摘要

Status epilepticus is often associated with endothelial dysfunction and increased vessels permeability. We discuss here the direct role of blood-brain barrier (BBB) dysfunction in epileptogenesis and brain damage. On the cellular level, astrocytes respond early to the efflux of serum proteins in the presence of dysfunctional BBB, with activation of the innate immune system and disturbed homeostasis of extracellular potassium and glutamate. In turn, there is enhanced excitability of neurons and altered network connectivity. Transforming growth factor beta (TGF-beta) signaling appears to be a potential new target for the prevention of epileptogenesis and secondary damage following status epilepticus.

  • 出版日期2011-10