OF PROPOSED RESEARCH In ischemic stroke, spreading depolarizations (SD) are widely recognized to be a major contributor in the progression of tissue damage and expansion of the core region into the ischemic penumbra - even after the restoration of blood flow. While short-term experimental data in anesthetized animals demonstrate the significant contribution of spreading depolarizations on infarct expansion in the initial hours after the onset of ischemia, long-term observations of SD triggers, frequency of occurrence, patterns of spread and initiation, and the impact on stroke outcome remain largely unknown. We propose to study the long- term evolution of SDs and the role of reperfusion after focal cerebral ischemia using a novel high-density cortical ?ECoG arrays (61 electrodes) non-anesthetized freely moving rats. We will provide crucial information about the long term contribution of SDs to secondary progression of tissue damage, delineate post-injury phases and SD triggers (i.e. physical stimulation) which is of high interest for the human ICU setting and could pave the way for phase specific, personalized new treatment strategies to inhibit secondary stroke progression (i.e. SD suppression).
statement: Spreading depolarizations contribute significantly to secondary cerebral infarct progression and stroke deterioration. The proposed study using novel high density cortical ?ECoG-arrays will provide crucial information about the long term contribution of SDs to secondary progression of tissue damage after stroke in freely moving rats. These recordings are likely to delineate post-injury phases and SD triggers (i.e. physical stimulation) which is of high interest for the human ICU setting and could pave the way for phase specific, personalized new treatment strategies to inhibit secondary stroke progression.
