• Publications
  • Influence
Metamorphosis of Subarachnoid Hemorrhage Research: from Delayed Vasospasm to Early Brain Injury
TLDR
The pathological mechanisms of early brain injury after SAH are reviewed and the status of current therapies are summarized, finding that many of these mechanisms evolve with time and participate in the pathogenesis of delayed ischemic injury and poor outcome.
Cerebral vasospasm after subarachnoid hemorrhage: the emerging revolution
TLDR
Alternative causes of neurological deterioration and poor outcome after subarachnoid hemorrhage are proposed, including delayed effects of global cerebral ischemia, thromboembolism, microcirculatory dysfunction and cortical spreading depression.
NLRP3 inflammasome contributes to inflammation after intracerebral hemorrhage
TLDR
This work investigated whether NLRP3 knockdown decreases neutrophil infiltration, reduces brain edema, and improves neurological function in an intracerebral hemorrhage mouse model, and determined whether mitochondrial reactive oxygen species (ROS) governed by mitochondrial permeability transition pores (mPTPs) would triggerNLRP3 inflammasome activation following ICH.
Early Brain Injury, an Evolving Frontier in Subarachnoid Hemorrhage Research
TLDR
It could be argued that the treatment of EBI may successfully attenuate some of the devastating secondary injuries and improve the outcome of patients with SAH and the reversal of vasospasm does not appear to improve patient outcome.
Signaling Pathways for Early Brain Injury after Subarachnoid Hemorrhage
TLDR
It is concluded that VEGF contributes to early brain injury after SAH by enhancing the activation of the MAPK pathways, and that the inhibition of these pathways might offer new treatment strategies for SAH.
Mechanisms of Early Brain Injury after Subarachnoid Hemorrhage
TLDR
Experimental data suggest that the apoptotic cascades occur very early after the initial insult and may be related directly to physiologic sequela commonly associated with SAH.
...
...