Imaging of stroke: Part 2, Pathophysiology at the molecular and cellular levels and corresponding imaging changes

Stroke is the third leading cause of death and the leading cause of severe disability. During the "decade of the brain" in the 1990s, the most promising development was the treatment of acute ischemic stroke. It is thought to result from a cascade of events from energy depletion to cell death. In the initial minutes to hour, clinical deficit does not necessarily reflect irreversible damage. The final outcome and residual deficit will be decided by how fast reperfusion is achieved, which in turn depends on how early the diagnosis is made. This article explains the pathophysiology of stroke at the molecular and cellular levels with corresponding changes on various imaging techniques.

The pathophysiology of stroke has several complex mechanisms. Understanding these mechanisms is essential to derive neuroprotective agents that limit neuronal damage after ischemia. Imaging and clinical strategies aimed at extending the therapeutic window for reperfusion treatment with mechanical and pharmacologic thrombolysis will add value to existing treatment strategies. Acute ischemic stroke is defined as abrupt neurologic dysfunction due to focal brain ischemia resulting in persistent neurologic deficit accompanied by characteristic abnormalities on brain imaging. Knowledge of the pathophysiologic mechanisms of neuronal injury in stroke is essential to target treatment. Neuroprotective and thrombolytic agents have been shown to improve clinical outcome. Physiologic imaging with diffusion-weighted imaging (DWI) and perfusion CT and MRI provide a pathophysiologic substrate of evolving ischemic stroke.