Focal cerebral ischemia and neurovascular protection: a bench-to-bedside update
Robert C Tasker1, Elizabeth D Duncan
1aDepartment of Neurology bDivision of Critical Care Medicine, Department of Anesthesiology, Perioperative and Pain Medicine, Boston Children's Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Purpose Of Review:
To date, many pharmacological approaches, or combination of approaches, have been applied to experimental models of focal cerebral ischemia (FCI), but their translation to clinically effective agents has proved unsuccessful. To date, only thrombolysis with recombinant tissue-type plasminogen activator, or other 'clot-breaking' or 'clot-removal' approaches, have proved effective for acute stroke. This review, therefore, focuses on the 'vascular' phenomena involved in the development of FCI.
Recent Findings:
Recent advances in the experimental literature on FCI describe the microvascular characteristics of the ischemic penumbra, the consequences of cortical spreading depression on impairing cerebral perfusion, and the potential neuroprotective mechanisms of ischemic preconditioning via antithrombotic effects on the neurovascular unit.
Summary:
This review provides a perspective about the neurovascular components contributing to the pathophysiology of FCI, and some relevant clinical strategies available on the horizon that hold promise for improved cerebral perfusion in FCI.
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