Logo for the University of Illinois at Chicago
    • Login
    View Item 
    •   INDIGO Home
    • Medicine, College of
    • College of Medicine at Chicago
    • Neurology and Rehabilitation, Department of
    • Publications - Neurology and Rehabilitation
    • View Item
    •   INDIGO Home
    • Medicine, College of
    • College of Medicine at Chicago
    • Neurology and Rehabilitation, Department of
    • Publications - Neurology and Rehabilitation
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Delayed Cerebral Ischemia after Subarachnoid Hemorrhage: Beyond Vasospasm and Towards a Multifactorial Pathophysiology.

    Thumbnail
    View/Open
    Main Article (958.9Kb)
    Date
    2017-10-23
    Author
    Geraghty, Joseph, R.
    Testai, Fernando, D.
    Publisher
    Current Medicine Group
    Metadata
    Show full item record
    Abstract
    PURPOSE OF REVIEW: Delayed cerebral ischemia (DCI) is common after subarachnoid hemorrhage (SAH) and represents a significant cause of poor functional outcome. DCI was mainly thought to be caused by cerebral vasospasm; however, recent clinical trials have been unable to confirm this hypothesis. Studies in humans and animal models have since supported the notion of a multifactorial pathophysiology of DCI. This review summarizes some of the main mechanisms under investigation including cerebral vascular dysregulation, microthrombosis, cortical spreading depolarizations, and neuroinflammation. RECENT FINDINGS: Recent guidelines have differentiated between DCI and angiographic vasospasm and have highlighted roles of the microvasculature, coagulation and fibrinolytic systems, cortical spreading depressions, and the contribution of the immune system to DCI. Many therapeutic interventions are underway in both preclinical and clinical studies to target these novel mechanisms as well as studies connecting these mechanisms to one another. Summary: Clinical trials to date have been largely unsuccessful at preventing or treating DCI after SAH. The only successful pharmacologic intervention is the calcium channel antagonist, nimodipine. Recent studies have provided evidence that cerebral vasospasm is not the sole contributor to DCI and that additional mechanisms may play equal if not more important roles.
    Citation
    Geraghty, J. R. and Testai, F. D. Delayed Cerebral Ischemia after Subarachnoid Hemorrhage: Beyond Vasospasm and Towards a Multifactorial Pathophysiology. Current Atherosclerosis Reports. 2017. 19(12). 10.1007/s11883-017-0690-x.
    Subject
    Cortical spreading depolarization
    Delayed cerebral ischemia
    Neuroinflammation
    Type
    Article
    Date available in INDIGO
    2018-06-19T20:18:36Z
    URI
    http://hdl.handle.net/10027/22355
    Collections
    • Publications - Neurology and Rehabilitation

    DSpace software copyright © 2002-2015  DuraSpace
    Contact Us | Send Feedback | Privacy Statement
    Theme by 
    Atmire NV

    Browse

    All of INDIGOCommunities & CollectionsBy Issue DateAuthorsTitlesSubjectsThis CollectionBy Issue DateAuthorsTitlesSubjects

    My Account

    LoginRegister

    Statistics

    View Usage Statistics

    DSpace software copyright © 2002-2015  DuraSpace
    Contact Us | Send Feedback | Privacy Statement
    Theme by 
    Atmire NV