Traumatic brain injury (TBI) remains a leading cause of mortality and morbidity worldwide. A major focus of preclinical research has focused on understanding the mechanisms of acute cell death after TBI; however, translation of these findings into the clinic has failed to improve long-term patient outcomes. Recent work suggests astrocytes, the predominant cell type within the human brain, may actively contribute to neurological demise by exacerbating secondary brain injury after TBI. Along these lines, astrocytes may promote neuroinflammation, increase the development of cerebral edema, and contribute to elevated intracranial pressure after brain injury. The primary goal of this mini-review is to summarize the growing body of literature that suggests reactive astrocytes influence the brain response to TBI. To maintain focus, we will limit our discussion to the mechanisms of cerebral edema.
- Cerebral blood flow
- Intracranial pressure
ASJC Scopus subject areas
- Clinical Neurology
- Cardiology and Cardiovascular Medicine