Published online by Cambridge University Press: 02 November 2009
The brain responds dynamically to ischemic insult. A brief period of focal ischemia may disrupt synaptic transmission and produce transient neurological deficits without causing permanent tissue injury. A somewhat more severe ischemic insult may sufficiently disrupt the cellular energetic state to impair maintenance of ionic gradients across cell membranes, producing cytotoxic edema. Early restoration of blood flow may permit cellular re-energization and restoration of ionic gradients, with edema resolution. However, some cells that initially restore membrane integrity experience a late, secondary stage of injury and delayed cell death. These findings, previously elucidated in animal models, have now been demonstrated for the first time in acute human brain ischemia by diffusion magnetic resonance imaging (MRI).
Standard brain imaging techniques, computed tomography (CT) and conventional MRI, are insensitive to these dynamic and regionally varying neural parenchymal responses to tissue ischemia. In contrast, the novel MRI technique of diffusion imaging permits visualization of these critical tissue processes, affording new insights into the physiopathology of human cerebral ischemia. We will here review recent diffusion MRI findings in two settings of transient cerebral ischemic insult in human patients: spontaneous transient ischemic attacks and thrombolysis induced cerebral reperfusion.
Transient ischemic attack
Transient ischemic attacks (TIAs) are defined as neurological symptoms due to focal cerebral ischemia that resolve completely within 24 hours. The 24 hour cutoff employed in this definition was first promulgated in the 1950s, based on limited data.