamycin (mTOR) expression of astrocytes in hippocampus of rats with sepsis associated encephalopathy (SAE). MethodsTotally, 90 cases of 30-day-old male Wistar rats were randomly divided into sham-operation group (n=10) and cecal ligation and puncture (CLP) group (n=80). Models of rats with sepsis were established by CLP. At 12 hours after CLP, if rats appeared lower neurobehavioral scores, abnormal electroencephalogram (EEG) and somatosensory evoked potential (SEP), they were diagnosed with SAE. And then, they were randomly divided into non-treated group and dexamethasone group. Rats in the dexamethasone group were injected with dexamethasone (1 mg/kg) via tail vein every other day for a total of 3 times. The same dose of saline was used in the non-treated group. The neurobehavioral score was measured, SEP and EEG were examined in the age of 40 days, and then the rats were killed and the hippocampus was taken. Expressions of mTOR protein were measured by Western blot. The glial fibrillary acidic protein (GFAP) and mTOR were detected by immunofluorescence assay, and the number of positive cells was calculated by image analysis system software. ResultsSix of 80 CLP rats died in 12 hours after operation, and 28 of 74 rats were diagnosed as SAE because they appeared lower neurobehavioral scores, abnormal EEG and SEP at 12 hours after CLP. The incidence of SAE was 37.84% (28/74). In the age of 40 days, compared with non-treated group, neurobehavioral score of rats in the dexamethasone group was low, the amount of alpha waves in EEG reduced, delta waves increased, the amplitude of P1 waves in SEP was decreased, and the latencies of P1 and N1 waves were prolonged (P＜0.05). GFAP immunofluorescence staining showed astrocytic body and processes were small in the sham operation group. However, astrocytes in the non-treated group had large body and hypertrophic processes, and compared with the sham operation group, the number of these cells increased significantly (P＜0.05). Astrocytic body and processes were small in the dexamethasone group compared with the non-treated group, and the number of cells also decreased (P＜0.05). The mTOR positive astrocytes in the non-treated group were more than those in the sham operation group (P＜0.05). But mTOR positive astrocytes in the dexamethasone group were fewer than those in the non-treated group (P＜0.05). ConclusionsAstrocytes are activated in the hippocampus of rats with SAE. They show features of reactive hyperplasia, and the expression of mTOR is up-regulated, while dexamethasone can inhibit effects on these.
Seventeen cases of pancreatic encephalopathy (PE) with acute pancreatitis were studied retrospectively. It was found that on the basis of brain damage caused by pancreatic enzyme, many factor might play a role in the development of PE. It suggests that PE should not be accepted as an operative indication separately in severe acute pancreatitis. Chinese medicine can benefit the patient in the treatment of this disease. Operation is the only choice while patient get worsened even after appropriate and enough nonoperative therapy, as well as while pancreatic necrosis become infected or pancreatic abcess formed. Mortality of PE in this series is 52.9%, slightly less than the level (66.7%-100%) reported by other authors.
Delayed encephalopathy due to acute carbon monoxide poisoning (DEACMP) is a serious complication of acute carbon monoxide poisoning. Patients with DEACMP often present with cognitive impairment, abnormal mental behavior, extrapyramidal system symptoms, pyramidal system symptoms, and may also have focal cortical dysfunction, which is closely related to the poor prognosis of the patients. Current research shows that the occurrence of DEACMP is related to multiple factors such as immune disorders, and glucocorticoids can exert certain therapeutic effects through immunosuppression. This article reviews the risk factors of DEACMP, the clinical research progress and possible mechanisms of glucocorticoid treatment for DEACMP, providing more references for the clinical treatment of DEACMP.