Intracerebral hemorrhage (ICH) is associated with high mortality and disability. Surgical treatment is the most preferred option for severe ICH. However, increasing evidence has shown that the duration of secondary brain injury (SBI) is longer and the damage is often more serious than the primary brain injury (PBI) induced by the directly mechanical effects of the hematoma.
The pathophysiological changes of the cascade events during SBI including red blood cell lysis, stimulation of the thrombin cascade, inflammatory response, cell apoptosis and necrosis, oxidative stress, etc., which lead to demyelination, neuronal death, glial scarring around the area of the initial damage, disruption of the blood-brain barrier and consequent brain edema. A better understanding of SBI following ICH will pave the way for developing new therapeutic option to significantly increase the survival rate and improves quality of life for survivors.
This Research Topic will provide a comprehensive overview on SBI following ICH, from underlying molecular and cellular pathophysiology to clinical transformation. We welcome the submission of original articles, reviews, perspectives and technical reports, but not limited to, the following topics:
• Pathophysiology mechanisms underlying the secondary brain damage.
• Drugs targeting on the immune or inflammatory response, cell apoptosis and necrosis, and signaling pathways, etc. involved in secondary brain damage following ICH.
• Inflammatory biomarkers or any other factors predicting the occurrence or prognosis of ICH.
• The application of novel technologies in studying ICH.
Intracerebral hemorrhage (ICH) is associated with high mortality and disability. Surgical treatment is the most preferred option for severe ICH. However, increasing evidence has shown that the duration of secondary brain injury (SBI) is longer and the damage is often more serious than the primary brain injury (PBI) induced by the directly mechanical effects of the hematoma.
The pathophysiological changes of the cascade events during SBI including red blood cell lysis, stimulation of the thrombin cascade, inflammatory response, cell apoptosis and necrosis, oxidative stress, etc., which lead to demyelination, neuronal death, glial scarring around the area of the initial damage, disruption of the blood-brain barrier and consequent brain edema. A better understanding of SBI following ICH will pave the way for developing new therapeutic option to significantly increase the survival rate and improves quality of life for survivors.
This Research Topic will provide a comprehensive overview on SBI following ICH, from underlying molecular and cellular pathophysiology to clinical transformation. We welcome the submission of original articles, reviews, perspectives and technical reports, but not limited to, the following topics:
• Pathophysiology mechanisms underlying the secondary brain damage.
• Drugs targeting on the immune or inflammatory response, cell apoptosis and necrosis, and signaling pathways, etc. involved in secondary brain damage following ICH.
• Inflammatory biomarkers or any other factors predicting the occurrence or prognosis of ICH.
• The application of novel technologies in studying ICH.
