Progress of the pathogenesis of status epilepticus and brain injury / 国际儿科学杂志

ABSTRACT

The pathogenesis of status epilepticus is closely associated with brain injury. Some animals experiments have proved that the activity of calcium / calmodulin-dependent protein kinase 2 ( CaM kinase Ⅱ ) ,oxidative stress, and the imbalance of nervous immune-endocrine factors are not only involved in the mechanisms of status epilepticus, but also act as the initial factor in neuronal injury. The pathophysiological changes after SE,such as acute brain ischemia, hypoxia and the reduced glucose utilization, over-excited neurons, N-methyl-Daspartate (NMDA) and non-NMDA receptor activated, a large amount of cation influx, can give rise to acute necrosis of neurons, also initiate the expression of apoptotic genes, at last leading to apoptosis by cell apoptotic enzymes cascade reaction. Studies have found that the pathway of death receptor activation, mitochondrial damage and endoplasmic reticulum stress mediated the neuronal apoptotic signal transduction after SE.