Pathophysiologic mechanisms of acute ischemic stroke: An overview with emphasis on therapeutic significance beyond thrombolysis

Jan 16, 2010Pathophysiology : the official journal of the International Society for Pathophysiology

Key biological processes in sudden stroke and their treatment beyond clot-busting drugs

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Abstract

Stroke is a major cause of death and disability globally, with only one FDA-approved treatment available.

The pathophysiology of stroke involves complex processes such as neuronal death, inflammation, and oxidative damage.
Restoration of cerebral blood flow and minimizing ischemic damage are key therapeutic goals in stroke management.
Current treatments include carotid endarterectomy and thrombolytics, but they remain suboptimal in effectiveness.
Only tissue-type plasminogen activator (tPA) is FDA-approved for ischemic stroke, with a limited therapeutic window.
There is ongoing frustration in finding effective neuroprotective agents for stroke.

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Stroke is a serious neurological disease, and constitutes a major cause of death and disability throughout the world. The pathophysiology of stroke is complex, and involves excitotoxicity mechanisms, inflammatory pathways, oxidative damage, ionic imbalances, apoptosis, angiogenesis and neuroprotection. The ultimate result of ischemic cascade initiated by acute stroke is neuronal death along with an irreversible loss of neuronal function. Therapeutic strategies in stroke have been developed with two main aims: restoration of cerebral flow and the minimization of the deleterious effects of ischemia on neurons. Intense research spanning over the last two decades has witnessed significant therapeutic advances in the form of carotid endarterectomy, thrombolytics, anticoagulant therapy, antiplatelet agents, neuroprotective agents, and treating associated risk factors such as hypertension and hyperlipidemia. However, the search for an effective neuroprotectant remains frustrating, and the current therapeutic protocols remain suboptimal. Till date only one FDA-approved drug is available for ischemic stroke; i.e., the serine protease tissue-type plasminogen activator (tPA), utility of which is limited by short therapeutic window. The objective of this review is to critically evaluate the major mechanisms underlying stroke pathophysiology, with emphasis on potential novel targets for designing newer therapeutic modalities.

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