Introduction

MRI is supremely sensitive to the abnormal accumulation of water, much more so than is CT, so it might be expected that MRI is superior to CT in the detection of ischemic infarction. Although this principle is applicable to subacute infarction, it is not the case in the first 6 hours after the onset of the ischemic insult. A basic understanding of the pathological processes which precede infarction is necessary in order to understand their MRI manifestations.

Pathology of ischemic infarction

Deprivation of oxygen supply to neurones, whether as a result of embolus, thrombosis or prolonged hypotension, leads initially to malfunction in as little as a few seconds, e.g. a Stokes-Adams attack, in which brainstem ischemia induces unconsciousness within seconds of cardiac asystole. If the ischemic insult is prolonged the highly energy dependent sodium pump mechanism, which is responsible for maintaining a tenfold difference in extracellular to intracellular sodium concentration, begins to fail and sodium, water and calcium ions pass from the extracellular to the intracellular space. The cell swells, producing ‘cytotoxic’ edema and the extracellular space is simultaneously reduced. If the diminished oxygen supply is maintained, the less energy-dependent capillary endothelial cells start to lose their function and the normally tight junctions between them begin to lose their integrity. Intravascular fluid leaks into the extravascular space, producing ‘vasogenic’ edema. Vasogenic edema spreads easily through the white matter due to its relatively less dense cellular density and more capacious extravascular space.