{"title":"癫痫持续状态在儿科实践:新生儿到青少年。","authors":"Asuri N Prasad, Shashi S Seshia","doi":"","DOIUrl":null,"url":null,"abstract":"<p><p>SE in the pediatric age group presents challenges in diagnosis and management. There is need for renewed consensus on the temporal definition of SE, both clinical and electrographic. SE in children exhibits an age-dependent vulnerability, with genetic predisposition and etiology as determinants of susceptibility. Nonepileptic phenomena may mimic SE. Clinical and electrographic SE in neonates are relatively rare, while serial (clinical and electrographic) and repetitive seizures are more common. Neurometabolic disease, chromosomal disorders, and abnormalities of cortical development are important etiological considerations. Abrupt discontinuation of or an aberrant response to AEDs can also precipitate SE. Metabolic perturbations and toxins can further aggravate the situation. Clinical and experimental data suggest that the longer a seizure lasts, the more difficult it becomes to control, and that seizures can have immediate and long-term adverse consequences on the immature and developing brain. Hence, treatment (usually with a benzodiazepine) should be started early in the clinical course. A trial of pyridoxine, biotin, or folinic acid should be considered in the appropriate clinical setting (e.g., neonates or young infants, in particular). Phenytoin/fosphenytoin and phenobarbital remain important treatment options. Pentobarbital and midazolam are preferred choices in the management of RSE. Once metabolic causes are excluded, children with RSE should be evaluated for surgical treatment early in the clinical course. Clinical guidelines based on best available evidence have to be periodically reviewed. The clinical consequences and management of electrographic SE, especially in the neonate, have to be addressed. Guidelines for continuous (video) EEG monitoring are needed to facilitate this task. AEDs that do not have an adverse effect on the developing brain have to be developed. Our review suggests a continuing need for prospective studies into all aspects of SE in the pediatric age group.</p>","PeriodicalId":7356,"journal":{"name":"Advances in neurology","volume":"97 ","pages":"229-43"},"PeriodicalIF":0.0000,"publicationDate":"2006-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Status epilepticus in pediatric practice: neonate to adolescent.\",\"authors\":\"Asuri N Prasad, Shashi S Seshia\",\"doi\":\"\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>SE in the pediatric age group presents challenges in diagnosis and management. There is need for renewed consensus on the temporal definition of SE, both clinical and electrographic. SE in children exhibits an age-dependent vulnerability, with genetic predisposition and etiology as determinants of susceptibility. Nonepileptic phenomena may mimic SE. Clinical and electrographic SE in neonates are relatively rare, while serial (clinical and electrographic) and repetitive seizures are more common. Neurometabolic disease, chromosomal disorders, and abnormalities of cortical development are important etiological considerations. Abrupt discontinuation of or an aberrant response to AEDs can also precipitate SE. Metabolic perturbations and toxins can further aggravate the situation. Clinical and experimental data suggest that the longer a seizure lasts, the more difficult it becomes to control, and that seizures can have immediate and long-term adverse consequences on the immature and developing brain. Hence, treatment (usually with a benzodiazepine) should be started early in the clinical course. A trial of pyridoxine, biotin, or folinic acid should be considered in the appropriate clinical setting (e.g., neonates or young infants, in particular). Phenytoin/fosphenytoin and phenobarbital remain important treatment options. Pentobarbital and midazolam are preferred choices in the management of RSE. Once metabolic causes are excluded, children with RSE should be evaluated for surgical treatment early in the clinical course. Clinical guidelines based on best available evidence have to be periodically reviewed. The clinical consequences and management of electrographic SE, especially in the neonate, have to be addressed. Guidelines for continuous (video) EEG monitoring are needed to facilitate this task. AEDs that do not have an adverse effect on the developing brain have to be developed. Our review suggests a continuing need for prospective studies into all aspects of SE in the pediatric age group.</p>\",\"PeriodicalId\":7356,\"journal\":{\"name\":\"Advances in neurology\",\"volume\":\"97 \",\"pages\":\"229-43\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2006-01-01\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Advances in neurology\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Advances in neurology","FirstCategoryId":"1085","ListUrlMain":"","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Status epilepticus in pediatric practice: neonate to adolescent.
SE in the pediatric age group presents challenges in diagnosis and management. There is need for renewed consensus on the temporal definition of SE, both clinical and electrographic. SE in children exhibits an age-dependent vulnerability, with genetic predisposition and etiology as determinants of susceptibility. Nonepileptic phenomena may mimic SE. Clinical and electrographic SE in neonates are relatively rare, while serial (clinical and electrographic) and repetitive seizures are more common. Neurometabolic disease, chromosomal disorders, and abnormalities of cortical development are important etiological considerations. Abrupt discontinuation of or an aberrant response to AEDs can also precipitate SE. Metabolic perturbations and toxins can further aggravate the situation. Clinical and experimental data suggest that the longer a seizure lasts, the more difficult it becomes to control, and that seizures can have immediate and long-term adverse consequences on the immature and developing brain. Hence, treatment (usually with a benzodiazepine) should be started early in the clinical course. A trial of pyridoxine, biotin, or folinic acid should be considered in the appropriate clinical setting (e.g., neonates or young infants, in particular). Phenytoin/fosphenytoin and phenobarbital remain important treatment options. Pentobarbital and midazolam are preferred choices in the management of RSE. Once metabolic causes are excluded, children with RSE should be evaluated for surgical treatment early in the clinical course. Clinical guidelines based on best available evidence have to be periodically reviewed. The clinical consequences and management of electrographic SE, especially in the neonate, have to be addressed. Guidelines for continuous (video) EEG monitoring are needed to facilitate this task. AEDs that do not have an adverse effect on the developing brain have to be developed. Our review suggests a continuing need for prospective studies into all aspects of SE in the pediatric age group.