So
far, intravenous tissue-type plasminogen activator (tPA) and mechanical
removal of arterial blood clot (thrombectomy) are the only available
treatments for acute ischemic stroke. However, the short therapeutic
window and the lack of specialized stroke unit care make the overall
availability of both treatments limited.
(And tPA has an appalling failure rate of 88% getting to full recovery.) Additional agents to combine
with tPA administration or thrombectomy to enhance efficacy and improve
outcomes associated with stroke are needed. Stroke-induced inflammatory
processes are a response to the tissue damage due to the absence of
blood supply but have been proposed also as key contributors to all the
stages of the ischemic stroke pathophysiology. Despite promising results
in experimental studies,
inflammation-modulating treatments have not
yet been translated successfully into the clinical setting. This review
will (a) describe the timing of the stroke immune pathophysiology; (b)
detail the immune responses to stroke sift-through cell type; and (c)
discuss the pitfalls on the translation from experimental studies to
clinical trials testing the therapeutic pertinence of immune modulators.
125 references to support this. Has your doctor read a single one?
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