Association of Neuroinflammation with Electroencephalographic Consequences of Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) is a form of hemorrhagic stroke that poses a serious public health concern due to its high mortality rate and long-term complications including neurobehavioral impairment and the development of lifelong epilepsy. One mechanism underlying these deficits is the prominent neuroinflammatory response observed throughout the brain after SAH and its potential role in driving epileptogenesis. While the development of abnormal electroencephalographic (EEG) activity in patients suffering from SAH is a well-documented epidemiological observation, to date no animal models have been developed to study these particular consequences of SAH. Here, we identify novel inflammatory biomarkers in patients with SAH, develop novel methods for analyzing EEG changes in established animal models of epilepsy, and then apply these methods for the first time in an animal model of SAH. Finally, we characterize the relationship between intracranial hemorrhage, activation of microglia, and modulate these inflammatory responses with the immunomodulatory agent fingolimod. Investigating the role of immune and inflammatory responses within the central nervous system after SAH offers the potential for the discovery of novel mechanistic and therapeutic targets which may have long-lasting benefits in survivors of SAH.