Research specifically targeting intracranial hemorrhage (ICH) has enjoyed a rejuvenated focus. This disease confers substantial morbidity and mortality worldwide. Its pathogenesis and potential treatments differ markedly from ischemic stroke. Substantial research focus ranges from toxic mediators of injury to pathways for neurogenesis. On the clinical side, the focus recently relates to stopping ongoing bleeding.
The 26th Princeton Conference facilitated the presentation of state-of-the-art basic and clinical ICH research. Dr John Zhang challenged everyone to consider that more than just vasospasm is responsible for neurological injury in subarachnoid hemorrhage. The concept of early brain injury involves several putative mechanisms that may be responsible for poor outcome in this disease. Dr Guohua Xi presented the intriguing story of thrombin’s influence on neurogenesis, angiogenesis, and plasticity in the brain after ICH. Dr Magdy Selim presented the early clinical work of using deferoxamine to chelate iron in the brain and prevent iron-related toxicity. Dr Jaroslaw Aronowski demonstrated the critical role of the microglia in containing the ICH and preventing neurotoxicity. Finally, Dr William Young examined the factors that make arteriovenous malformations bleed and how to remedy this occurrence.
The future directions of ICH research and treatment are dependent on finding new targets for intervention. They will likely be based on keen observations of the role blood components have on injury, on prevention of the injury from occurring, containing it once it begins, and recovery of brain function after injury. For us to truly understand this disease, all possible mechanisms must be considered. For ICH, this involves mechanical, toxic, inflammatory, coagulation, and vascular biology issues, just to name a few. It is greatly encouraging to see that researchers are broadening their view of therapeutic targets for ICH and that therapies have already transitioned from bench to bedside.
- Accepted July 30, 2008.